essay neuro exam

NeurologyResidents

Resources for future neurologists.

• Neurological Examination Templates

Normal Neurological Examination

GEN : NAD, pleasant, cooperative CVS : RRR, no carotid bruit CHEST : No signs of resp distress, on room air ABD : Soft, NTTP NEURO MENTAL STATUS: AAOx3, memory intact, fund of knowledge appropriate LANG/SPEECH : Naming and repetition intact, fluent, follows 3-step commands CRANIAL NERVES: II: Pupils equal and reactive, no RAPD, no VF deficits, normal fundus III, IV, VI: EOM intact, no gaze preference or deviation, no nystagmus. V: normal sensation in V1, V2, and V3 segments bilaterally VII: no asymmetry, no nasolabial fold flattening VIII: normal hearing to speech IX, X: normal palatal elevation, no uvular deviation XI: 5/5 head turn and 5/5 shoulder shrug bilaterally XII: midline tongue protrusion MOTOR : 5/5 muscle power in Rt shoulder abductors/adductors, elbow flexors/extensors, wrist flexors/extensors, finger abductors/adductors.  5/5 in Rt hipflexors/extensors, knee flexors/extensors, ankle dorsiflexors and planter flexors.

5/5 muscle power in Lt shoulder abductors/adductors, elbow flexors/extensors, wrist flexors/extensors, finger abductors/adductors.  5/5 in Lt hipflexors/extensors, knee flexors/extensors, ankle dorsiflexors and planter flexors.

REFLEXES : 2/4 throughout, bilateral flexor plantar response, no Hoffman's, no clonus SENSORY : Normal to touch, pinprick, vibration, temp all limbs No hemineglect, no extinction to double sided stimulation (visual & tactile) Romberg absent COORD : Normal finger to nose and heel to shin, no tremor, no dysmetria STATION : normal stance, no truncal ataxia GAIT : Normal; patient able to tip-toe, heel-walk.

GEN : NAD, pleasant, cooperative

CVS : RRR, no carotid bruit

CHEST : No signs of resp distress, on room air

ABD : Soft, NTTP

Mental Status:  Alert and oriented x3. Language is fluent with good comprehension.

Cranial Nerve:  Pupils are equal, round, and reactive to light. Visual fields are intact to confrontation. Normal fundi. Ocular movements are intact. Face is symmetric at rest and with activation with intact sensation throughout. Hearing intact to finger rub bilaterally. Muscles of tongue and palate activate symmetrically. No dysarthria. Strength is full in sternocleidomastoid and trapezius bilaterally.

Motor:  Muscle bulk and tone are normal. Strength is 5/5 in all four extremities both proximally and distally. Intact fine motor movements bilaterally. There is no pronator drift or satelliting on arm roll.

Sensory:  Sensation is intact to light touch, pinprick, vibration, and proprioception throughout. Romberg is negative.

Reflexes:  2+ and symmetric at the biceps, triceps, brachioradialis, patella, and Achilles bilaterally. Plantar response is flexor bilaterally.

Coordination:  No dysmetria on finger-nose-finger or heel-knee-shin. Normal rapid alternating movements. Fast finger tapping with normal amplitude and speed.

Gait:  Narrow based with normal stride length and good arm swing bilaterally. Able to walk on heels, toes, and in tandem.

• Mental status:  The patient is alert, attentive, and oriented.
• Speech : clear and fluent with good repetition, comprehension, and naming. She recalls 3/3 objects at 5 minutes.
• Cranial nerves: CN II: Visual fields are full to confrontation. Fundoscopic exam is normal with sharp discs. Pupils are 4 mm and briskly reactive to light. Visual acuity is 20/20 bilaterally. CN III, IV, VI: EOMI, no nystagmus, no ptosis CN V: Facial sensation is intact to pinprick in all 3 divisions bilaterally. CN VII: Face is symmetric with normal eye closure and smile. CN VII: Hearing is normal to rubbing fingers CN IX, X: Palate elevates symmetrically. Phonation is normal. CN XI: Head turning and shoulder shrug are intact CN XII: Tongue is midline with normal movements and no atrophy.
• Motor : There is no pronator drift of out-stretched arms. Muscle bulk and tone are normal. Strength is full bilaterally.
•   Reflexes : Reflexes are 2+ and symmetric at the biceps, triceps, knees, and ankles. Plantar responses are flexor.

Sensory : Light touch, pinprick, position sense, and vibration sense are intact in fingers and toes.

Coordination : Rapid alternating movements and fine finger movements are intact. There is no dysmetria on finger-to-nose and heel-knee-shin. There are no abnormal or extraneous movements. Romberg is absent.

Gait/Stance: Posture is normal. Gait is steady with normal steps, base, arm swing, and turning. Heel and toe walking are normal. Tandem gait is normal when the patient closes one of her eyes.

GEN:  NAD CVS : RRR, CHEST : No signs of resp distress ABD : Soft, NTTP NEURO:   HC:   AF : Soft and flat   Mental status : Alert, awake   CN : Pupils b/l equal and reactive, EOMI, VF seem intact, face symmetrical, facial sensation intact b/l, head turn seems normal.   Motor : Moving all 4 extremities equally   Sensory : Intact to tickle in all 4 extremities and face b/l   Reflexes : +ve b/l palmar and plantar grasp, +rooting, +suck, + moro's, b/l babinksi present

GEN : NAD, pleasant, playing, running around in room. CVS : RRR, CHEST : No signs of resp distress ABD : Soft, NTTP NEURO:   Mental status : Alert, awake, oriented to mom, dad, playing   Language : Speaks in one or two words.   CN : Pupils b/l equal and reactive, EOMI, VF seem intact, face symmetrical, facial sensation intact, haed turn seems normal.   Motor : Moving all 4 extremities equally   Sensory : Intact to touch in all 4 extremities and face b/l   Reflexes : 2/4 throughout, no Hoffman's, no clonus, bilateral flexor planter responses   Coord /Rhombergs/Stance/Gait : walking and running in room, normal gait, no ataxia.

Neurological Examination in Specific Situations:

--> Parkinsonian gait & bilateral rigidity, the rest of motor/sensory exam is normal - UPDRS motor part is added to describe parkinsonian features.

NEURO : Mental Status :  The patient is alert, attentive, and oriented to time, place and person. Speech: clear and fluent with good repetition, comprehension, and naming. She recalls 3/3 objects at 5 minutes. Cranial nerves: CN II: Visual fields are full to confrontation. Fundoscopic exam is normal with sharp discs. Pupils are 4 mm and briskly reactive to light. Visual acuity is 20/20 bilaterally. CN III, IV, VI: EOMI, no nystagmus, no ptosis CN V: Facial sensation is intact to pinprick in all 3 divisions bilaterally. CN VII: Face is symmetric with normal eye closure and smile. CN VII: Hearing is normal to rubbing fingers CN IX, X: Palate elevates symmetrically. Phonation is normal. CN XI: Head turning and shoulder shrug are intact CN XII: Tongue is midline with normal movements and no atrophy.

Motor: There is no pronator drift of out-stretched arms. Muscle bulk is normal. Strength is 5/5 throughout. Tone is increased (rigidity) in both upper and lower extremities and around the neck. Deltoid Biceps Triceps Wrist ext Finger abd Hip flex Hip ext Knee flex Knee ext Ankle flex Ankle ext

Reflexes: Reflexes are 2+ and symmetric at the biceps, triceps, knees, and ankles. Plantar responses are flexor. Sensory: Light touch, pinprick, position sense, and vibration sense are intact in fingers and toes. Coordination: Rapid alternating movements and fine finger movements are intact. There is no dysmetria on finger-to-nose and heel-knee-shin. There are no abnormal or extraneous movements. Romberg test is negative. Gait/Stance: Stooped posture, short steppage gait with decreased arm associative movements. Turns in block but no gait freezing.

UPDRS: (each item scored from 0 to 4, 0 is normal) -Speech -Facial expression -Resting tremors -Postural/action tremors -Rigidity -Finger taps -Hand movements -Rapid alternating movements -Leg agility -Arising from a chair -Posture -Gait -Postural stability -Bradykinesia TOTAL SCORE:

Gen : Laying in bed, no apparent distress CVS : RRR, no carotid bruit CHEST : No signs of resp distress, on room air ABD : Soft, NTTP Neuro :  Mental status:    Psychomotor activity : normal.    Affect :  normal.    Judgement :  fair.    Insight : fair.    Orientation : Orineted to time place and person.    Attention :  normal attention span, can spell WORLD backwords, could do serial 7 subtractions.    Memory : impaired delayed recall, could remember only 1 of 3 objects in 5 minutes - longterm memory appears normal.    Excutive functions : could replicate a cube, draw a clock.    Abstraction : Could relate different objects (fruits, tools).    Language : fluent. CNs : Pupils b/l equal 3mm, reactive, EOMI seems intact, face symmetric, tongue midline. Motor : Limited due to patient not following commands but moving all 4 extremities equally and spontaneously. Roughly 4+/5 throughout Sensory : Intact to pin prick in all 4 extremities and face bilaterally. Reflexes : 2/4 throughout, bilateral flexor plantar response, no Hoffman's, no clonus Coordination no observed nystagmus or appendicular ataxia on spontaneous movements

Gen : Laying in bed, no distress CVS : RRR, no carotid bruit CHEST : No signs of resp distress, on room air ABD : Soft, NTTP Neuro : MS : awake, alerts to name but not attentive , not following commands Language : says few sentences - requires repeated stimulation to follow simple commands CNs : Pupils b/l equal 3mm, reactive, EOMI seems intact, face symmetric, tongue midline. Motor : Limited due to patient not following commands but moving all 4 extremities equally and spontaneously. Roughly 4+/5 throughout Sensory : reacts to pain in all extremities Reflexes : 2/4 throughout, bilateral flexor plantar response, no Hoffman's, no clonus Coordination no observed nystagmus or appendicular ataxia on spontaneous movements

Gen : Laying in bed, eyes closed, not following commands consistently CVS : RRR, no carotid bruit CHEST : No signs of resp distress ABD : Soft, NTTP Neuro : MS : sleepy, awakens to repeated stimuli, not attentive, sometime tracks but not following commands. Language : Not following simple commands, occasionally saying yes to random questions. CNs : Pupils b/l equal 3mm, reactive, EOMI seems intact, face symmetric, tongue midline. Rest of cranial nerves are intact. Motor : Limited due to patient not following commands but withdraws to pain in all extrenities equally. Sensory : reacts to pain in all extremities Reflexes : 2/4 throughout, bilateral flexor plantar response, no Hoffman's, no clonus Coordination: no evident nystagmus or ataxia Gait : deferred due to mental status

Stuperus difficutl to arouse – withdraws Gen : Laying in bed, eyes closed, not following commands CVS : RRR, no carotid bruit CHEST : No signs of resp distress ABD : Soft, NTTP Neuro : MS : stuperous, opens her eyes only to pain, not attentive, not tracking, not following commands Language : Not following simple commands, non-verbal. CNs : Pupils b/l equal 3mm, reactive, cephalo-ocular reflex intact, face symmetric, tongue midline. Rest of cranial nerves are intact. Motor : Limited due to patient not following commands but withdraws to pain in all extremities. Sensory : reacts to pain in all extremities Reflexes : 2/4 throughout, bilateral flexor plantars Coordination: deferred - unresponsive  Gait : deferred due to mental status

Gen : Laying in bed, eyes closed, no spontaneous movements CVS : RRR, no carotid bruit CHEST : No signs of resp distress ABD : Soft, NTTP Neuro : MS : no response to verbal or painful stimuli    Language : intubated - comatose CNs : Pupils b/l equal 2mm with sluggish reaction, cephalo-ocular reflex intact, face symmetric, cough and gag present, rest of cranial nerves exam is limited by mental status. Motor : no response to painful stimulation 0/5 throughout Sensory : no response to pain Reflexes : no reflexes could be elicited    Coordination: not assessed, patient is unresponsive GAIT : deferred due to mental status

General : lying down in bed, no apparent distress - sedated - no spontaneous movements CVS : RRR, no carotid bruit. Lungs : on mechanical ventillation, clear breath sounds Abdomen : Soft, NTTP Extremities : no edema or cyanosis Neuro: MENTAL STATUS: sedated on propofol LANG/SPEECH : non-verbal (sedated) CRANIAL NERVES: Pupils are equal and reactive, face symmetric - poor cough and gag to suctioning, rest of cranial nerves were deferred due to sedation. MOTOR : no spontaneous movements - no withdrawal to pain on either side (sedated) REFLEXES : hyporeflexic bilaterally SENSORY : no reaction to pain in both sides COORD : deferred - sedated GAIT : deferred - sedated

General : no apparent distress CVS : RRR, no carotid bruit Chest : No signs of resp distress, clear breath sounds Abdomen : Soft, NTTP Extremities : no edema or cyanosis Neuro: MENTAL STATUS: awake, alert, globally aphasic (can't assess fund of knowledge). LANG/SPEECH : global aphasia CRANIAL NERVES: II: Pupils equal and reactive, no RAPD, Rt hemianopia III, IV, VI: EOM intact, right gaze preference VII: Rt facial weakness VIII: normal hearing to speech Rest of cranial nerves unremarkable MOTOR : Withdraws Rt UE and LE to pain but no spontaneous movement 5/5 in Lt upper and lower extremities REFLEXES : 2/4 throughout, Rt extensor plantar response SENSORY : reacts to pain in all limbs  Gait : deferred due to weakness

MENTAL STATUS: AAOx3 LANG/SPEECH : dysarthria with intact naming and repetition - follows commands appropriately CRANIAL NERVES : II: Pupils equal and reactive, no RAPD, Lt hemianopia III, IV, VI: EOM intact, no gaze preference or deviation, no nystagmus. V: normal VII: Lt facial weakness VIII: normal hearing to speech Rest of cranial nerves are intact MOTOR: 1 /5 in Lt upper extremity and 1/5 in Lt lower extremity 5/5 in Rt upper and lower extremity REFLEXES: 2/4 throughout, left extensor plantar SENSORY : decreased to touch and pain prick on left side COORD : Normal finger to nose on right side - no dysmetria or tremors. Gait : deferred due to weakness

Notes for Neurological Exam Templates:

• Although billing is not required for residents, it is a good habit for senior residents to learn and follow the correct billing maneuvers.
• Comprehensive single system exam (neurological) with auscultation of either the carotid or the heart.
• For more information on billing, please refer to out page: Billing
• A Life-saving diagnosis, just by luck!
• Child Neurology
• Neuro-Anatomy
• Neuro-Muscular
• Neuro-Pathology
• Neurological Examination
• Neuropharmacology
• Billing-Hospitals
• Billing-physicians
• Billing-Updates
• BoardReview
• Botox Injections
• Business of Medicine
• Case – Her Eyes Were The Clue
• Case – It’s all about localization !
• Epilepsy, EEG & EMU
• CME & MOC
• Compensation
• CT Anatomy – Gyri
• Epic EMR Templates
• Epilepsy Updates
• Evidence Based Neurology
• Famous Neurologists
• History of Neurology
• Interesting Books
• Interesting Cases
• It’s not a rare disease anymore !
• Joint Steroid Injection
• Maintenance of Certification
• Malpractice Insurance
• Miscellaneous
• Neuro-Immunology
• Neuro-Immunology Updates
• Neuro-Infectious
• Neuro-Radiology
• Neurolgy Blogs
• Neurology Board Preparation
• Neurology Lists
• Neurology Reference Handbook
• Neurology vs Oncology, Localization wins!
• NeuroMuscular Updates
• NeuroSonology-NeuroVascular Ultrasound
• Multiple Sclerosis
• Parkinsonism
• AIS after tPA/Thrombectomy
• ICH intubated (ICU)
• ICH not intubated (ICU)
• Ischemic stroke without tPA or intervention
• Myasthenic Crisis
• SAH Intubated (ICU)
• SAH not intubated (ICU)
• Status Epilepticus
• On-Call Templates
• Central line
• Lumbar Puncture
• AIS after tPA
• AIS without tPA
• Patients Biographies & Diaries
• Physicians Biographies & Diaries
• Puzzling Case
• Radiology – Angiography
• Radiology – Arterial Territories
• Radiology – Brain MRA
• Radiology – CT Brain Gyri
• Radiology – CT Brain Lobes
• Radiology – MRA 3D
• Radiology – MRI Brain Gyri
• Radiology – MRI Brain, CSF Spaces
• Radiology – MRI Brain, Deep Nuclei
• Radiology – MRI Brain, Limbic System
• Reset Password
• Sclaes & Scores
• Stroke & Vascular Neurology
• Stroke Clinical Trials
• Tensilon (edrophonium) Test
• Text Editor
• Slide Anything Popup Preview

An official website of the United States government

The .gov means it's official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you're on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings
• Browse Titles

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

StatPearls [Internet].

Neurologic exam.

Mahsa Shahrokhi ; Ria Monica D. Asuncion .

Affiliations

Last Update: January 16, 2023 .

• Definition/Introduction

The neurological examination is an assessment tool to determine a patient's neurologic function. It is beneficial in a variety of ways as it allows the localization of neurologic diseases and helps in ruling in or ruling out differential diagnoses. Neurological diseases can present a myriad of ways, including cognitive/behavioral, visual, motor, and sensory symptoms. Certain red flags during examination allow early detection of life-threatening neurologic diseases and recognize disorders that may negatively impact the quality of life. [1]

The neurologic examination is useful in both ambulatory and emergency settings. It provides the physician a tool to recognize neurologic involvement in certain disease states, and thereby allow proper work-up and treatment for these patients. It is also beneficial in intensive care units, particularly in monitoring neurologic sequelae of diseases like strokes, intracranial tumors, and traumatic brain injury. [2] [3]  In emergent settings, rapid assessment of the severity of an injury and neurologic involvement is crucial and leads to fast decision-making in patient management, as well as improvement of patient survival rates. [4]

• Issues of Concern

The neurological exam can be intimidating and challenging to perform for most physicians. It is particularly challenging to perform in certain age groups like infants, younger children, and older uncooperative adults. [5]  In the examination of a pediatric patient, proper diagnoses begin with understanding which specific age groups are prone to developing certain disease processes. It is also important to keep in mind that the manifestation of certain neurologic illnesses can be vastly different in children and adults.

The assessment of how a patient feels about their symptoms can provide a better insight into their quality of life. [6]  

Physicians encounter an extensive range of patients with different illnesses daily. These can range from relatively benign to life-threatening conditions. This range of potentials highlights the importance of a physician's ability to recognize red flags early on in the disease processes. These red flags are picked up in history or during a neurological examination. A good example would be a patient who presents with chronic headaches, which can be a benign condition like migraine or life-threatening like a tumor. The presence of nausea and vomiting in the patient's history may still be present in migraines or may be a sign of increased intracranial pressure. An abnormal neurological examination can then direct the physician to the diagnosis (e.g., ataxic gait in this patient points to a cerebellar lesion). The physician can then refer the patient for appropriate diagnostic imaging and direct the management. [7]  

Recognizing red flags can be challenging for physicians, particularly when it comes to neurologically related disorders. The complexity of the neurologic examination, the interpretation of results, and the correlation to the neuroaxis are often challenging. This fact highlights the need for increased awareness of what constitutes a proper neurological examination and what each specific finding suggests. It is also important to note that some positive results, especially in isolation, can be a normal variant.

A neurological examination should also be tailored and focused on specific disease presentations. Certain maneuvers can be incorporated to increase the sensitivity of an exam for a certain symptom; an elderly patient with memory deficits will require a more in-depth cognitive assessment than a young patient with ptosis.

• Clinical Significance

A basic neurologic examination can be performed rapidly with practice. The presence of an abnormal result usually warrants further investigation and referrals to specific specialties. It helps to recognize and therefore manage diseases earlier in their course. A complete neurologic examination should contain an assessment of sensorium, cognition, cranial nerves, motor, sensory, cerebellar, gait, reflexes, meningeal irritation, and long tract signs. Specific scales are useful to improve interobserver variability.

Glasgow Coma Scale

The Glasgow coma scale (GCS) is a standard to determine the level of awareness in trauma or critically ill patients who present with impaired consciousness. It is a 15 point scale that gives a general idea of the extent of brain injury. [12] The GCS is divided and scored according to eye-opening, verbal response, and motor response. The eye-opening response is scored as spontaneous – 4, opens to verbal command – 3, opens to pain – 2, and no response – 1. The verbal response is scored as oriented – 5, confused – 4, inappropriate responses – 3, incomprehensible sounds – 2, and no response – 1. The motor response is scored as obeys commands – 6, spontaneous movement or localizes to painful stimuli – 5, withdrawal from pain – 4, abnormal flexion (decorticate) – 3, abnormal extension (decerebrate) – 2, and no response – 1. The scores are added and classified as follows: Minor brain injury – 13 to 15 points, moderate brain injury- 9 to 12 points, and severe brain injury- 3 to 8 points. [8]

Mental Status

The mental status examination begins during the interview. Assessment of the patient's cognitive abilities such as language usage, chronology in the recollection of events, and significance of answers will give a clinician a general feel of the patient's condition. A quick mental status exam may involve asking for orientation to time, place, and person. A healthy patient is recognized to be "awake," "alert" (responding appropriately), and "oriented" (aware of self, place, and time). If disorientation or memory lapses (especially in the elderly) are present, a mini-mental status examination can be done. This will assess further the patient's orientation, registration, attention, recall, language, repetition, complex commands, and visuospatial function. Any abnormality in a specific function may warrant further investigation that is not covered by this article. Abnormalities in these areas can point to lesions in specific areas of the cortex (e.g., difficulty in repetition may involve the arcuate fasciculus of the dominant hemisphere—the pathway between Wernicke's area and Broca's area). Mood and affect also require assessment. [9]

Cranial Nerves 

The cranial nerves innervate the structures in the head and neck. The olfactory nerve and optic nerve exit from the cerebrum. The cranial nerves 3 to 12 exit from the brainstem. Abnormality in cranial nerve function helps in localizing the lesion to a specific level of the brain or brainstem. Cranial nerves have motor, sensory and autonomic functions. It is important to note that, in general, a singular cranial nerve deficit points to a lesion of the peripheral nerve. A lesion in the brainstem, being a busy structure, will involve multiple cranial nerve deficits, as well as motor and sensory tracts to the extremities.

Olfactory nerve (Cranial nerve I) - This is the least tested of cranial nerves in the clinical setting. To test function involves the assessment of the patient's sense of smell. Start with one nostril while covering the opposing nostril to allow for proper detection of any abnormal findings. Do this for both sides. The most common causes of anosmia, the loss of smell, are the following: infections, allergies, or nasal polyps. Other causes include trauma (fracture of the cribriform plate), Parkinson disease, lesions at the base of the skull (meningioma), or rare genetic conditions. [10]

Optic nerve (Cranial nerve II) – Assessment of the optic nerve function includes a test for visual acuity and visual fields. Each eye is tested separately. Most problems with visual acuity are ophthalmologic in origin; however, damage to this nerve, like pseudobulbar neuritis or pressure from a pituitary tumor, can present with monocular blindness and visual field cuts. The extent of involvement will depend on what they can see during the examination as compared to the baseline. [11] Furthermore, the pupillary light reflex can be tested by shining a light directly into the eye. The afferent limb of this reflex is found on the optic nerve; the sensory input. Shining a light on one eye should show a constriction of the pupils on both eyes. The failure of the pupils to constrict could indicate either an optic nerve lesion, a lesion of the efferent limb (oculomotor nerve), or any lesion along the pathway. A dilated pupil that is unresponsive to light may indicate a lesion on the efferent limb of the pathway, while a constricted pupil can point to a lesion on the cervical sympathetic chain. A fundoscopic examination is also done to visualize the optic disk. Abnormalities like papilledema or retinal hemorrhages are red flags that can point to life-threatening conditions like increased intracranial pressure and subarachnoid hemorrhage. [12]

Oculomotor, trochlear, and abducens nerves (Cranial nerve III, IV, and VI)  are the nerves for extraocular muscle movement. Assessment involves drawing an invisible "H" in front of the patient and asking the patient to follow with their eyes. Abnormal findings present as disconjugate gaze or double vision. The involvement of the third cranial nerve by compression (aneurysm of the posterior communicating artery) leads to dilated pupil, ptosis, and eyes looking outward and downward. Lateral rectus palsy is due to the involvement of the sixth cranial nerve; it can be a false localizing sign in increased intracranial pressure (bilateral lateral rectus palsy). The involvement of the pathways in the brainstem (e.g., lacunar infarct, multiple sclerosis) can lead to internuclear ophthalmoplegia. This condition occurs when the medial longitudinal fasciculus (MLF), a heavily myelinated pathway that allows for coordinated horizontal gaze, is damaged. [13]

Trigeminal nerve (Cranial nerve V)   – this nerve supplies the sensation to the face, the motor nucleus is responsible for biting and chewing. Assessment of this nerve involves asking the patient to clench their jaw and test for the sensation of the ophthalmic, maxillary, and mandibular branches. Therefore, a weakness of the muscle of mastication or sensory deficit on the ipsilateral side suggests its involvement. This is also the afferent pathway for the blink reflex (the efferent pathway being the facial nerve). A corneal reflex is usually performed in comatose patients to assess brainstem function. An absence in an awake patient may point to a localized lesion affecting either the trigeminal nerve the facial nerve or both. [14]

The facial nerve (Cranial nerve VII) supplies the muscles of facial expression, stapedius muscle, and taste to the anterior two- of the tongue. Assessment of this nerve involves asking the patient to move their facial muscles by asking them to raise their eyebrows, close their eyes tightly, smile, and blow up their cheeks. The location of weakness in facial muscles can differentiate between peripheral or central involvement. A weakness with the movement of the entire right side of the face is indicative of either a peripheral lesion or damage to the facial nucleus on the ipsilateral side, like in Bell's palsy or a pontine infarct. A weakness of the lower half of the face with sparing of the forehead is suggestive of a lesion above and contralateral to the facial nerve (stroke involving the motor cortex). This is because the forehead has innervation from both the left and right sides of the motor cortex.  [15] Damage to the facial nerve can also present with hyperacusis and loss of taste to the anterior 2/3 of the tongue.

The vestibulocochlear nerve (Cranial nerve VIII) supplies functions in hearing and equilibrium. Gross assessment of function can be done by whispering words behind the patient, rubbing fingers or hair together close to the ear, and asking if the patient can hear. If a hearing deficit is established, doing a Weber and Rinne test can differentiate sensorineural from conductive hearing loss. A normal Rinne exam will exhibit air conduction (AC) greater than bone conduction (BC). A conductive hearing loss will show BC greater than AC. In patients with sensorineural hearing loss, AC will be greater than BC, but for a shorter duration when compared to a normal subject. A normal Weber test shows hearing the sound/vibration equally in both ears. A conductive hearing loss will lateralize the sound to the abnormal ear while a sensorineural hearing loss will lateralize to the normal ear. [16]

The glossopharyngeal and vagus nerves (Cranial nerve IX and X) innervate the pharynx and posterior third of the tongue. The vagus nerve innervates the pharynx, larynx, and gastrointestinal tract motility and function. Assessment of these nerves includes listening as the patient talks, watching out for hoarseness, or nasal speech. The patient can also be asked to swallow some water and observed for coughing or gurgling speech, which may indicate weakness of the muscles involving swallowing. Ask the patient to open the mouth and say "ah," and observe the palatal arch for asymmetry. The deviation of the uvula to one side indicates a vagal nerve lesion on the opposite side. [17]

The spinal accessory nerve (Cranial nerve XI) innervates the muscles of the thorax, back, and shoulders. Assessment involves asking the patient to turn their head to the side against resistance and shrug their shoulders. The weakness of the sternocleidomastoid or atrophy of the trapezius muscle may indicate involvement. [18]

The hypoglossal nerve (Cranial nerve XII) innervates the motor component of the tongue. Assessment involves inspection of the tongue in the relaxed position inside the mouth, the presence of increased corrugation and fasciculations may indicate a lower motor neuron involvement. Also, ask the patient to stick out the tongue, the deviation to one side is indicative of a lesion on the same side. [19]

The inspection of the muscles is the first step in doing the motor examination. Any visible scars, deformities, fasciculations, and asymmetry (swelling or atrophy) should be noted. This is followed by palpation to assess for mass lesions or tenderness if present.

The range of motion (ROM) is used to assess tone and helps localize injury or disease to the joints or muscles. On doing the passive ROM, the physician check's for flaccidity, spasticity, and rigidity. The active ROM can give a clue to strength and pain-related causes of decreased range. The presence of spasticity or flaccidity can help differentiate an upper motor neuron from a lower motor neuron cause of weakness, while the presence of cogwheel rigidity points to a specific disease like Parkinsonism. [20]

Finally, the assessment of muscle strength is done. The manual muscle testing is scored as follows: [21] [22] 0 - None: No visible or palpable contraction, 1 - Trace: Visible or palpable contraction (only slight), 2 - Poor:  Full ROM with gravity eliminated, 3 - Fair: Full ROM against gravity, 4 - Good: Full ROM against gravity with moderate resistance, and 5 - Normal: Full ROM against gravity with maximum resistance. 

Assessment of muscle strength should occur in an orderly fashion. Testing should be done to differentiate proximal from distal muscle weakness, as well as compare the left and right sides. The location of the weakness concerning other neurologic deficits can help differentiate a cortical lesion (hemiplegia from a stroke), from a brainstem lesion (crossed deficits from an MS plaque), from a spinal cord lesion (presence of dermatomal level), from a peripheral nerve lesion (neuropathy or radiculopathy), and a muscular disease (myasthenia gravis). 

Sensory Exam

The sensory exam involves the assessment of patient-reported symptoms that includes a diminished or exaggerated perception of sensation. Modalities tested include pain, temperature, vibration, and position sense. The location and pattern of sensory deficits are also helpful in localization. Pain sensation is assessed by using a sterile pin and test for sharpness or dullness. A tuning fork can be used to evaluate vibration sense. A piece of cotton can serve to assess for light touch, while the assessment for position sense can be done by testing the distal phalanx and asking the patient the position of the digit with eyes closed. An abnormal sensation can involve the sensory cortex, the thalamus, the brainstem, the spinal cord, and the peripheral nerves. Cortical lesions present with diminished sensation on the contralateral side, spinal cord lesions present as a sensory level, radiculopathies involve a specific dermatome, and neuropathies can have a glove and stocking distribution. [23]

The assessment of a patient's gait can be as simple as watching the patient walk into the room. It is essential to keep in mind that gait changes can be brought about by several factors, including weakness, neuropathies, arthritic changes, excess weight, and pain. A specific gait disorder that is recognized can point to a particular disease process or neurologic involvement.

Assessment of the gait involves observing the stance, the stride, the balance, and the heel strike. Balance and strength could have further evaluation by asking the patient to walk on their tiptoes or heels and walking in tandem (the heel of the front foot touching the toe of the back foot in a straight line). Recognition of an extensive list of different gaits linked to various pathologies is crucial in the early detection of neurological diseases. [24]  Assessment of the gait also allows an understanding of a patient's level of functioning. [25]  

Some common abnormal gait recognized include: [24]  

• Antalgic gait - altered gait due to pain, such as "limping." 
• Paretic gait - due to partial paralysis/weakness (e.g., steppage gait)
• Spastic gait - due to stiffness of the limbs
• Ataxic gait - broad-based and uncoordinated gait, might be due to cerebellar or sensory involvement.
• Hypokinetic - shuffling and slow gait, might be due to basal ganglia involvement.
• Dyskinetic - disturbance due to involuntary movements like dystonia or athetosis

Deep Tendon Reflexes                                            

The assessment of the deep tendon reflexes can be done by tapping a specific tendon with a reflex hammer and observing for a reflex muscle contraction. These tests a specific spinal cord level (biceps C5-C6, triceps C7, knees L3-L4, ankles S1-S2) and help in localizing the level of a lesion. Reflexes are scored as follows: 0 - absent, 1+ - trace, 2+ - normal, 3+ - brisk, 4+ - nonsustained clonus, and 5+ - sustained clonus.

Decreased deep tendon reflex is usually suggestive of a lower motor neuron lesion, like radiculopathy, but may also occur in spinal shock. On the other hand, the presence of hyperreflexia and clonus points to an upper motor neuron lesion. [26] [27]

Other reflexes include the Babinski reflex and the Hoffman reflex. The Babinski reflex involves stimulation of the lateral plantar aspect of the foot, the presence of an upgoing big toe indicates a positive result. Variations of this reflex include Chaddock reflex - stimulation of the lateral aspect of the foot, Oppenheim reflex - stroking the anterior and medial tibia downward, and Gordon reflex - squeezing the calf muscle; the presence of the upgoing big toe indicates a positive response. On the upper extremity, a Hoffman reflex can be done by flicking the distal digit of the middle finger with the positive response being the involuntary flexion of the other fingers, including the thumb. A positive Hoffman reflex indicates cervical cord involvement. A positive response in these tests helps differentiate an upper motor lesion from a lower motor lesion.

Meningeal Signs

The presence of meningeal signs reflects an irritation of the meninges. Maneuvers include assessment of nuchal rigidity by passive flexion of the patient's neck, and the presence of pain and resistance indicates a positive result. Other maneuvers include the Kernig sign, where a passive extension of the knee while the leg is flexed at the hip in a supine patient causes pain, and the Brudzinki sign, where passive neck flexion causes reflex knee flexion in the supine position. [28]  The usual causes of meningeal irritation include CNS infections and subarachnoid hemorrhage.

It is crucial to remember that when examining a patient, a focused physical and neurologic exam is complementary to a detailed history and is key in achieving proper diagnoses. [29]  

• Nursing, Allied Health, and Interprofessional Team Interventions

Although a full neurological examination with its specific maneuvers and domains is within the comfort zone of neurologists, it is an essential tool in the arsenal of primary care physicians. Localizing a disease to the neuroaxis will assist them in the appropriate management and referral to appropriate specialties. Also, basic neurologic assessment should be a point of emphasis for other health care professionals, especially in areas with a high likelihood of seeing neurologic cases such as in emergency rooms, intensive care units, and post-operative monitoring. [30]  

• Review Questions
• Access free multiple choice questions on this topic.
• Comment on this article.

Disclosure: Mahsa Shahrokhi declares no relevant financial relationships with ineligible companies.

Disclosure: Ria Monica Asuncion declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Shahrokhi M, Asuncion RMD. Neurologic Exam. [Updated 2023 Jan 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

In this Page

Bulk download.

• Bulk download StatPearls data from FTP

Related information

• PMC PubMed Central citations
• PubMed Links to PubMed

Similar articles in PubMed

• The neuromythology of silicone breast implants. [Neurology. 1996] The neuromythology of silicone breast implants. Rosenberg NL. Neurology. 1996 Feb; 46(2):308-14.
• Review American Medical Society for Sports Medicine position statement: concussion in sport. [Br J Sports Med. 2013] Review American Medical Society for Sports Medicine position statement: concussion in sport. Harmon KG, Drezner JA, Gammons M, Guskiewicz KM, Halstead M, Herring SA, Kutcher JS, Pana A, Putukian M, Roberts WO. Br J Sports Med. 2013 Jan; 47(1):15-26.
• Review Dementia -- Caring, Ethics, Ethnical and Economical Aspects: A Systematic Review [ 2008] Review Dementia -- Caring, Ethics, Ethnical and Economical Aspects: A Systematic Review Swedish Council on Health Technology Assessment. 2008 Jun
• Review Evaluation of red flags minimizes missing serious diseases in primary care. [J Family Med Prim Care. 2018] Review Evaluation of red flags minimizes missing serious diseases in primary care. Ramanayake RPJC, Basnayake BMTK. J Family Med Prim Care. 2018 Mar-Apr; 7(2):315-318.
• The Neurological Exam of a Comatose Patient: An Essential Practical Guide. [Malays J Med Sci. 2020] The Neurological Exam of a Comatose Patient: An Essential Practical Guide. Zakaria Z, Abdullah MM, Halim SA, Ghani ARI, Idris Z, Abdullah JM. Malays J Med Sci. 2020 Oct; 27(5):108-123. Epub 2020 Oct 27.

Recent Activity

• Neurologic Exam - StatPearls Neurologic Exam - StatPearls

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

Connect with NLM

National Library of Medicine 8600 Rockville Pike Bethesda, MD 20894

Web Policies FOIA HHS Vulnerability Disclosure

Help Accessibility Careers

Home » Feature » How to Pass the Neuro-Psychiatric Exam: 2023 Guide

How to Pass the Neuro-Psychiatric Exam: 2023 Guide

The  Neuro-Psychiatric Examination tests the mental stability, adaptability, and psychological functioning of applicants before they are recruited into service. The purpose of the exam is to filter applicants if they are really suitable for the uniformed services of the government. It is one of the most decisive parts of the recruitment process in the PNP , BFP, BJMP, BuCor , and all the branches of the AFP. In fact,  only 25% of the applicants pass the Neuro-Psychiatric exam, making it the most dreaded part of the application process.

The  Neuro-Psychiatric Exam is comprised of two parts- the written and the personal interview. It includes a 35-item Aptitude (Adaptation) Test,  Guilford Zimmerman Temperament Survey , Applicant Risk Profiler, The Industrial Sentence Completion Test, Work Environment Preference Schedule (WEPS), Hand Test, and the “Drawing”. Sounds scary, right? Well, here are some tips and pieces of advice to help you pass this crucial part of your application. Please read on.

6 Important Tips to Pass the Neuro-Psychiatric Exam

To help you succeed in passing the Neuro-Psychiatric Exam, we recommend a book called Neuro-Psychiatric Exam Guide for Police (PNP), Fire (BFP), BJMP, Coast Guard & AFP Applicants . It is available in Shopee and can be paid via the COD option.

Are you still searching for ways how to successfully hurdle this important part of your application? Check these important tips on how to pass the Neuro-Psychiatric Exam like a boss.

1. Follow instructions

In every exam, following the instructions is as important as knowing the right answer to every question. Knowing how to follow instructions is a good indicator that you will be a good policeman, fireman, jail officer, or soldier as these services require utmost compliance with instructions. When you are told to write your name in block capitals, do it exactly as you are told.

Neuro-psychiatric examinations often involve complex tasks and assessments that require careful observation and attention to detail. Whether it’s reading a passage and answering questions or completing a visual puzzle, make sure you take the time to thoroughly understand the instructions and the requirements of each task. Paying attention to details can help you avoid careless mistakes and demonstrate your ability to analyze information accurately.

2. Manage your time during the exam

As I’ve said earlier, the Aptitude, or what we call the IQ test is composed of 35 questions. You have to answer all these questions in just 15 minutes. That means you only have about two minutes to answer each item. The proctors are strict regarding the time limit, so never think that they will give you a time extension. Develop a strategy to allocate your time wisely, ensuring that you devote sufficient time to each section while leaving enough time for reviewing and double-checking your answers. The trick is to answer the easy questions first, then go back to the difficult ones in case you still have time. This way, you can maximize the time and increase your chances of completing the test.

Practicing under timed conditions beforehand can help you become more comfortable with the time constraints and improve your efficiency during the actual exam.

3.  Be consistent with your answers

Be mindful of your answers to every question of the exam. Always remember your answer to a particular question because you will be asked similar and related questions in the next following items. You have to be consistent with your answers. Remembering and providing consistent information throughout the examination demonstrates your attentiveness and reliability. In contrast, inconsistent answers may indicate that you are untruthful and just telling lies. By remaining consistent, you will enhance your chances of passing the examination successfully.

4. Learn how to draw

When I say learn how to draw, it does not mean you have to be like Michaelangelo or Da Vinci. If you are told to draw people, do not draw stick figures. Instead, focus on basic human anatomy and proportionality. Draw people with complete parts like ears, eyes, hairs, fingers, etc. Pay attention to details such as body posture, facial expressions, and gestures, as they can provide valuable insights into the individual’s emotional state. Make evident distinctions between males and females e.g., mustache for males and long hair for females. After that, you describe each drawing or make a story out of it in 4-5 sentences.

Remember that the purpose of drawing in this context is not to showcase artistic talent, but rather to communicate information and convey observations accurately. Some of the concepts included here are tricky, and everything being drawn could mean something to the psychologists. Therefore, be careful.

5. Hone your English skills

Sometimes, the exam may include essay exercises. The purpose is to evaluate the incident reporting skills of the applicants. Practice your English writing skills, be precise, and pay attention to the grammar rules. Remember, clear and concise communication is crucial in showcasing your knowledge and competence in the neuro-psychiatric examination.

6. Prepare for the interview

The final part of the exam is the one-on-one interview with a psychologist to assess how you will present yourself under pressure. Answer all the questions with wit, consistency, and fluency. Do not make unnecessary body and hand movements or gestures during the interview. Maintain a calm and composed demeanor throughout the process. Remember to take deep breaths, maintain eye contact, and listen attentively to the interviewer’s questions before formulating your responses. Be honest about your limitations and strengths, as this will demonstrate self-awareness and authenticity. Be snappy and stand firm when talking. Lastly, always be humble.

To wrap it up

The neuro-psychiatric test wants to know if you have the mindset of an average person. Do not pretend that you are an extraordinary one and just be yourself. Be consistent in your answers, bring out the good in yourself, and do not show any violence in your words. Lastly, never leave anything unanswered. Those unanswered questions might determine the result of the neuro-psych whether you are RECOMMENDED or NOT RECOMMENDED. Good luck and may the odds be in your favor.

I usually told my former students and friends and those who are asking some pieces of advice from me before they take their exams these things mentioned above. I emphasized on consistency of answers, I used to work in a Psych department. Also, be descriptive on your drawings and you need to be able to explain what you have drawn. Most of those who ask help from me are now policemen, seeing them around in town and thanking me makes me happy at least. I agree with the author. So have confidence, be ready and be prepared, be humble and …  Read more »

I just hope I can pass the neuro-psychiatric exam for PNP soon. In god’s perfect timing. please lord let the light be in me.

Do i need to be honest even though i have a lot of negativism and lack of confidence .

ff, I lied in my neuro exam too.

How many months/year Neuro exam expire.. or how.long its validity

very nice advice

• Civil Service Exam Reviewer
• L TO Portal Registration Guide
• How to Renew a Driver's License
• National ID Tracker
• Civil Service Exam Application
• Privacy Policy
• Terms of Service

All content provided on this website is for informational purposes only. The owner of this website makes no representations as to the accuracy or completeness of any information on this site or found by following any link on this site. The owner will not be liable for any errors or omissions in this information or for the availability of this information. The owner will not be liable for any losses, injuries, or damages from the display or use of this information.

You may not use the content of this blog for commercial purposes without prior formal written consent from us. These terms and conditions of use are subject to change at any time and without notice.

TOPNOTCHER PH is a participant in the Shopee Affiliate Program, an affiliate advertising program designed to provide a means for us to earn advertising fees by linking to SHOPEE.PH. As a Shopee Affiliate, we earn from your qualifying purchases through our links without extra cost to you.

© 2024 TOPNOTCHER.PH

• Advanced Life Support
• Endocrinology
• Gastroenterology
• Infectious disease
• Intensive care
• Palliative Care
• Respiratory
• Rheumatology
• Haematology
• Endocrine surgery
• General surgery
• Neurosurgery
• Ophthalmology
• Plastic surgery
• Vascular surgery
• Abdo examination
• Cardio examination
• Neurolo examination
• Resp examination
• Rheum examination
• Vasc exacmination
• Other examinations
• Clinical Cases
• Communication skills
• Prescribing

Questions about the neurological exam

Questions about the neurological examination

Neuro exam questions for doctors, medical student exams, finals, OSCES, MRCP PACES and USMLE

• Fasciculations are usually best seen up the deltoid in the upper limb.
• They may be elicited by gently flicking the muscle if there is a clinical suspicion (e.g. weakness and wasting)
• Both spacticity and rigidity are forms of increased tone (increased resistance to stretch)
• Spacticity is often described as “clasp knife” as resistance will change throughout movement.
• Rigidity is an extrapyramidal pathway issue and is knows as “lead pipe” rigidity as it feel as if you are bending a lead pipe.
• When tremor is superimposed it is described as “cog-wheel” rigidity
• Muscle power is assessed in the clinical exam using MRC grading scale for power.
• 5: Full Strength (or what is likely normal for the patient – e.g. can be less than your strength if you’re a 6 foot amateur wrestler and your patient is an tiny 80-year old woman)
• 4 – Movement against partial resistance
• 3 – Movement against gravity (e.g. can lift heel off bed)
• 2 – Movement with gravity eliminated (i.e. can move horizontally on the bed)
• 1 – Feeble contractions (e.g. twitch)
• 0 – Absent voluntary contraction

Testing power in the upper limbs

• Jendrassik’s manoeurve is used to reinforce reflexes.
• Ask the patient to clench their teeth or grasp hands together and pull apart just as you strike with the tendon hammer.
• Though there is no universally defined system for grading reflexes, they can be described as absent  ,  hyporeflexic (present with reinforcement), normal or brisk
• These are often written as: – ,  + , ++ or +++ respectively
• Biceps: C5/6
• Triceps: C7/8
• Brachioradialis (supinator): C6
• In normal tone the foot will flop in the opposite direction as the way the knee is moved. In increased tone the foot will remain in line with the knee
• In a patient with normal tone, the heel will remain on the bed, but with increased tone the foot will leave the bed
• The presence of greater than five beats of clonus (or sustained rhythmical contraction while the tendon is stretched) indicates increased tone

Testing power in the lower limbs

Question 10

• A gait due to pain in one area – tends to involve putting one leg down for a shorter time than the other, creating an asymmetrical gait
• The patient will also be unable to walk heel-to-toe, a more sensitive test of ataxia
• Classically seen in extra-pyramidal disease
• May be indicative of inner ear disorder
• Occurs in foot drop, a person will lift their foot far above the ground in order to avoid catching their toes on the ground while walking. The patient will also have difficulty walking on their heels
• If the gait does not fit any obvious pattern, see if it is distractable or changes over time. This may point more towards a psychologically mediated gait disturbance

Question 11

• Romberg’s test is a method of assessing propioception and can be positive in sensory ataxia (peripheral neuropathy) and in tabes dorsalis  (affecting the sensory pathways of the spinal cord)
• Ask the patient to stand with their feet close together and stretch out their arms. Make sure you position the patient so that if they did fall you can catch them or that they fall onto a bed
• After giving reassurance that you will catch them if they fall, ask the patient to close their eyes
• In a positive Romberg’s test the patient will fall with their eyes closed but not with their eyes open, as the visual input that was compensating for the lack of propioceptive input is removed
• In cerebellar dysfunction the patient will be just as unsteady with their eyes open as closed

Question 12

• Outer shoulder/regimental badge area: axillary nerve C6
• Outer forearm: lateral cutaneous C5
• Thumb: median nerve C6
• Middle finger: median nerve C7
• Little finger: ulnar nerve C8
• Back of the hand – radial side: radialnerve C5-T1
• Medial antecubital fossa: medial cutaneous T1

Question 13

•  Inner thigh: upper L1, mid L2
• Medial side of knee: L3
• Medial malleolus: L4
• Big toe: L5
• Popliteal fossa: S2
• Anal sensation/tone: S3 and S4

Click here for how to do the perfect neuro exam  

Perfect revision for medical student exams, OSCES, finals, PACES and USMLE

Click here for how to do an exam presentation of someone with UMN lesion

• Preface to 6th Edition
• Case Studies
• Examination Questions

Pretest and Post-Test Exams

Neurological Assessment

Neurological Exam

Reviewed by Psychology Today Staff

A neurological assessment is an evaluation of a person’s nervous system , which includes the brain, spinal cord, and the nerves that connect these areas to other parts of the body. A neurological exam is done to assess for any abnormalities in the nervous system that can cause problems with daily functioning.

A complete exam is conducted by a neurologist and it includes evaluation of an individual’s speech, awareness of environment, motor function and balance (walking ability, muscle strength, and tone), sensation, reflexes, coordination, and the 12 cranial nerves of the brain. These nerves are involved in smell, vision, pupil activity, eye movement, taste, hearing, swallowing, and movement of the face, neck, and shoulders.

This assessment is often conducted if a person has experienced trauma or head injury , or reports a range of symptoms that may include dizziness, blurry vision, confusion, or difficulty with motor functions. This is done to detect neurological damage or disease.

• The Neuro Exam Step-by-Step
• When to Conduct a Neurological Assessment
• What More Can You Expect in a Neuro Exam?

These following nerves and functions are generally tested in such an exam:

Cranial Nerves

The cranial nerves control eye muscles, jaw muscles, and the tongue. Other cranial nerves include the optic nerve for vision, the vestibulocochlear nerve for hearing and balance, and the olfactory nerve for smell. Difficulties with any of these may indicate a neurological problem.

For the sense of smell, test tubes are filled with common odors like cinnamon or coffee, which are placed under each nostril. You will be asked to identify the odors.

The neurologist will ask you to wrinkle your nose and bare your teeth to test your facial nerves.

Similar to a normal eye exam, vision is tested by identifying letters or numbers. The physician will test your field of vision as well: You look straight ahead and cover one eye, the physician then waves a finger from the side of your head to the middle.

Motor System and Coordination

Mobility, coordination, and fine motor skills are tested. With your eyes shut and arms outstretched, can your finger touch your nose? Can you button and unbutton your shirt? Can you spin around once, and in how many steps?

The neurologist may test your reflexes by tapping your knee with a hammer.

The physician may use soft fabric and a needle to gauge your ability to feel pain and touch. Also, can you feel warm or cold water?

Cognitive Function and Memory

Language and math skills are also examined. The physician will ask you the current date and year, your occupation, where you work, your current location. Difficulties answering these questions may indicate problems that need further attention .

Autonomic Nervous System

The autonomic nervous system controls your body's vital functions, such as your pulse, breathing, body temperature, and digestion. A neurological exam also includes questions about bowel movements, urination, and blood pressure.

A neuro assessment is conducted if a person has experienced trauma or head injury , or reports a range of symptoms that may include dizziness, blurry vision, confusion, or difficulty with motor functions. This is done to detect neurological damage or disease. The physician may order an EEG (electroencephalography) or an EMG (electromyography) or scans such as the fMRI (functional magnetic resonance imaging).

Yes, these tests are different. A neuropsychological exam evaluates an individual’s ability to read, speak, reason, comprehend others, dedicate information to memory, and stay focused. This assessment includes more than just tests, but tests are a key component. It will help health providers determine whether changes in cognitive function have been caused by normal aging or by other conditions.

Yes, these tests are different. The mini mental status exam is used to rule out cognitive decline , such as in dementia . The MMSE assesses an individual’s sense of location, ability to complete simple math, sense of time and date, overall cognitive function, and simple abilities such as listing common objects.

The BCSE is similar to the MMSE, as they are both designed to assess overall cognitive function. The BCSE is used when, for example, Alzheimer’s or dementia or learning difficulties are suspected. This brief exam, completed in about 10-20 minutes, also gauges a person’s estimation of time, verbal fluency, memory, and other abilities.

To rule out the worst medical complications, physicians can use the three-minute neurological exam. This quick assessment will help evaluate, for example, whether a person’s headaches are caused by a brain tumour or hemorrhaging. This analysis includes the patient removing his shoes and standing with eyes closed, walking on the tips of his toes, the finger-to-nose test, eye movements, certain reflexes, among other checks.

The typical neurological exam will include a general physical assessment and a discussion of symptoms and medical history, putting any neurological abnormalities into context. The health provider will use tools such as lights, reflex hammers, tuning forks, as well as tools for an eye examination to test these various functions. This exam looks for problems such as strokes, tumors, Parkinson’s disease, tremors, multiple sclerosis, and many other disorders.

Vital signs include breathing patterns, oxygen level, heart rate, blood pressure, and temperature. A person with compromised neurological function will have changes in these signs.

Gait, balance, and coordination are controlled by the cerebellum. Irregular movement may mean there is a problem, such as multiple sclerosis, Huntington's, or stroke.

Vision as well as hearing are always evaluated because if one cannot see or hear well, it won’t be possible to process, understand, and remember information registered through the eyes and ears. Your pupils size, shape, and how they react, can also inform you if there is a problem.

The exam often includes non-invasive measures of brain activity including an EEG (electroencephalography), which captures brain wave activity, or an EMG (electromyography), which captures nerve activity from the brain or spinal cord to a peripheral nerve such as in the arm or leg.

CAT scans such as the fMRI (functional magnetic resonance imaging) are used if a neurodevelopmental condition such as autism spectrum disorder or a neurodegenerative disorder such as Alzheimer's disease or Parkinson's needs to be ruled in or out, an assessment may be paired with neuropsychological tests as well. This involves pen and paper tests as well as clinical interviews.

An abundance of evidence supports the relationship between anesthesia and memory loss. The severity and frequency of exposure to anesthesia could lead to mild cognitive impairment.

Has your loved one told you something happened that you’re not sure is true? It could be a false memory.

Personal Perspective: I'd waited for this appointment for months, and nothing would keep me from it. Little did I know, a surprise awaited me.

Many people, including therapists, remain unfamiliar with functional neurological disorder (FND), even though its diagnosis has increased exponentially.

AI can detect emotions on par with human performance from audio clips as short as 1.5 seconds, new research shows.

A new AI deep-learning model can distinguish between women and men from brain scans of neural activity with over 90% accuracy.

Neuroscientists created a method to track when brain cell activity decreases or switches off after a burst of activity using optogenetics and proteomics.

Personal Perspective: Is it time we started thinking differently in terms of neurotypes and health?

Assessment for autism, ADHD, or neurodiversity can be a lot to consider. Here's what to expect if decide to go forward.

Autism is a neurodevelopmental disorder, meaning that it is present throughout a person’s lifetime. Here are key features to look for throughout the developmental period.

• Find a Therapist
• Find a Treatment Center
• Find a Psychiatrist
• Find a Support Group
• Find Online Therapy
• International
• New Zealand
• South Africa
• Switzerland
• Asperger's
• Bipolar Disorder
• Chronic Pain
• Eating Disorders
• Passive Aggression
• Personality
• Goal Setting
• Positive Psychology
• Stopping Smoking
• Low Sexual Desire
• Relationships
• Child Development
• Self Tests NEW
• Therapy Center
• Diagnosis Dictionary
• Types of Therapy

At any moment, someone’s aggravating behavior or our own bad luck can set us off on an emotional spiral that threatens to derail our entire day. Here’s how we can face our triggers with less reactivity so that we can get on with our lives.

• Emotional Intelligence
• Gaslighting
• Affective Forecasting
• Neuroscience

SITE CONTENTS • ... Listed by Exam • ... Listed by Topic

Having trouble adding our QuickTime movies to your PowerPoint or Keynote presentation? Link to our QuickTime Instruction Page .

Masks Strongly Recommended but Not Required in Maryland, Starting Immediately

Due to the downward trend in respiratory viruses in Maryland, masking is no longer required but remains strongly recommended in Johns Hopkins Medicine clinical locations in Maryland. Read more .

• Vaccines  
• Masking Guidelines
• Visitor Guidelines  

Neurological Exam

What is a neurological exam.

A neurological exam, also called a neuro exam , is an evaluation of a person's nervous system that can be done in the healthcare provider's office. It may be done with instruments, such as lights and reflex hammers. It usually does not cause any pain to the patient. The nervous system consists of the brain, the spinal cord, and the nerves from these areas. There are many aspects of this exam, including an assessment of motor and sensory skills, balance and coordination, mental status (the patient's level of awareness and interaction with the environment), reflexes, and functioning of the nerves. The extent of the exam depends on many factors, including the initial problem that the patient is experiencing, the age of the patient, and the condition of the patient.

Why is a neurological exam done?

A complete and thorough evaluation of a person's nervous system is important if there is any reason to think there may be an underlying problem, or during a complete physical. Damage to the nervous system can cause problems in daily functioning. Early identification may help to find the cause and decrease long-term complications. A complete neurological exam may be done:

During a routine physical

Following any type of trauma

To follow the progression of a disease

If the person has any of the following complaints: 

Blurry vision

Change in behavior

Change in balance or coordination

Numbness or tingling in the arms or legs

Decrease in movement of the arms or legs

Injury to the head, neck, or back

Slurred speech

What is done during a neurological exam?

During a neurological exam, the healthcare provider will test the functioning of the nervous system. The nervous system is very complex and controls many parts of the body. The nervous system consists of the brain, spinal cord, 12 nerves that come from the brain, and the nerves that come from the spinal cord. The circulation to the brain, arising from the arteries in the neck, is also frequently examined. In infants and younger children, a neurological exam includes the measurement of the head circumference. The following is an overview of some of the areas that may be tested and evaluated during a neurological exam:

Mental status. Mental status (the patient's level of awareness and interaction with the environment) may be assessed by conversing with the patient and establishing his or her awareness of person, place, and time. The person will also be observed for clear speech and making sense while talking. This is usually done by the patient's healthcare provider just by observing the patient during normal interactions.

Motor function and balance. This may be tested by having the patient push and pull against the healthcare provider's hands with his or her arms and legs. Balance may be checked by assessing how the person stands and walks or having the patient stand with his or her eyes closed while being gently pushed to one side or the other. The patient's joints may also be checked simply by passive (performed by the healthcare provider) and active (performed by the patient) movement.

Sensory exam. The patient's healthcare provider may also do a sensory test that checks his or her ability to feel. This may be done by using different instruments: dull needles, tuning forks, alcohol swabs, or other objects. The healthcare provider may touch the patient's legs, arms, or other parts of the body and have him or her identify the sensation (for example, hot or cold, sharp or dull).

Newborn and infant reflexes. There are different types of reflexes that may be tested. In newborns and infants, reflexes called infant reflexes (or primitive reflexes ) are evaluated. Each of these reflexes disappears at a certain age as the infant grows. These reflexes include:

Blinking. An infant will close his or her eyes in response to bright lights.

Babinski reflex. As the infant's foot is stroked, the toes will extend upward.

Crawling. If the infant is placed on his or her stomach, he or she will make crawling motions.

Moro's reflex (or startle reflex). A quick change in the infant's position will cause the infant to throw the arms outward, open the hands, and throw back the head.

Palmar and plantar grasp. The infant's fingers or toes will curl around a finger placed in the area.

Reflexes in the older child and adult. These are usually examined with the use of a reflex hammer. The reflex hammer is used at different points on the body to test numerous reflexes, which are noted by the movement that the hammer causes.

Evaluation of the nerves of the brain. There are 12 main nerves of the brain, called the cranial nerves . During a complete neurological exam, most of these nerves are evaluated to help determine the functioning of the brain:

Cranial nerve I (olfactory nerve). This is the nerve of smell. The patient may be asked to identify different smells with his or her eyes closed.

Cranial nerve II (optic nerve). This nerve carries vision to the brain. A visual test may be given and the patient's eye may be examined with a special light.

Cranial nerve III (oculomotor). This nerve is responsible for pupil size and certain movements of the eye. The patient's healthcare provider may examine the pupil (the black part of the eye) with a light and have the patient follow the light in various directions.

Cranial nerve IV (trochlear nerve). This nerve also helps with the movement of the eyes.

Cranial nerve V (trigeminal nerve). This nerve allows for many functions, including the ability to feel the face, inside the mouth, and move the muscles involved with chewing. The patient's healthcare provider may touch the face at different areas and watch the patient as he or she bites down.

Cranial nerve VI (abducens nerve). This nerve helps with the movement of the eyes. The patient may be asked to follow a light or finger to move the eyes.

Cranial nerve VII (facial nerve). This nerve is responsible for various functions, including the movement of the face muscle and taste. The patient may be asked to identify different tastes (sweet, sour, bitter), asked to smile, move the cheeks, or show the teeth.

Cranial nerve VIII (acoustic nerve). This nerve is the nerve of hearing. A hearing test may be performed on the patient.

Cranial nerve IX (glossopharyngeal nerve). This nerve is involved with taste and swallowing. Once again, the patient may be asked to identify different tastes on the back of the tongue. The gag reflex may be tested.

Cranial nerve X (vagus nerve). This nerve is mainly responsible for the ability to swallow, the gag reflex, some taste, and part of speech. The patient may be asked to swallow and a tongue blade may be used to elicit the gag response.

Cranial nerve XI (accessory nerve). This nerve is involved in the movement of the shoulders and neck. The patient may be asked to turn his or her head from side to side against mild resistance, or to shrug the shoulders.

Cranial nerve XII (hypoglossal nerve). The final cranial nerve is mainly responsible for movement of the tongue. The patient may be instructed to stick out his or her tongue and speak.

Coordination exam:

The patient may be asked to walk normally or on a line on the floor.

The patient may be instructed to tap his or her fingers or foot quickly or touch something, such as his or her nose with eyes closed. 

Find a Treatment Center

• Neurology and Neurosurgery

Find Additional Treatment Centers at:

• Howard County Medical Center
• Sibley Memorial Hospital
• Suburban Hospital

Request an Appointment

Facioscapulohumeral Muscular Dystrophy in Children

Moyamoya Disease

Motor Stereotypies

Related Topics

Want to create or adapt books like this? Learn more about how Pressbooks supports open publishing practices.

6.10 Neurological Assessment

Now that we have reviewed tests included in a neurological exam, let’s review components of a routine neurological assessment typically performed by registered nurses. The neurological assessment begins by collecting subjective data followed by a physical examination.

Subjective Assessment

Subjective data collection guides the focus of the physical examination. Collect data from the patient using effective communication and pay particular attention to what the patient is reporting, including current symptoms and any history of neurological illness. Ask follow-up questions related to symptoms such as confusion, headache, vertigo, seizures, recent injury or fall, weakness, numbness, tingling, difficulty swallowing (called dysphagia ) or speaking (called dysphasia ), or lack of coordination of body movements. [1]

See Table 6.10a for sample interview questions to use during the subjective assessment

Table 6.10a Interview Questions Related to Subjective Assessment of Neurological System

Life Span Considerations

At birth, the neurologic system is not fully developed. The brain is still developing, and the newborn’s anterior fontanelle doesn’t close until approximately 18 months of age. The sensory and motor systems gradually develop in the first year of life. The newborn’s sensory system responds to stimuli by crying or moving body parts. Initial motor activity is primitive in the form of newborn reflexes. Additional information about newborn reflexes is provided in the “ Assessing Reflexes ” section. As the newborn develops, so do the motor and sensory integration. Specific questions to ask parents or caregivers of infants include the following:

• Have you noticed your infant sleeping excessively or having difficulty arousing?
• Has your infant had difficulty feeding, sucking, or swallowing?

Depending on the child’s age and developmental level, they may answer questions independently or the child’s parent/guardian may provide information. Specific questions for children include the following:

• Have you ever had a head injury or a concussion?
• Do you experience headaches? If so, how often?
• Have you had a seizure or convulsion?
• Have you noticed if your child has any problems with walking or balance?
• Have you noticed if your child experiences episodes of not being aware of their environment?

Older Adults

The aging adult experiences a general slowing in nerve conduction, resulting in a slowed motor and sensory interaction. Fine coordination, balance, and reflex activity may be impaired. There may also be a gradual decrease in cerebral blood flow and oxygen use that can cause dizziness and loss of balance. Examples of specific subjective questions for the older adult include the following:

• Have you ever had a head injury or recent fall?
• Do you experience any shaking or tremors of your hands? If so, do they occur more with rest or activity?
• Have you had any weakness, numbness, or tingling in any of your extremities?
• Have you noticed a problem with balance or coordination?
• Do you ever feel lightheaded or dizzy? If so, does it occur with activity or change in position?

Objective Assessment

The physical examination of the neurological system includes assessment of both the central and peripheral nervous systems. A routine neurological exam usually starts by assessing the patient’s mental status followed by evaluation of sensory function and motor function. Comprehensive neurological exams may further evaluate cranial nerve function and deep tendon reflexes. The nurse must be knowledgeable of what is normal or expected for the patient’s age, development, and condition to analyze the meaning of the data that are being collected.

Nurses begin assessing a patient’s overall neurological status by observing their general appearance, posture, ability to walk, and personal hygiene in the first few minutes of nurse-patient interaction. For additional information about obtaining an overall impression of a patient’s status while performing an assessment, see the “ General Survey ” chapter.

Level of orientation is assessed and other standardized tools to evaluate a patient’s mental status may be used, such as the Glasgow Coma Scale (GCS), NIH Stroke Scale, or Mini-Mental State Exam (MMSE). Read more information about these tools under the “ Assessing Mental Status ” section earlier in this chapter.

The nurse also assesses a patient’s cerebellar function by observing their gait and balance. See the “ Assessing Cerebellar Function ” section earlier in chapter for more information.

Auscultation

Auscultation refers to the action of listening to sounds from the heart, lungs, or other organs with a stethoscope as a part of physical examination. Auscultation is not typically performed by registered nurses during a routine neurological assessment. However, advanced practice nurses and other health care providers may auscultate the carotid arteries for the presence of a swishing sound called a bruit . Bruits suggest interference with cerebral blood flow that can cause neurological deficits.

Palpation during a physical examination typically refers to the use of touch to evaluate organs for size, location, or tenderness, but palpation during the neurologic physical exam involves using touch to assess sensory function and motor function. Refer to sections on “ Assessing Sensory Function ,” “ Assessing Motor Strength ,” “ Assessing Cranial Nerves ,” and “ Assessing Reflexes ” earlier in this chapter for additional information on how to perform these tests.

See Table 6.10b for a summary of expected and unexpected findings when performing an adult neurological assessment.

Table 6.10b Expected Versus Unexpected Findings on Adult Neurological Assessment

• This work is a derivative of Clinical Procedures for Safer Patient Care by British Columbia Institute of Technology licensed under CC BY 4.0 ↵

Difficulty swallowing.

Difficulty speaking.

A swishing sound heard upon auscultation.

Nursing Skills - 2e Copyright © 2023 by Chippewa Valley Technical College is licensed under a Creative Commons Attribution 4.0 International License , except where otherwise noted.

Share This Book

Internet Book of Critical Care (IBCC)

Online Medical Education on Emergency Department (ED) Critical Care, Trauma, and Resuscitation

Neurological examination & neuroanatomy

May 14, 2022 by Josh Farkas

• Rapid Reference 🚀

Neurological examination

• Level of consciousness
• Motor responses to pain
• Breathing patterns
• Approach to anisocoria
• Unilateral pupillary abnormalities
• Horner's syndrome
• Bilateral pupillary abnormalities
• CN3-Oculomotor nerve
• CN6-Abducens nerve
• Testing of horizontal gaze abnormalities
• Peripheral CN6-abducens lesion
• Lateral gaze palsy
• INO (internuclear ophthalmoplegia)
• WEBINO (well-eyed internuclear ophthalmoplegia)
• One-and-a-half syndrome
• CN5-Trigeminal nerve
• CN7-Facial nerve
• Corneal reflex
• Blink reflex
• Cough reflex
• CN11-Spinal Accessory nerve
• CN12-Hypoglossal nerve
• Motor pathways & weakness
• Deep tendon reflexes
• Babinski sign
• Hoffmann sign
• Extremity coordination
• Vibration & proprioception
• Pain & temperature
• Visual pathway
• Pointers on localizing motor & sensory loss

Neuroanatomy & Lesion Localization

• Cerebral hemispheres
• Weber syndrome
• Claude syndrome
• Benedikt syndrome
• Parinaud syndrome
• Marie-Foix syndrome
• Wallenberg syndrome
• Foville syndrome
• Dejerine syndrome
• Bilateral hemispheric dysfunction
• Uncal herniation
• Downward central herniation
• Upward transtentorial herniation
• Tonsillar herniation
• Falcine herniation
• Brainstem displacement from a cerebellar mass
• Questions & discussion

(back to contents)

ability to follow commands?

• Ask to blink and to look up/look down (to evaluate for locked in state).
• 💡 Avoid asking to squeeze fingers, as this is potentially a grasp reflex. (Nelson, 2020)

ability to track or attend a stimulus?

• Apraxia of eyelid opening often occurs with non-dominant hemisphere lesions, but it can also occur with lesions in the medial frontal lobe, rostral brainstem, or basal ganglia (Parkinson's disease and Parkinson-plus syndromes). 🌊
• Both eyes are affected.
• The most potent visual stimulus is one's face. A smartphone may be used in selfie mode to determine if the patient will track to an image of their own face.
• ? Blink to threat (more on the blink reflex here: 📖 ).

how to examine

• For awake patients, ask them to move their extremities.
• Supraorbital pressure may be helpful, as this facilitates differentiation between localization versus withdrawal.
• A sternal rub may be less precise, but it provides very potent stimulation. This may be useful for patients who are unresponsive to less aversive stimuli.
• ⚠️ Sternal rub is contraindicated in patients status post recent surgical sternotomy. (Dunser 2019)

observe for

• Grimacing without withdrawal may suggest an intact sensory response, with motor paralysis.
• Extremity flexion without grimacing in the lower extremity may be seen in the presence of brain death, due to a spinal reflex known as triple flexion. Triple flexion is also suggested if the patient responds exactly the same way, regardless of where their foot is stimulated (e.g., dorsum vs. sole). ( 24636925 )
• Presence of any asymmetry (e.g., an asymmetric grimace or motor response implies the presence of a focal lesion).
• Motor responses to pain (listed below).

potential motor responses to pain

• (1) Stimulation of the supraorbital ridge or temporomandibular joint, causing the patient to bring their hand to their head.
• (2) Arm crosses midline, in efforts to alleviate a painful stimulus on the contralateral side.
• Withdraws to pain (GCS M4) : The patient moves their arm in response to pain. This may include crude movements, or flexion of the arm towards the source of pain. The patient is able to move somewhat, but not in a meaningful way to evade the source of pain.
• Flexor posturing (decorticate; GCS M3) is loosely associated with damage at the level of the thalamus.
• Extensor posturing (decerebrate; GCS M2) is loosely associated with damage at the level of the midbrain. This may be associated with downward herniation, or compression of the brainstem by posterior fossa lesions. However, occasionally severe toxic/metabolic etiologies may also cause decerebrate posturing (e.g., hepatic encephalopathy); normal pupillary size and response may support a toxic/metabolic etiology.
• No motor response (GCS M1) : Lesions below the pons may cause loss of all motor responsiveness (other than spinal reflexes such as triple flexion of the lower limbs).

how to observe breathing patterns

• Nonintubated patient: simple observation.
• Intubated patient: lift sedation (e.g., propofol) and place the patient on a pressure support mode (e.g., 10 cm pressure support with 5 cm PEEP). This allows patients to drive the rate and depth of respiration without interference, thus revealing their native breathing pattern.
• ⚠️ Localization is much less precise than has been suggested. ( 27907952 )

Cheyne-Stokes respiratory pattern

• This is defined as a sinusoidal breathing pattern, reflective of a delayed feedback loop involved in regulating CO2 levels (e.g., commonly seen in severe heart failure with poor cardiac output). Generation of this pattern requires intact brainstem respiratory reflexes .
• Heart failure with impaired cardiac output.
• Bilateral forebrain dysfunction (e.g., metabolic encephalopathies such as uremia, in which Cheyne-Stokes respiration is common). (Alpert 2019)
• Bilateral thalamic injury (e.g., downward transtentorial herniation).
• Acute stroke (especially extensive hemorrhagic stroke, but can occur with lacunar infarctions). ( 32924623 )

central neurogenic hyperventilation

• Diagnosis requires an ABG/VBG that demonstrates a primary respiratory alkalosis.
• (1) Midbrain or pontine lesions.
• (2) Bihemispheric lesions.

apneustic breathing

• This is a rare pattern that involves end-inspiratory pauses (figure above).
• Generally associated with bilateral pontine dysfunction (especially pontine infarction due to basilar artery occlusion).
• Rarely, may be seen in severe metabolic encephalopathies. (Alpert 2019)

cluster breathing

• Irregular clusters of breaths occur. This may mimic a Cheyne-Stokes pattern, but it lacks any smooth, sinusoidal transition between apnea and hyperventilation.
• Cluster breathing may reflect lower pontine or high medullary injury .
• Common causes include: stroke, cerebellar hemorrhage with brainstem compression, or anoxic encephalopathy. ( 32924623 )

ataxic (Biot's) breathing

• Breaths have various amplitude and length, with interspersed periods of apnea.
• ⚠️ This suggests an unstable respiratory rate that may progress to apnea. (Louis 2021)
• May reflect damage to the dorsomedial medulla (e.g., as a component of Wallenberg syndrome 📖 ). This should always raise concern for a medullary infarct .
• Often occurs as a preterminal event due to medullary damage as a result of tonsillar herniation. (Alpert 2019)
• May be associated with injury to the medulla (e.g., as a component of area postrema syndrome due to neuromyelitis optica spectrum disorders 📖 or in lateral medullary syndrome).

common signs of aphasia

• Paraphasias (substitution of one word for a similar word).
• Dysnomia (poor word retrieval).
• Abnormal speech fluency.
• Poor repetition (e.g., inability to repeat a sentence or phrase).
• Naming of objects is almost invariably impaired (regardless of the type of aphasia). (Albert 2019)

types of aphasia

• Broca's aphasia (nonfluent aphasia, with difficulty producing speech that frustrates the patient) – posterior inferior frontal lobe.
• Wernicke's aphasia (fluent, with poor comprehension) – superior temporal gyrus.
• Global aphasia – often due to a large lesion near the Sylvian fissure.
• Transcortical aphasias are marked by the ability to repeat normally, but deficiencies in either fluency or comprehension. These localize to areas outside of the perisylvian region.
• Localizes to the dominant (usually left) medial occipital cortex involving the splenium of the corpus callosum. It is a disconnection syndrome that results from disruption of interhemispheric communication across the corpus callosum. Normally, visual information from the nondominant visual cortex must be transmitted across the corpus callosum in order to be decoded into language. Writing remains intact because the angular gyrus and associated expressive language centers (Broca area) are intact and connected. ( 18533088 )
• Usually due to a PCA (posterior cerebral artery) stroke.
• If detected, this has strong localizing value. ( 18533088 )
• Alexia with agraphia (inability to write or to read) – May associate with lesions in the angular gyrus, or with Wernicke's aphasia. (Albert 2019)
• ⚠️ It takes months for an aphasia syndrome to have reliable localizing value. In acute neurological disorders, precise subtyping of aphasia may not localize accurately.

(1) historical features to consider

• History of ocular trauma or surgery?
• Check old photographs (chronic anisocoria?, chronic ptosis?).
• Exposure to topical medications? (including nebulized ipratropium).

(2) determine if its a sympathetic lesion or a parasympathetic lesion

• Anisocoria is greater in the dark (inability to dilate). This is especially noticeable within ~5-10 seconds of turning down the lights ( dilation lag ).
• Both eyes are briskly responsive to light (able to constrict).
• Small pupil is abnormal (unilateral miosis ).
• This often implies the presence of Horner's syndrome (especially if there is also ptosis ). More on the evaluation of possible Horner's syndrome below. 📖
• Anisocoria is greater in the light (inability to constrict).
• Larger pupil has a sluggish response to light ( impaired constriction ).
• Larger pupil is abnormal (unilateral mydriasis ).
• This is discussed further immediately below 👇.
• (If anisocoria is similar in light or dark this suggests the possibility of physiological anisocoria).

(2b) unilateral parasympathetic lesion (mydriasis) – differential diagnosis

• (1) Herniation syndrome compressing the nerve sheath.
• (2) Midbrain lesion affecting the CN3-oculomotor nucleus.
• (2) Focal seizure .
• Ipratropium got into the patient's eye (following nebulized administration).
• Patient touched their scopolamine patch and then rubbed their eyes.
• Dilated eye examination by an ophthalmologist.
• Isolated pupil dilation with light-near dissociation (reaction to accommodation is normal).

physiological anisocoria (benign variant) has the following features: 🌊

• (1) Degree of anisocoria is <1 mm.
• (2) Normal response to light and accommodation (this exonerates CN3).
• (3) Lack of ptosis.
• (4) Degree of anisocoria is similar in light and darkness (this exonerates the sympathetic system).
• (5) Chronic (may be seen on prior photographs, such as a driver's license).
• May indicate increased intracranial pressure (e.g., due to an acute hemispheric mass effect). (Wijdicks 2019) Ovoid pupils commonly precede anisocoria (unequal pupil size). (Dunser 2019)
• Oval or irregular pupils may be associated with midbrain pathology. (Alpert 2019)

RAPD (relative afferent pupillary defect, aka Marcus Gunn pupil)

• Usually caused by optic nerve pathology (or profound, extensive retinal disease).
• One pupil is less responsive to light, but does constrict when light is shone on the contralateral pupil (a consensual response).
• Swinging flashlight test: A flashlight is swung back and forth between the eyes, illuminating each eye for about two seconds. To avoid a near pupil response, the patient should fixate on a distant object and light should be shown on the eyes from below. The test is positive if the affected eye has reduced constriction and more rapid dilation (escape). In more severe cases, the affected eye may frankly dilate when light is shining on it.
• 🎥 : Relative afferent pupillary defect

diagnosis of Horner's syndrome

• Ptosis involves the upper and lower lids. Thus, the most accurate way to evaluate this is distance between the upper and lower eyelids (“palpebral length”).
• Examination in a darkened room may cause the normal pupil to dilate, thereby accentuating the difference between the pupils. The difference is greatest shortly after darkening the room ( dilation lag ; see the video below).
• Both pupils are briskly reactive to light (unlike anisocoria due to parasympathetic dysfunction).
• 🎥 Horner's syndrome: Dilation lag
• 🎥 Horner's syndrome: Ciliospinal reflex

differential diagnosis: other causes of unilateral ptosis

• Lesion of the CN3 (oculomotor nerve), which generally would be associated with a dilated pupil – more on this below. 📖
• Weakness of the levator palpebrae superioris due to neuromuscular pathology (e.g., myasthenia gravis) or muscular pathology (e.g., ocular myopathy).
• Sagging eyelids in the elderly (blepharoptosis) or due to prior eye surgery.

causes of Horner's syndrome

• Large thalamic hemorrhage , or posterolateral thalamic lesion. 🌊
• Early phase of central herniation syndromes (either upwards or downwards herniation). 📖
• Inferior lateral pons (Marie-Foix syndrome 📖 ).
• Lateral medulla (Wallenberg's syndrome 📖 ).
• Spinal cord lesion (C1-T2 level). (Alpert 2019)
• Brachial plexus lesion .
• Cancer in the lung apex (Pancoast tumor).
• Thoracic surgery or chest tube placement.
• Internal carotid artery dissection . 📖
• Neck surgery .
• Cavernous sinus pathology .

bilateral dilated & fixed

• Bilateral midbrain damage causing loss of parasympathetic output from CN3-oculomotor (most often due to early transtentorial herniation).
• Extremely deep metabolic coma (e.g., hypothermia, barbiturates, bupropion, lidocaine, sympathomimetics).
• Anticholinergic drugs at high dose (especially atropine).
• Botulism. 📖

bilateral dilated & reactive

• Anticholinergic drugs.
• Withdrawal from alcohol or benzodiazepines.
• Sympathomimetics (e.g., amphetamine, cocaine, methamphetamines, MDMA).
• Serotonin syndrome.
• Generalized seizure, including the postictal period.

bilateral mid-position & fixed

• Bilateral midbrain damage with loss of sympathetic and parasympathetic output (most commonly seen after herniation, or in patients with brain death).
• Profound barbiturate coma (but not high doses of IV benzodiazepines or propofol). ( 27907952 )
• Hypothermia.

bilateral mid-position & reactive (normal pupils)

• (#1) Most likely, this may be toxic/metabolic coma, causing diffuse dysfunction of the cerebral cortex.
• (#2) Lesions in the dorsolateral, upper-mid pons.
• (#3) Bilateral thalamic dysfunction.
• Neuromuscular blocking medications (note that smooth muscles of the iris don't get paralyzed).

bilateral small pupils

• Medications (e.g., cholinergic agonists, opioids, clonidine, ACE-inhibitors).
• Usually due to extensive pontine hemorrhage (“pontine pupils”).
• May occur in the early phase of central herniation syndromes (either upwards or downwards herniation).
• Argyll Robertson pupils (bilateral small, irregular, and often asymmetric pupils that retain responsiveness to accommodation, but not to light; video example 🎥 ).

features of CN3 palsy

• (1) Pupil dilation – May be the first finding due to external compression of the nerve, since parasympathetic fibers run along the outside of the nerve.
• (2) Ptosis (CN3 supplies the levator palpebrae, which elevates the eyelid).
• (3) Eye position is down and out (due to unopposed actions of abducens and superior oblique muscles).

clues to further localization

• Bilateral ptosis and bilateral superior rectus palsy (suggests lesion of the CN3 nucleus, given bilateral innervation of these muscles).
• Contralateral hemiplegia (as a component of Weber syndrome 📖 ).
• Contralateral ataxia (as a component of Benedikt syndrome 📖 ).
• Contralateral tremor (as a component of Claude's syndrome 📖 ).
• Intrinsic nerve micro-infarction due to diabetes/hypertension may cause abnormal eye position without affecting the pupils, because this affects the innermost fibers of the nerve. This clinical presentation is less worrisome for a mass lesion.
• However, another possibility that should be considered here is superior divisional CN3 palsy , which presents as ptosis and limited upward eye movement without pupillary involvement. This is most commonly associated with lesions in the anterior cavernous sinus or superior orbital fissure that compress the superior division of the nerve. However, other causes may include intrinsic brainstem disease, aneurysms, or leptomeningeal carcinomatosis. ( 32924623 )

important causes of CN3-oculomotor dysfunction

• Brainstem lesions involving the CN3 nucleus.
• 🚨 Uncal herniation (usually ipsilateral). 📖
• Meningitis.
• Aneurysm of the posterior communicating artery, posterior cerebral artery, superior cerebellar artery, or internal carotid artery. (Alpert 2019, 32924623 ) Aneurysms of the anterior communicating artery or posterior cerebral artery may rarely cause contralateral CN3 dysfunction, possibly due to compression of the nerve against the tentorium. ( 32924623 )
• Skull base tumors.
• Cavernous sinus disorder (additional nerves are usually involved including trochlear, abducens, and division V1 of the trigeminal).
• Postoperative.
• Idiopathic intracranial hypertension. ( 32924623 )

manifestation of CN6 palsy

• Inability to abduct the ipsilateral eye (i.e., temporal, or outward movement).

sub-localization of CN6 palsy

• (1) Involvement of nearby CN7-facial , causing facial weakness.
• (2) Inability to adduct the contralateral eye (complete lateral gaze palsy 📖 , due to damage to the pontine lateral gaze center).
• (3) Contralateral hemiparesis . If the pontine lesion also involves the corticospinal tract, eyes deviate away from the lesion (and toward the paretic limb). This is sometimes called “wrong way eyes,” since it is the opposite of the more commonly seen pattern which occurs with destructive lesions of the frontal lobe (wherein eyes look away from the paretic limb). Wrong way eyes usually indicate a contralateral pontine lesion involving the abducens nucleus, but this can also be caused by thalamic hemorrhage. (Berkowitz 2017)
• Abducens nucleus damage is a component of inferior medial pontine syndrome ( Foville syndrome ). 📖

causes of CN6 palsy

• Abducens nerve palsy is frequently a nonspecific sign of increased intracranial pressure. (This may result from any process that exerts downward pressure on the brainstem.)
• Elevated intracranial pressure may especially be suggested by bilateral CN6 palsies.
• (More on the diagnosis of elevated intracranial pressure here: 📖 )
• Pontine pathology (additional abnormalities would usually be expected, as described above).
• Wernicke encephalopathy .
• Cavernous sinus lesion (should see other cranial nerves involved as well, especially CN3-oculomotor and/or CN4-trochlear).
• Meningitis , syphilis, or Lyme disease.
• Skull base neoplasm.
• Microvascular ischemia (e.g., diabetes, hypertension, smoking).
• Multiple sclerosis.

neuroanatomy of horizontal gaze

• Gaze may be stimulated from the frontal eye fields, or as a reflex via the vestibular nerve (e.g., cold caloric reflexes).
• In both scenarios, gaze starts with CN 6 stimulating ipsilateral abduction. CN 6 communicates with the contralateral CN3 via the MLF (medial longitudinal fasciculus), to coordinate contralateral eye adduction .

how to test gaze abnormalities

• Awake & communicative patient: Ask the patient to follow your finger, or ask them to look to the right and the left. This stimulates a pathway involving the frontal eye fields and the PPRF (paramedian pontine reticular formation). It also requires the patient to have intact hearing and language comprehension.
• When the head is rotated, the eyes normally turn in the opposite direction (thereby staying fixated in roughly the same direction). This test shouldn't be performed in patients with C-spine injury (among whom cold caloric testing may be used instead).
• This is easily tested, as a front-line evaluation of eye movements in comatose patients. Intact oculocephalic reflexes argue strongly against a structural cause of coma. However, this reflex may be muted in deep metabolic coma, so symmetric absence of eye movements doesn't necessarily indicate a structural lesion.
• If the oculocephalic reflex is absent, cold caloric testing should be performed, since cold caloric testing provides a stronger stimulus to more rigorously evaluate eye movements.
• In awake patients, the oculocephalic reflex is overcome by voluntary gaze control. ( 24636925 ) If it's unclear whether an abnormal oculocephalic reflex is due to voluntary gaze control versus brainstem pathology, this may also be sorted out using cold caloric testing (discussed further below).
• This involves slowly flushing the ear with 50 ml of ice water, with the head of the bed inclined at a 30-degree angle (to properly align the semicircular canal). At least five minutes should be allowed to pass in between testing each ear.
• In a comatose patient with intact brainstem reflexes, this will cause the eyes to rotate towards the stimulated ear.
• ⚠️ Cold calorics may elicit nausea and vomiting in awake or mildly somnolent patients.

response to cold calorics often reveals an objective assessment of the patient's level of consciousness

• In patients without structural brainstem lesions, cold calorics will provide an objective determination of the patient's level of consciousness. This may be especially useful to expose states such as functional coma. Responses may be classified along a spectrum, as follows (Alpert 2019)
• #1) Completely normal response : Contralateral nystagmus occurs, without significant eye deviation. The cerebrum maintains complete control of eye position, albeit with some slow deviations (due to cold caloric stimulation) that are promptly corrected via nystagmus (fast-phase nystagmus occurs away from the cold ear). In a patient who appears to be clinically comatose, this unexpected finding would suggest functional coma (pseudocoma), malingering, or akinetic mutism.
• #2) Mildly abnormal response : Eyes deviate towards the cold ear, with contralateral nystagmus. The cerebrum loses control of eye position, but it is still attempting to drag the eye back to a normal position. This could be seen with bilateral hemispheric dysfunction causing lethargy or obtundation.
• #3) Ipsilateral eye deviation only : Eyes deviate towards the cold ear, without nystagmus. This reflects intact function of the brainstem, with no input from the cerebrum. Clinically this pattern may be seen in a patient with bilateral hemispheric dysfunction causing stupor/coma.
• #4) No response at all : Brainstem reflexes to caloric stimulation are mute. Absent vestibulo-ocular reflexes usually indicate brainstem pathology (e.g., this is seen in brain death). However, this may also be seen in very deep toxic/metabolic coma (e.g., phenytoin, tricyclic antidepressants, sedatives) or following administration of paralytics. Thus, the differential diagnosis here may include various brain-death mimics (more on these here 📖 ).

Below are some more common horizontal gaze abnormalities. These may be elicited when patients try to move their eyes, or by vestibulo-ocular reflexes.

frontal lobe damage causes a gaze preference

• Cortical damage (e.g., stroke) ➡️ Eyes deviate towards the lesion & away from the paretic limb.
• ⚠️ Postictal findings after a seizure will mimic those seen during a stroke.
• Eyes are able to cross the midline during cold calorics or doll's eyes maneuvers (thus, this is a gaze preference ). In contrast, gaze paralysis is caused by brainstem lesions (more on these below).

peripheral lesion of CN6-abducens

• This causes an ipsilateral inability to abduct the eye (in response to any stimuli).
• More on abducens nerve (CN6) palsy: 📖 .

lateral gaze palsy (damage to CN6-abducens nucleus or PPRF)

• Unlike frontal lobe lesions, pontine lesions cause gaze paralysis , which cannot be overcome by the oculocephalic reflex or cold caloric stimulation.
• Further discussion of abducens nucleus damage: 📖 .
• Damage to the PPRF (paramedian pontine reticular formation) would cause an identical pattern of abnormalities in response to volitional eye movements triggered via the frontal eye fields. However, PPRF damage wouldn't be expected to affect the oculocephalic or vestibulo-ocular reflexes.

INO (internuclear ophthalmoplegia, due to unilateral MLF damage)

• A lesion of the MLF impairs the ability of the ipsilateral eye to adduct.
• Convergence (bilateral adduction) is preserved, since this doesn't depend on the MLF pathway. Preservation of convergence demonstrates that the CN3 and medial rectus muscles are functional – they just aren't being triggered properly during horizontal gaze. (However, skew deviation can occur in patients with internuclear ophthalmoplegia, which may make it difficult to test convergence.)
• If the patient is awake , there may be nystagmus of the normal abducting eye (as if trying to tell the other eye to come along). (Berkowitz 2017)
• Causes of internuclear ophthalmoplegia include multiple sclerosis, pontine stroke, or tumor. Among patients <50 years old, multiple sclerosis is most likely. (Alpert 2019)
• 🎥 : Internuclear ophthalmoplegia examples.

WEBINO (wall-eyed bilateral internuclear ophthalmoplegia, due to bilateral MLF damage)

• Neither eye is able to adduct properly.
• Sometimes, the eyes may be abducted at baseline, creating a “wall-eyed” appearance.
• Bilateral damage to the CN3 nuclei may cause a similar pattern, with inability of either eye to adduct. However, this would be expected to cause additional abnormalities (e.g., ptosis and pupil dilation – see the section on CN3 dysfunction: 📖 ).
• Progressive supranuclear palsy may present similarly, but vestibulo-ocular reflexes remain intact. ( 32924623 )
• Common causes: multiple sclerosis, brainstem tumor, or stroke.
• Less common causes: cryptococcus, neuromyelitis optica spectrum disorder.
• 🎥 : WEBINO

one-and-a-half syndrome

• This results from a medial, dorsal (posterior), caudal pontine lesion that affects the CN6 nucleus and the ipsilateral MLF (e.g., Foville syndrome 📖 ).
• (1) The only possible horizontal gaze is abduction of the contralateral eye towards the unaffected side. This often induces nystagmus in abduction.
• (2) Convergence is intact.
• (3) Patients often have ipsilateral facial weakness, due to involvement of the nearby facial nerve (CN7) nucleus. This may be termed an “eight-and-a-half” syndrome (i.e., 7+1.5 = 8.5). (Albin 2022)
• More common: Ischemic stroke, demyelinating disease (e.g., multiple sclerosis), infection.
• Less common: Head trauma, mass lesions (e.g., brain tumors or arteriovenous malformations).
• 🎥 : One-and-a-half syndrome

skew deviation (one eye looks up, other looks down)

• Skew deviation suggests a unilateral cerebellar lesion or a unilateral brainstem lesion (usually involving the CN8 nucleus). Asymmetric dysfunction of the vestibular system causes the brain to think the head is tilted when it is not. (Berkowitz 2017)
• In the context of a comatose patient, skew deviation may suggest a basilar artery occlusion . (Wijdicks 2021)

upward gaze may be caused by:

• Usually due to bihemispheric damage (e.g., following severe anoxic injury).
• Brainstem injury. (Torbey, 2019)
• Oculogyric crisis.

downward gaze may be caused by:

• Bilateral hemispheric dysfunction (e.g., anoxic injury, metabolic coma).
• Thalamic injury (e.g., hemorrhage).
• (Hydrocephalus is a common cause.)

horizontal conjugate roving eye movements

• This refers to spontaneous, synchronized movements of the eyes back and forth. Some texts differentiate between “ conjugate roving ” versus “ ping-pong ” movements, but they seem to be fundamentally similar phenomena. Spontaneous roving eye movement is often seen in patients with a reduced level of consciousness. (Wijdicks 2019)
• These movements reveal normal function of midbrain and pons.
• (1) Bilateral cerebral hemispheric dysfunction. In the context of coma, horizontal conjugate eye movements exonerate the brainstem, thereby implying that the coma is due to bilateral cerebral hemispheric dysfunction (e.g., a toxic/metabolic coma). Severe bilateral hemispheric infarction can also cause this. ( 32924623 )
• (2) Lesions in the cerebellar vermis may also cause horizontal conjugate roving eye movements (but such lesions in isolation wouldn't be expected to cause coma). ( 28187795 )
• 🎥 : Ping-pong gaze.

ocular bobbing or dipping

• Bobbing (rapid down, slow up) suggests a pontine lesion (video below). ( 28187795 )
• Dipping (slow down, rapid up) might suggest bihemispheric dysfunction (e.g., anoxia or a metabolic disorder)(video below). ( 28187795 ) However, ocular dipping may be caused by a variety of lesions, so it lacks definitive localizing value. (Flemming 2022)
• 🎥 : Ocular bobbing.
• 🎥 : Ocular dipping.

nystagmus – see section below 📖

• Opsoclonus is a dyskinesia marked by rapid, involuntary, chaotic, multidimensional conjugate eye movements without inter-saccadic intervals (“saccadomania” – example in the video below). ( 33232023 )
• Ocular flutter is similar, but ocular flutter occurs only in the horizontal direction.
• Nystagmus may appear similar, but nystagmus involves both a fast (saccadic) phase and a slow phase.
• OMS (opsoclonus-myoclonus syndrome) is associated with paraneoplastic syndromes or viral infection (opsoclonus combined with myoclonus and/or ataxia, encephalopathy, generalized tremor).
• Toxicologic : Amitriptyline, barbiturates, benzodiazepines, ketamine, lithium 📖 , organophosphates, phencyclidine, phenytoin, salicylates, sympathomimetics (amphetamines, cocaine, serotonin syndrome), toluene, venlafaxine.
• Parainfectious: Often seen in younger patients, may associate with truncal myoclonus and ataxia. Causes include HIV, enterovirus, mumps, Zika virus, CMV, COVID-19.
• Paraneoplastic: Often seen in older patients; causes include small cell lung cancer, breast cancer, and ovarian cancer.
• Stroke (may occur as a component of lateral medullary syndrome).
• Brain tumor.
• Brainstem encephalitis.
• Demyelinating disorders (including multiple sclerosis, neuromyelitis optica spectrum disorders, and MOG-IgG associated).
• Traumatic brain injury.
• Wernicke encephalopathy.
• Hyperosmolar hyperglycemic state.

Nystagmus is named after the fast phase. The differential diagnoses below focus on more acute and common forms relevant to critical care, without attempting to be comprehensive. (Frucht 2022)

central nystagmus (often due to brainstem pathology) 🌊

• Wernicke encephalopathy. 📖
• Antiepileptic agents.
• Alcohol, sedatives (intoxication is a common cause).
• Chiari I malformation.
• Cervicomedullary junction or cerebellar lesions; or less often pontine or medullary lesions (e.g., tumor, stroke, demyelination).
• Infection (e.g., West Nile encephalomyelitis).
• Paraneoplastic.
• Medications (e.g., amiodarone, antiepileptic agents, lithium, opioids) or alcohol use.
• B12 or magnesium deficiency. 📖
• Hydrocephalus. ( 32924623 )
• Medullary lesions, or less commonly midbrain lesions (e.g., stroke, demyelination).
• Paraneoplastic disorders.
• Convergence-retraction nystagmus – see Parinaud syndrome. 📖
• Pure rotatory nystagmus (best noted by looking at the blood vessels in the sclera). This is most common with brainstem lesions involving the vestibular nuclei, especially medullary lesions as a component of Wallenberg syndrome 📖 . (Alpert 2019)
• Pendular nystagmus (symmetrically oscillating eye movements with no dominant direction; usually congenital but can occur due to demyelination, following brainstem stroke, Whipple disease, or toluene abuse).
• 💡 Brainstem lesions are a more common cause of nystagmus than pure cerebellar pathology. (Alpert 2019)
• Seizures may cause horizontal nystagmus, with the fast phase directed contralateral to the epileptic focus. (Alpert 2019) This may be mediated by stimulation of frontal eye fields (discussed further above 📖 ).
• Nystagmus may last for the duration of the seizure. Most seizures are self-limiting within <5 minutes, so nystagmus would last for only a few minutes. However, patients with persistent NCSE (nonconvulsive status epilepticus) could experience ongoing nystagmus (more on nonconvulsive status epilepticus here: 📖 ).
• Other than during seizure, cortical lesions don't cause nystagmus. (Alpert 2019)

peripheral nystagmus

• May be overcome by visual fixation.
• May be associated with ear pathology (e.g., hearing loss).
• Direction of the nystagmus is generally the same (with the fast phase towards the normally functional side). However, vestibular disease may cause direction-changing positional nystagmus in supine patients, wherein the direction of the nystagmus varies depending on which ear is facing downward.
• Nystagmus may be either horizontal or a combination of horizontal and rotatory (clockwise when the fast phase is to the left or counterclockwise when the fast phase is to the right). (Alpert 2019)
• Nystagmus is most marked when looking away from the lesion (looking in the direction of the fast phase).
• No features of additional brainstem pathology.
• Peripheral nystagmus is caused by lesions of the semicircular canals within the ear or CN8-vestibulocochlear (e.g., Meniere's disease, vestibular neuronitis, benign paroxysmal positional vertigo).

functions of CN5-trigeminal

• Numb chin syndrome is often a manifestation of multiple sclerosis or systemic malignancy. ( 32924623 )
• Muscles of mastication (each trigeminal nucleus is innervated bilaterally by the motor cortex, so unilateral lesions in the motor cortex usually cause no deficit in jaw movement). (Blumenfeld 2022)

involvement in reflexes

• The V1 division of the trigeminal nerve is involved in the corneal reflex : 📖 .
• The jaw jerk reflex involves purely CN5-trigeminal (which mediates both afferent and efferent limbs). The jaw jerk is normally absent or minimal. A brisk jaw jerk reflex suggests bilateral upper motor neuron pathology, above the level of the trigeminal motor nuclei (as may be seen in amyotrophic lateral sclerosis or diffuse white matter disease). (Alpert 2019; Blumenfeld 2022)
• 🎥 : Jaw jerk reflex.

The primary function of the facial nerve is to innervate the facial musculature . The facial nerve is involved in the efferent limb of the corneal reflex (discussed further below 📖 ).

upper motor neuron lesion (e.g., motor cortex)

• Weakness predominantly involves the lower face. (The forehead receives bilateral innervation from both cortical hemispheres, so it is spared.)
• Emotional expression (e.g., spontaneous smiling) may be preserved, because the frontal lobe and extrapyramidal systems also provide stimulation to the facial nucleus. However, patients may be unable to smile upon command!
• Caused by any lesion within the corticobulbar tract that lies above the facial nucleus (e.g., the motor cortex).

lower motor neuron lesion (facial nerve or facial nucleus in brainstem)

• Weakness of the entire ipsilateral face.
• Hyperacusis.
• A lower motor neuron lesion usually indicates a lesion within the facial nerve (e.g., Bell's palsy).
• However, a lower motor neuron lesion can involve the cranial nerve nucleus, or the nerve fascicle as it exits the brainstem – so this can occur in the context of brainstem pathology. Lesions of the facial nucleus usually localize to the posterior, inferior pons (e.g., Foville syndrome 📖 or Marie-Foix syndrome 📖 ).

neuroanatomy

• The afferent limb involves the ophthalmic division of the trigeminal nerve (V1). The efferent limb of the reflex occurs via CN7-facial.
• Stimulating one eye should elicit blinking bilaterally .

eliciting the corneal reflexes

• Dropping saline from a sterile saline flush is the kindest and gentlest approach to eliciting corneal reflexes. If this succeeds in eliciting corneal reflexes, then it may be concluded that the patient has intact corneal reflexes.
• Gently touching the edge of the cornea with gauze provides a stronger stimulus to elicit corneal reflexes, so this may be used if there is doubt about the reflex. Ensure that you are truly touching the cornea (rather than the sclera of the eye).

interpretation

• ⚠️ The corneal reflex may be sensitive to sedation.
• Unilateral pontine injuries may cause an ipsilateral loss of the corneal reflex. (Nelson, 2020)
• If the contralateral eye blinks but the ipsilateral eye does not, this indicates an ipsilateral facial nerve (CN7) paralysis.
• Bell's phenomenon: Conjugate upward deviation of the eyes without eyelid closure. Normally the eyes often elevate when they close, but we are unable to observe this. Seeing the eyes elevate indicates intact sensation (CN5) and intact pathways to CN3 (to elevate the eye), with dysfunction of the eyelid (CN7) – essentially revealing a CN7 palsy . (Torbey, 2019)
• Jaw deviates away from the side of corneal stimulation, along with bilateral eye blinking.
• Implies a structural lesion injuring the trigeminal nucleus above the mid-pons level. (Torbey, 2019) Potential causes include herniation, intrinsic upper brainstem lesions, amyotrophic lateral sclerosis, or multiple sclerosis.
• 🎥 : Corneomandibular reflex

blink to visual threat

• Involves: Optic nerve, a functioning visual cortex, and the facial nerve (CN7).
• (Shown in a video here .)

blink to auditory stimulus (aka, acoustic reflex)

• Tested by applying a loud auditory stimulus near the patient (e.g., clap).
• Unlike a visual threat, this does not require signal processing in the cortex. The acoustic loop runs through the brainstem. Thus, patients in persistent vegetative state may blink after a sound – without awareness of the sound. (Wijdicks 2019)

CN9 and CN10 generally function as a single entity

• CN9 and CN10 lie in very close proximity, with disease processes often involving both nerves. For example, motor fibers of both nerves originate from the nucleus ambiguus in the medulla.
• It's difficult to separately examine CN9 vs. CN10 during a basic neurologic examination, since their functions overlap.
• For general clinical purposes, it's reasonable to consider CN9/10 as a single functional entity.

functions of CN9/10

• Pharyngeal sensation and musculature (swallowing).
• Laryngeal muscles (speaking, mostly via the recurrent laryngeal nerve which is a branch of CNX-vagus).
• Aortic arch and carotid artery baroreceptors.
• CN10-vagus provides parasympathetic innervation to the heart, lung, and upper gastrointestinal tract.

clinical examination of CN9/10:

• Symmetric upward movement of the uvula suggests intact function of CN9/10.
• Unilateral damage to CN9/10 causes the uvula to be pulled towards the normal side.
• Bilateral damage to CN9/10 causes the uvula to remain immobile ; this may correlate with dysphagia (especially with liquids). (Alpert 2019)
• CN10-vagus innervates the vocal cords.
• Lesions to CN10 may be suggested by a breathy, nasal, or hoarse voice. (However, dysarthria may result from abnormalities in CN 5, 7, 9, 10, or 12 – so this isn't necessarily specific to a lesion of CN10).
• CN10-vagus is required for the afferent pathway of the cough reflex (section below).

basics of the cough reflex

• The cough reflex involves the vagus nerve (CN10, near the medulla). This reflex will be preserved in most coma states (which usually involve higher brain centers).
• Reliably eliciting the cough reflex requires an intubated patient, in whom endobronchial stimulation can be applied by suctioning the endotracheal tube.
• The cough reflex is one of the most durable reflexes, which is generally preserved even in severe brain injury. For example, following anoxic brain injury, lack of a cough reflex after 24 hours carries a likelihood ratio of 85 for poor neurologic outcome. ( 14970067 )

causes of an absent cough reflex include

• Damage to the medulla (e.g., tonsillar herniation, brain death).
• Extremely profound toxic/metabolic coma (e.g., barbiturate or baclofen overdose).
• Neuromuscular paralysis (e.g., lingering effects of rocuronium used for intubation).

💡 When encountering a patient who lacks a cough reflex without any obvious cause, always consider the possibility of a lingering neuromuscular paralytic agent . If the patient otherwise appears paralyzed (e.g., absent deep tendon reflexes), this should be immediately evaluated at the bedside using a peripheral nerve stimulator .

⚠️ please stop gagging patients

• The presence of a gag reflex does not indicate that the patient is able to protect their airway. Airway protection involves swallowing reflexes, which are far more complex than a simple gag reflex.
• Many people normally lack a gag reflex. Therefore, absence of a gag reflex isn't necessarily pathological, nor does this reveal any definitive information.
• Gagging patients may induce emesis, which could lead to aspiration.
• Further discussion of why gagging patients should be abandoned is here .

(One exception is that among patients with known posterior circulation strokes, serial evaluation of the gag reflex might help track the evolution of brainstem function over time.)

• CN11 is a motor nerve that innervates the trapezius (which raises the shoulder) and the sternocleidomastoid muscles . Contraction of one sternocleidomastoid turns the head, whereas contraction of both is involved in head flexion.
• Unilateral upper motor neuron lesion in the cortex causes contralateral weakness of the trapezius, with relative sparing of sternocleidomastoid strength. Similar to the upper facial muscles, the sternocleidomastoid muscle is controlled by the bilateral cerebral hemispheres. (Blumenfeld 2022) However, a focal seizure tends to cause contralateral neck flexion, suggesting that dominant control of each sternocleidomastoid muscle comes from the ipsilateral cerebral hemisphere.

clinical examination

• Trapezius strength is assessed by asking the patient to shrug their shoulders.
• Sternocleidomastoid strength may be assessed by asking the patient to turn their head in both directions. For a supine patient, lifting their head off the pillow requires the bilateral sternocleidomastoid muscles.

neck flexion weakness

• Bilateral weakness of the sternocleidomastoid muscles causes weakness of head flexion (e.g., patient may be unable to lift their head off the pillow).
• Common causes include myasthenia gravis, myopathy, and Guillain-Barre syndrome.
• Weakness of neck flexion may tend to track with respiratory muscle weakness . This could reflect that they share the same segmental innervation. ( 35863882 )
• Dysfunction of CN12-hypoglossal causes the tongue will deviate towards the paretic side.

causes of CN12 dysfunction include:

• Internal carotid dissection.
• Medial medullary syndrome (Dejerine syndrome). 📖

corticospinal tract (aka pyramidal system)

• Upper motor neuron cell bodies lie in the motor cortex (within the precentral gyrus).
• Their axons travel in the subcortical white matter within the posterior limb of the internal capsule.
• They run through the cerebral peduncles into the ventral/anterior brainstem.
• They cross (decussate) at the junction of the medulla and the cervical spinal cord.
• They run down the posterolateral spinal cord.
• Finally, upper motor neuron axons synapse onto lower motor nerves within the anterior horn of the spinal cord grey matter.

more on localization of weakness here: 📖

evaluation of reflexes:

• 0 = Absent.
• 1+ = Reduced, or seen only on reinforcement.
• 2+ = Normal.
• 3+ = Brisk.
• 4+ = Hyperreflexia associated with unsustained clonus.
• 5+ = Hyperreflexia with sustained clonus.
• 💡 Deep tendon reflexes are normal if they are 1+, 2+, or 3+ as long as they are symmetric and there isn't a dramatic difference between arms versus legs. (Blumenfeld 2022)
• Spreading of reflexes to muscles that aren't being tested is a reflection of hyperreflexia.

neuroanatomy of commonly tested reflexes:

• Biceps: C5-C6.
• Brachioradialis: C6.
• Triceps: C7.
• Patellar: L4.
• Achilles: S1.

For supine patients, patellar and ankle reflexes require supporting the joint in a mildly flexed position, as shown below. Crossing the patient's legs at the shins may also be helpful. A video on reflex testing is here .

general comments

• Clonus may be conceptualized as a form of profound hyperreflexia, wherein each muscle contraction triggers another reflexive contraction.
• Nonsustained clonus (<5-10 beats) that is symmetric may be normal. However, sustained clonus (>5-10 beats) is always abnormal. ( 30521283 ) Unfortunately there is some confusion about how to define “sustained clonus,” with some authors using this to refer to clonus that occurs indefinitely. ( 33522735 )
• As part of the physical examination, ankle clonus is generally tested (video below). However, clonus may occur at other joints as well (e.g., it could be inadvertently triggered while testing a patellar reflex).
• Spontaneous clonus is triggered by minor movement, leading to rhythmic, large muscle contractions. This may be confused with seizures.
• 🎥 : Clonus

causes of clonus include:

• Upper motor neuron dysfunction as spasticity develops (e.g., due to stroke, trauma, cerebral palsy, or multiple sclerosis).
• 💡 Toxicological clonus may be suggested by symmetric clonus and diffuse hyperreflexia (without any focal neurological signs).
• Serotonin syndrome 📖 is the most common toxicological association. Clonus due to serotonin syndrome is usually most prominent in the legs.
• Anticholinergic toxicity.
• Baclofen withdrawal.
• Preeclampsia. 📖
• Paraneoplastic or autoimmune encephalopathies.
• Sympathetic hyperactivity due to various etiologies. 📖

how to evaluate

• The patient's leg should be extended at the knee.
• Firm pressure with a somewhat sharp object should be applied to the lateral portion of the sole of the foot near the heel and slowly moved upwards. If there is no response, the stimulus can be turned when it reaches the base of the fifth toe and continued medially towards the ball of the foot. (Alpert 2019)
• Flexion (downward movement) is normal.
• Upwards (extension) movement is abnormal, termed a “positive Babinski sign.”
• It may sometimes to difficult to sort out a withdrawal response versus a Babinski sign. The Chaddock maneuver may also be used to elicit the same reflex, but this is less likely to elicit a withdrawal response. (Alpert 2019)
• A video showing evaluation of the Babinski sign.

significance

• A Babinski sign (upward extension of the large toe) is always abnormal [in adults]. This is an indication of upper motor neuron disease.
• A unilateral Babinski sign indicates pathology somewhere within the corticospinal tract (contralateral cerebral hemisphere, contralateral brainstem, or ipsilateral spinal cord).
• In isolation , this often suggests spinal cord pathology.
• A bilateral Babinski sign may result from brainstem or cerebral hemisphere dysfunction (e.g., due to bilateral brain injury, general anesthesia, coma from organ failure, or seizure). (Wijdicks 2021)
• Babinski sign may develop quickly (including even within the postictal phase after a seizure). ( 18674480 )
• Flicking the third digit causes flexion of the first and second digits.
• 🎥 : Hoffman's sign.
• The Hoffman sign is generally indicative of an upper motor neuron lesion (e.g., a cervical myelopathy).
• If the Hoffman sign is positive in both hands symmetrically, this may be a normal variant. (Albert 2019)

🎥 : How to evaluate muscle tone

causes of increased motor tone or rigidity 

• Intoxication (e.g., serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia).
• Withdrawal of Parkinson's medications. 📖
• Upper motor neuron lesion (involving the corticospinal tract).
• Basal ganglia dysfunction.
• Bilateral frontal lobe dysfunction may cause paratonic rigidity (discussed further below).

causes of flaccidity

• Acute upper motor neuron lesion (especially spinal cord injury) – may initially cause flaccidity, before development of spasticity. This may occur in the context of spinal shock. 📖
• Lower motor neuron lesion.
• Intoxication.
• Chemical paralysis.

multifocal myoclonus – more on this here 📖

Asterixis (negative myoclonus).

• Asterixis refers to sudden, brief, arrhythmic lapses of sustained posture due to involuntary interruption in muscle contraction. ( 27807107 )  
• This is commonly assessed by asking the patients to hold their hands outstretched, as if they were stopping traffic.  Asterixis may begin after a latent period of 30 seconds, so be cautious about immediately concluding that there is no asterixis. ( 27807107 )  
• Asterixis is usually an asymptomatic examination finding, but it can cause symptoms.

causes include

• Hepatic encephalopathy (although asterixis may be lost in the most severe stages of hepatic encephalopathy).
• Uremic encephalopathy .
• Hypercapnia and/or hypoxemia.
• Hypoglycemia.
• Severe electrolyte abnormalities (hypokalemia, hypomagnesemia). ( 36625084 )
• Urea cycle defects causing hyperammonemia.
• Wilson's disease.
• Antiseizure medications (e.g., phenytoin, valproate, carbamazepine, gabapentin).
• Anticholinergics.
• Benzodiazepines.
• Hemorrhage (subdural, subarachnoid, or intraparenchymal).
• Infarction.
• Neoplasia (primary or metastatic).
• Cerebral toxoplasmosis.
• Viral encephalitis.

fasciculations

• Fasciculations are small involuntary muscle contractions that don't cause movement across a joint.
• Any disease involving the lower motor neurons.
• Electrolyte abnormalities (e.g., hypomagnesemia, hypokalemia).
• Hyperthyroidism.
• Medication side effect (e.g., steroid, acetylcholinesterase inhibitors, isoniazid, bronchodilators, caffeine).
• Benzodiazepine withdrawal.
• Following brain death.

tremor: more common causes in the ICU

• Cerebellar lesion (intention tremor).
• Midbrain lesion (postural tremor).
• Beta-agonists.
• Dopamine antagonists.
• Amiodarone.
• Cyclosporine, Tacrolimus.
• Lithium 📖 .
• Withdrawal (e.g., alcohol or opioid). (Wijdicks 2021)
• (Tremors may occur as a component of acute onset parkinsonism, discussed further here: 📖 )

paratonic rigidity (gegenhalten)

• Paratonic rigidity is a form of hypertonia marked by involuntary variable resistance to passive movements (especially a quick movement of the arm). Resistance occurs with a force equal and opposite to that applied by the examiner. This may be misinterpreted as oppositional behavior. (Alpert 2019)
• Frontal lobe disorders, especially bilateral frontal lobe dysfunction (may be accompanied by a grasp reflex). (Louis 2021)
• Metabolic encephalopathy.
• Catatonia. 📖

Gait often cannot be tested in critically ill patients, but extremity coordination may be tested as follows (video here ):

• Finger-nose-finger test.
• Rapid alternating movements (dysdiadochokinesia).

differential diagnosis of discoordination

• Contrary to popular belief, poor performance on the above tests doesn't necessarily indicate a cerebellar lesion. Instead, it may reflect a pathology involving the cerebellum, proprioception, vision, basal ganglia, or motor pathways.
• Cerebellar pathology is likely only if abnormalities in other subsystems have been excluded (e.g., adequate vision, intact strength, normal reflexes, intact proprioception, and absence of other features of basal ganglia dysfunction).

neuroanatomy of vibration & proprioception: posterior (dorsal) column – medial lemniscus pathway

• Nucleus gracilis (from the lower body; more medial).
• Nucleus cuneatus (from the upper body; more lateral).
• Neurons from these nuclei decussate in the base of the medulla (similarly to the corticospinal tract), subsequently forming the medial lemniscus.
• The medial lemniscus travels to the VPL (ventral posterior lateral) nucleus of the thalamus, which is also the destination of the anteriolateral (spinothalamic) tract.
• Finally, neurons project through the posterior limb of the internal capsule to the primary somatosensory cortex.

evaluation: vibration sense

• Start by stimulating the pulp of digits (e.g., toes or fingers). If this isn't sensed, then stimulate more proximally until the patient is able to perceive vibration. Avoid stimulation over bones, as the bone may transmit vibration proximally.
• Ideally this is performed with a tuning fork (preferably a 128-Hz or 64-Hz tuning fork, but 256-Hz may also be adequate). (Blumenfeld 2022) However, a tuning fork is often unavailable.
• Smartphone applications may be used to provide these frequencies (e.g., a free iphone app onsA440 allows for production of a 128-Hz sound that generates perceptible vibration if the phone speaker is gently held to the skin). To avoid cross-contamination, cover the phone with a clear plastic bag before contacting the patient. Vibration may not be effectively transmitted unless the speaker is held fully over the skin. The examiner may touch the patient's skin next to the phone to confirm that vibration is being effectively transmitted to the patient.

evaluation: position sense

• Position sense may be evaluated by determining if the patient can sense very subtle adjustments to finger or toe position, either upwards or downwards. The digit should be gently grasped from the sides , to avoid providing tactile clues regarding which direction the digit is being moved (video here ). Only small movements are necessary, as normal perception should allow for the detection of movements which are barely perceptible to the eye. (Blumenfeld 2022)

neuroanatomy of pain and temperature: anterolateral (spinothalamic) tract

• It takes 2-3 spinal segments for the fibers to reach the opposite side of the spinal cord. Thus, a lateral cord lesion will affect contralateral pain sensation beginning a few segments below the level of the lesion. (Blumenfeld 2022)
• Eventually, these neurons join the medial lemniscus in the pons and travel together with the dorsal column neurons to the ventral posterolateral nucleus of the thalamus.
• Clinically, pain perception can be measured by determining whether a pin is perceived as feeling sharp.
• Temperature may be evaluated by asking the patient to close their eyes and then touching the skin with either a plastic cup of ice water or a cup of warm water (items easily obtainable in an ICU). Another technique is wiping the skin with an alcohol prep pad, which generates a cool patch of skin due to evaporative cooling – this should generally be perceived as being cold. ( 25340491 )
• Pain sensation may be evaluated by determining whether the patient can perceive a gentle stimulation from a pin or broken wooden swab as “sharp” (video here ). The skin should be stimulated very gently and not broken. Nonetheless, a clean pin should be used for each patient and disposed of subsequently.

monocular vision loss

• Lens (e.g., cataract).
• Anterior chamber (e.g., uveitis).
• Retina (e.g., retinal ischemia).
• Optic nerve problem (e.g., optic neuropathy).

bitemporal hemianopsia

• Pathology at the optic chiasm.
• Often due to pituitary lesions.
• Sellar meningioma or craniopharyngioma.
• Aneurysm of the distal carotid.

homonymous hemianopsia

• Occipital lobe (45%).
• Optic radiations (32%).
• Optic tracts (10%).
• Lateral geniculate body of the thalamus (1%).

homonymous quadrantanopia

• Generally localizes to the optic radiation or the occipital lobe.

cortical blindness

• Severe, bilateral occipital lobe damage may cause the brain to be unable to understand visual information. This can be caused by bilateral PCA (posterior cerebral artery) strokes.
• Anton syndrome: Patient is unaware that they are blind.
• Charles Bonnet syndrome: Release hallucinations occur, often involving small people. The patient generally knows that these are not real.

Neglect may often be evaluated during other components of the neurological examination (e.g., while testing for facial sensation to evaluate the trigeminal nerve).

evaluation of neglect

• Simultaneous stimulation on both sides of the body may be recognized only on one side (extinction on double simultaneous stimulation). This is easily tested when examining skin sensation (cranial nerve V) or testing visual fields.
• Patients may ignore half of the room (e.g., paying attention to the examiner only if approached from the patient's right side).
• The neglected side has intact strength, but is moved only if attention is strongly directed towards it. (Blumenfeld 2022)
• During strength testing, if asked to perform a motor task bilaterally (e.g. “step down on the gas”), the patient may perform the task only unilaterally.
• Constructional neglect: If asked to draw a clock, half of the clock may be ignored.

causes of neglect

• Obvert neglect usually reflects right parietal lobe dysfunction, causing left-sided neglect. However, this may also result from right frontal lesions, right thalamic or basal ganglia lesions, or rarely right midbrain lesions. (Blumenfeld 2022)
• Left parietal lobe dysfunction can cause right-sided neglect, but this is usually more subtle.

Below are some general rules of thumb. Please note that they are not uniformly valid (for example, in a patient with numerous distributed lesions).

loss of specific sensory modes

• The dorsal columns and spinothalamic tracts merge together in the lower medulla.
• Selective loss of some modes of sensation (e.g., vibration but not pain) indicates a lesion below the lower medulla.
• a lesion above the lower medulla.
• a lesion in the spinal cord involving all tracts.

facial involvement

• (+) Facial involvement (either sensory or motor) requires a lesion in the brainstem or higher up in the neuraxis ( not the spinal cord).

isolated bilateral motor loss, or isolated bilateral sensory loss

• This generally suggests a lesion in the spinal cord, or in the peripheral nerves (or the neuromuscular junction or muscle, in the case of weakness).
• Bilateral findings imply bilateral lesions, which will generally cause some other abnormality.
• An exception is that a medial lesion affecting the bilateral leg areas of the motor cortices may cause paraplegia and incontinence mimicking a spinal cord lesion. This can result from bilateral anterior cerebral artery infarction or a tumor near the midline. However, this lesion will typically also cause cognitive deficits (more on anterior cerebral infarction: 📖 ).

frontal lobe

• Broca's area lies in the inferior frontal gyrus. Damage may cause a nonfluent aphasia with preserved comprehension. Broca's area may sometimes lie on the right side in left-handed patients.
• Poor executive function, abulia (apathy). ( 27907952 ) Damage may cause behavioral disinhibition.
• Activation of the frontal eye fields drives the eyes to look towards the contralateral side.
• Seizure involving the frontal lobe will activate the frontal eye fields, causing the eyes to deviate away from the lesion (looking towards the shaking extremity).
• Stroke involving the frontal lobe will inactivate the frontal eye fields, causing the eyes to deviate towards the lesion (looking away from the paretic extremity).
• Perseveration.
• Impaired digit span.
• Mesial frontal lobe (akinetic-mute): minimal spontaneous action/speech.
• Impulsive, emotionally labile.
• Inappropriate jocularity.
• Hypersexuality.

temporal lobe

• Lesions in the medial temporal lobes (including the hippocampus) cause amnesia . This is especially problematic if the dominant hippocampus is damaged.
• Right temporal lobe – music-melody perception ( 27907952 )
• Left temporal lobe: Wernicke's area is located in the posterior temporal gyrus. Damage may cause a receptive aphasia that results in fluent production of nonsensical speech.
• Damage to the Meyer loop visual fibers could cause a superior quadrantanopia .
• Apathy may result from left temporal injury. ( 27907952 )

parietal lobe: Spatial attention and praxis

• The parietal lobe combines information from the somatosensory cortex and the visual cortex to determine where objects are in space.
• Lesions cause neglect : objects in half of space fall off the patient's radar.
• Neglect is more common in lesions of the nondominant parietal lobe (usually a right-sided parietal lobe causing left-sided neglect). This may cause anosognosia – patients are unaware of neurologic deficits.
• Predominantly occurs in the dominant parietal lobe.
• Lesions in the angular gyrus of the dominant hemisphere can cause Gerstmann's syndrome: Left-right confusion, inability to count (acalculia), inability to name fingers (finger agnosia), and inability to write (agraphia).
• Dominant parietal lobe lesions may cause apraxia bilaterally. (Praxis begins in the left parietal lobe, and then information is sent to the bilateral prefrontal motor areas, which each direct praxis on the contralateral side of the body.).
• Eyelid opening apraxia is discussed above. 📖
• (1) Simultanagnosia – inability to perceive global elements. Patients have problems with visuospatial attention.
• (2) Optic ataxia: Difficulty with finger-nose movements because patients cannot locate elements in space. There is poor reaching under visual guidance (yet intact ability to return the finger to the nose).
• (3) Ocular apraxia (inaccurate saccades).

occipital lobe

• Either occipital lobe may cause a visual field cut.
• The left side of the brain is generally involved in language .
• Lesions in the left occipital association cortex may cause alexia without agraphia. 📖
• Right “what” pathway of the occipital & nearby temporal lobe impairs facial recognition. Damage may cause prosopagnosia (inability to recognize people).

Some generalizations may be helpful in lesion localization:

(#1/3) vertical localization within brainstem

• Midbrain: CN 2-4 (pupils, vertical eye movements).
• Pons: CN 5-8 (vestibular, horizontal eye movements, facial weakness).
• Medulla: CN9-12 (tongue, larynx).

(#2/3) anterior (ventral) vs. posterior (dorsal)

• Anterior lesion: Corticospinal tract.
• Cerebellar peduncles (causes ipsilateral ataxia).
• Sensory function of cranial nerves.
• Lesion in a cranial nerve nucleus (e.g., nuclear CN3 palsy 📖 ).

(#3/3) medial vs. lateral

• Motor nuclei of cranial nerves.
• Corticospinal tract (motor pathway).
• Causes INO (internuclear ophthalmoplegia). 📖
• Lesion is ipsilateral to the eye that cannot adduct.
• Medial lemniscus (vibration/proprioception).
• Descending sympathetics (ipsilateral Horner's syndrome).
• Spinothalamic tract (ascending pain/temperature).
• Sensory nuclei of CN5-trigeminal (facial sensation).
• Spinocerebellar tract (ipsilateral ataxia).

unilateral ventral (anterior) midbrain peduncle = Weber syndrome

• (1) Ipsilateral CN3 palsy due to involvement of the CN3 fascicle.
• (2) Contralateral hemibody weakness (corticospinal tract).
• May be caused by occlusion of the paramedian branches at the top of the basilar artery.

unilateral dorsomedial midbrain (Claude syndrome)

• (1) Ipsilateral CN3 palsy (fascicle of CN3).
• (2) Contralateral tremor and ataxia (red nucleus & cerebellothalamic fibers).

unilateral paramedian midbrain (Benedikt syndrome)

• This is a combination of Weber and Claude syndromes, due to infarction of an area overlapping both regions.
• (2) Contralateral hemibody weakness (cerebral peduncle).
• (3) Contralateral tremor and ataxia (red nucleus & cerebellothalamic fibers).
• (4) May have contralateral rigidity (substantia nigra).

bilateral ventral (anterior) midbrain ( 27907952 )

• Abnormal consciousness or agitated delirium (reticular activating system).
• Vertical gaze palsy (colliculi).
• Miosis (sympathetic nerve).

dorsal midbrain syndrome (aka Parinaud syndrome, pretectal syndrome, Sylvian aqueduct syndrome, posterior commissure syndrome)

• Impaired upgaze (initially this may be evident only with saccades, but eventually a complete paralysis of upgaze may occur).
• Convergence-retraction nystagmus may be triggered by upward gaze. Simultaneous activation of all extraocular muscles cause retraction of the eyes into the orbit.
• Pupils are usually large and poorly responsive to light, but they do respond to accommodation (“light-near dissociation”).
• Eyelid retraction may occur (Collier's sign).
• Typically localizes to lesions in the midbrain around the cerebral aqueduct and involving the corpora quadrigemina and posterior commissure. ( 32924623 )
• Hydrocephalus , particularly fourth ventricular outflow obstruction. 📖
• Tumor (e.g., pineal tumor or tectal glioma).
• 🎥 : Parinaud's syndrome.

lateral mid-pontine syndrome

• Ipsilateral ataxia (due to involvement of middle cerebellar peduncle).
• Contralateral impairment in arm/leg pain and temperature sensation (spinothalamic tract involvement).
• Ipsilateral facial numbness ( CN5-trigeminal ).
• Ipsilateral paralysis of mastication (motor component of CN5-trigeminal ).

inferior lateral pontine syndrome (Marie-Foix syndrome)

• Impairment of pain and temperature sensation in the ipsilateral face ( CN5-trigeminal nucleus & tract) and the contralateral arm/leg (spinothalamic tract).
• Ipsilateral Horner's syndrome (descending sympathetic chain).
• Ipsilateral facial paralysis ( CN7-facial ).
• Vertigo/hearing loss ( CN8-vestibulocochlear nerve nucleus or ischemia of the vestibular apparatus/cochlea itself, which is supplied via the AICA).
• Caused by occlusion of the AICA (anterior inferior cerebellar artery).

lateral medullary syndrome (Wallenberg syndrome)

• Ipsilateral ataxia, vertigo, nystagmus, and nausea (due to involvement of inferior cerebellar peduncle & CN8-vestibular nuclei).
• Ipsilateral Horner's syndrome (descending sympathetic fibers in lateral medulla).
• Hoarseness and dysphagia (involvement of the nucleus ambiguous, CN10-vagus ).
• 🫁 Rarely, may also cause central hypoventilation syndrome with loss of respiratory drive when asleep (aka, Ondine's curse).
• Caused by occlusion of the vertebral artery, or (less commonly) the PICA (posterior inferior cerebellar artery).

medial mid-pontine syndrome

• Contralateral hemibody weakness (corticospinal tracts).
• Contralateral vibration/proprioception loss (medial lemniscus).
• Ipsilateral ataxia (superior cerebellar peduncle).

inferior medial pontine syndrome (Foville syndrome)

• Due to occlusion of basilar perforators (paramedian branches).
• Ipsilateral CN7 -facial weakness (facial colliculus).
• Ipsilateral conjugate gaze palsy (nucleus of CN6 -abducens), possibly accompanied by one-and-a-half syndrome if the MLF (medial longitudinal fasciculus) is also involved. 📖

medial medullary syndrome (Dejerine syndrome)

• Contralateral arm/leg weakness, usually sparing the face (corticospinal tracts).
• Tongue deviation towards the lesion (Ipsilateral CN12-hypoglossal nucleus).
• Contralateral reduced position and vibration sense (medial lemniscus).
• Due to paramedian branches of anterior spinal artery or vertebral artery.

vermis ( 27907952 )

• Ataxia of gait (truncal ataxia, which affects the proximal musculature).
• Dysarthria.

hemisphere ( 27907952 )

• Incoordination and dysmetria (dentate nucleus).
• Appendicular ataxia (affecting the ipsilateral limbs).
• Ataxic speech (may sound drunk).
• Very deep intoxication (e.g., barbiturate or baclofen overdose) may cause loss of cranial nerve reflexes.
• Anticholinergic poisoning or anoxic-ischemic injury may cause loss of pupillary reactivity.
• Spontaneous eye movements can occur (e.g., roving conjugate gaze, dipping with slow downgaze followed by rapid upgaze, or ping-pong gaze back and forth). ( 28187795 )
• Upward or downward eye deviation can occur.
• Adventitious limb movements may be seen. If present, multifocal myoclonus , asterixis , or tremor support a metabolic etiology. ( 28187795 ) Any motor signs are usually symmetric.
• Gegenhalten (paratonic rigidity) may be seen. (Louis 2021)

clinical findings in uncal herniation

• Initially, the pupil is dilated and sluggish. Parasympathetic fibers run along the outside of CN3-oculomotor, so pupillary dilation can occur first .
• With progression, the pupil becomes fixed and dilated. Impaired consciousness is almost always present by the time the pupil is fixed and dilated. (Nelson, 2020)
• With progression, oculomotor paralysis occurs (causing the eye to be locked in a down-and-out orientation).
• Ipsilateral ptosis results from denervation of the levator palpebrae superioris. ( 26704760 )
• (Further discussion of CN3-oculomotor palsy above 📖 ).
• Hemiparesis may be accompanied by hyperreflexia and a positive Babinski's sign.
• If untreated, this may eventually compress the midbrain (e.g., causing bilateral fixed & dilated pupils, with decorticate or decerebrate posturing).

Kernohan's notch phenomenon

• Definition: Lateral displacement of the midbrain can compress the contralateral cerebral peduncle. This causes weakness ipsilateral to the herniation (a false localizing sign).
• The CN3-oculomotor palsy sometimes remains correctly localizing (ipsilateral to the herniation). 📄 Thus, Kernohan's notch phenomenon could be suggested by ipsilateral pupillary dilation and weakness. ( 32938557 )

key radiological findings

• The earliest finding may be effacement of the suprasellar cistern .
• Widening of the ipsilateral perimesencephalic cistern (since the midbrain is pushed away from the hernia).
• Hydrocephalus may be seen (especially involving the contralateral lateral ventricle).

• Uncal herniation is often the first event in downward transtentorial herniation, followed by herniation of more posteriorly located brain tissue.
• Compression of the PCA (posterior cerebral artery) may cause infarction of the medial temporal and occipital lobe (white arrowhead in the figure above).
• Compression of the aqueduct of Sylvius may cause hydrocephalus.
• Compression of the reticular activating system in the midbrain may cause unconsciousness.

posterior lateral downward transtentorial herniation

• Uncal herniation (discussed above) refers to downward herniation of the anterior portion of the temporal lobe.
• Less commonly, mass lesions located more posteriorly within the head may cause downward herniation of the posterior portion of the temporal lobe. This may cause impingement on the lateral part of the quadrigeminal plate cistern. ( 31589570 )
• Involvement of the tectum at the level of the superior colliculus may cause Parinaud syndrome.
• Compared to uncal herniation, there is less involvement of CN3-oculomotor nerve or the PCA (posterior cerebral artery).

Downward central herniation often occurs in combination with downward lateral herniation.

clinical features

• Disruption of the reticular activating system causes drowsiness and confusion .
• Miotic (small) pupils are initially a prominent sign, often with restricted upgaze (Parinaud syndrome) . Uncommonly, a unilateral Horner's syndrome may occur early on (before transitioning to bilateral small pupils). (Alpert 2019)
• ⚠️ Initially, this may resemble an intoxication causing small pupils (e.g., cholinergic agonists, opioids, clonidine, ACE-inhibitors). There may initially be conjugate roving eye movements, simulating a toxic/metabolic coma.
• Coma deepens.
• Midbrain dysfunction emerges: pupils may become fixed & mid-position .
• Abnormal motor responses (e.g., posturing) may be an early clue to a structural etiology of the coma. Decorticate and later decerebrate posturing occur, with bilateral extensor Babinski reflexes.
• Pontine dysfunction emerges, with loss of vestibulo-ocular reflexes and corneal reflexes .
• Pathological breathing patterns may emerge (e.g., central neurogenic hyperventilation).
• Breathing may slow and become irregular (ataxic breathing).
• Cushing's reflex may occur with hypertension and bradycardia. Pupils may temporarily dilate due to a surge of epinephrine release.

clinical findings

• Vertical gaze palsy may be followed by stupor/coma. ( 34618757 )
• Pupils may be fixed and either midposition or dilated.
• Cerebral aqueduct compression may result in acute hydrocephalus .
• Patients may also have impaired swallowing and aspiration, due to compression of the brainstem.
• Branches of the SCA (superior cerebellar arteries) and the PCA (posterior cerebral arteries) may be compressed, causing infarction of the superior portion of the cerebellar hemisphere and the occipital lobe. ( 31589570 )
• (1) Mass effect from the posterior cranial fossa, especially a mass originating near the opening of the tentorium cerebelli (e.g., within the cerebellar vermis).
• (2) Sudden relief of supratentorial intracranial hypertension (e.g., due to placement of an external ventricular drain).

radiologic findings

• The quadrigeminal cistern is distorted.
• Stiff neck may be a very early sign. (Alpert 2019)
• Cranial nerve palsies and stupor/coma result from brainstem compression.
• Decerebrate posturing may occur initially, but eventually flaccid paralysis occurs.
• Cushing reflex may occur including hypertension, bradycardia, and slow respirations. ( 34618757 ) Compression of the medulla may eventually lead to central hypoventilation with respiratory arrest .
• Acute hydrocephalus may occur (due to compression of the fourth ventricle). This may accelerate the process of herniation and consciousness impairment.
• Tonsillar herniation may cause infarction of the PICA (posterior inferior cerebellar artery), causing infarction of the cerebellum and lateral medulla. ( 32924623 )
• Contralateral leg weakness is a central finding, due to compression of the ipsilateral anterior cerebral artery. P osturing of the leg may also be seen.
• Mental status is relatively unaffected, as compared to other herniation syndromes. However, there may be apathy and indifference. ( 31589570 )

anatomic considerations

• The cingulate gyrus herniates underneath the falx cerebri. This may eventually cause necrosis of the ipsilateral cingulate gyrus.
• ACA (anterior cerebral artery) infarction may occur. ( 32924623 )
• Falcine herniation may compromise both foramina of Monro, causing dilation of the contralateral ventricle (the ipsilateral ventricle tends to be directly compressed).
• Ultimately, this may progress to central downwards herniation over time (due to increasing edema of herniated tissue).
• Pupillary reflexes are often intact (since these are located in the midbrain, which is above the level of compression).
• Absent corneal reflexes and abnormal vestibulo-ocular reflexes are often seen. Skew deviation may occur (one eye looks up, the other looks down).
• Ocular bobbing can occur, or nystagmus that may be direction-changing or vertical. ( 28187795 )
• Extensor or flexor posturing can occur.

To keep this page small and fast, questions & discussion about this post can be found on another page here .

Acknowledgement: Thanks to Dr. Casey Albin (@caseyalbin) for thoughtful comments on this chapter.

Guide to emoji hyperlinks

• 📄 = Link to open-access journal article.
• 24636925 Singhal NS, Josephson SA. A practical approach to neurologic evaluation in the intensive care unit. J Crit Care. 2014 Aug;29(4):627-33. doi: 10.1016/j.jcrc.2014.02.014 [ PubMed ]
• 27807107   Ellul MA, Cross TJ, Larner AJ. Asterixis. Pract Neurol. 2017 Jan;17(1):60-62. doi: 10.1136/practneurol-2016-001393  [ PubMed ]
• 27907952 Wijdicks EF. Neurology of Critical Care. Semin Neurol. 2016 Dec;36(6):483-491. doi: 10.1055/s-0036-1592108 [ PubMed ]
• Berkowitz, A. (2016). Lange Clinical Neurology and Neuroanatomy: A Localization-Based Approach (1st ed.). McGraw Hill / Medical.
• Dünser, M. W., Dankl, D., Petros, S., & Mer, M. (2018). Clinical Examination Skills in the Adult Critically Ill Patient (1st ed. 2018 ed.). Springer.
• Alpert, J. N. (2018). The Neurologic Diagnosis: A Practical Bedside Approach (2nd ed. 2019 ed.). Springer.
• Torbey, M. T. (2019). Neurocritical Care (2nd ed.). Cambridge University Press.
• Nelson, S. E., & Nyquist, P. A. (2020). Neurointensive Care Unit: Clinical Practice and Organization (Current Clinical Neurology) (1st ed. 2020 ed.). Springer.
• 30521283 Zimmerman B, Hubbard JB. Clonus. 2021 Aug 12. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan– [ PubMed ]
• 30743297 Edmundson C, Bird SJ. Acute Manifestations of Neuromuscular Disease. Semin Neurol. 2019 Feb;39(1):115-124. doi: 10.1055/s-0038-1676838 [ PubMed ]
• 31589570 Riveros Gilardi B, Muñoz López JI, Hernández Villegas AC, Garay Mora JA, Rico Rodríguez OC, Chávez Appendini R, De la Mora Malváez M, Higuera Calleja JA. Types of Cerebral Herniation and Their Imaging Features. Radiographics. 2019 Oct;39(6):1598-1610. doi: 10.1148/rg.2019190018 [ PubMed ]
• 33232023 Margolin E, Jeeva-Patel T. Opsoclonus. 2021 Nov 19. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan– [ PubMed ]
• 33522735 Hardy TA. Spinal Cord Anatomy and Localization. Continuum (Minneap Minn). 2021 Feb 1;27(1):12-29. doi: 10.1212/CON.0000000000000899 [ PubMed ]
• Wijdicks, E. F. M. (2021). Examining Neurocritical Patients (1st ed. 2021 ed.). Springer.
• Louis ED, Mayer SA, Noble JM. (2021). Merritt’s Neurology (Fourteenth). LWW.
• Blumenfeld, H. (2022). Neuroanatomy through Clinical Cases (3rd ed.). Sinauer Associates is an imprint of Oxford University Press.
• Albin, C. S. W., & Zafar, S. F. (2022). The Acute Neurology Survival Guide: A Practical Resource for Inpatient and ICU Neurology (1st ed. 2022 ed.). Springer.
• 32924623 Li B, Sursal T, Bowers C, Cole C, Gandhi C, Schmidt M, Mayer S, Al-Mufti F. Chameleons, red herrings, and false localizing signs in neurocritical care. Br J Neurosurg. 2022 Jun;36(3):298-306. doi: 10.1080/02688697.2020.1820945 [ PubMed ]
• Flemming, K. D. (2022). Mayo Clinic Neurology Board Review (Mayo Clinic Scientific Press) (2nd ed.). Oxford University Press.

The Internet Book of Critical Care is an online textbook written by Josh Farkas ( @PulmCrit ), an associate professor of Pulmonary and Critical Care Medicine at the University of Vermont.

We are the EMCrit Project , a team of independent medical bloggers and podcasters joined together by our common love of cutting-edge care, iconoclastic ramblings, and FOAM.

Resus Leadership Academy

Subscribe by Email

Insert/edit link.

Enter the destination URL

Or link to existing content

Neurologic Examination

• Mental Status |
• Cranial Nerves |
• Motor Nerves |
• Sensory Nerves |
• Coordination, Balance, and Gait |
• Autonomic Nervous System |
• Blood Flow to the Brain |

When a neurologic disorder is suspected, doctors usually evaluate all of the body systems during the physical examination, but they focus on the different parts of the nervous system. Examination of the nervous system—the neurologic examination—includes evaluation of the following:

Mental status

Cranial nerves

Motor nerves

Sensory nerves

Coordination and balance

Walking (gait)

Doctors may evaluate some areas more thoroughly than others depending on what type of disorder they suspect. For example, the neurologic examination can also help identify the cause of a muscle malfunction (such as weakness or paralysis) because normal muscle contraction depends on stimulation by a nerve (see figure Using the Brain to Move a Muscle ).

A neurologic examination differs from a psychiatric examination, which focuses on a person's behavior. However, the two examinations overlap somewhat because abnormalities in the brain can cause abnormal behavior. Abnormal behavior can be a clue to a physical problem in the brain.

Mental Status

Doctors evaluate the following:

Orientation to time, place, and person

Various abilities, such as thinking abstractly, following commands, using language, and solving math problems

The mental status evaluation consists of a series of questions and tasks, such as naming objects, recalling short lists, writing sentences, and copying shapes. The person’s answers are recorded and scored for accuracy. If the person reports feeling depressed, doctors ask if there have been any thoughts of suicide.

Cranial Nerves

There are 12 pairs of cranial nerves , which connect the brain with the eyes, ears, nose, face, tongue, throat, neck, upper shoulders, and some internal organs (see table Viewing Cranial Nerves ). How many nerves doctors test depends on what type of disorder they suspect. For example, the 1st cranial nerve (the nerve of smell) is not usually tested when a muscle disorder is suspected, but it is tested in people recovering from serious head trauma (because smell is often lost).

A cranial nerve may be damaged anywhere along its length as a result of any of the following:

Impaired blood flow

An autoimmune disorder

An infection

Increased pressure in the skull (intracranial pressure)

The exact site of the damage can often be identified by testing the functions of a particular cranial nerve.

Motor Nerves

Motor nerves carry impulses from the brain and spinal cord to voluntary muscles (muscles controlled by conscious effort), such as muscles of the arms and legs. Muscle weakness or paralysis of a muscle may indicate damage to any of the following:

The muscle itself

A motor nerve

The nerve's connection to the muscle ( neuromuscular junction )

The spinal cord

Doctors look for abnormalities such as the following:

A decrease in muscle size (wasting, or atrophy)

An increase in muscle size

Tremor (rhythmic shaking of a body part) and other unintended (involuntary) muscle movements

Muscle twitching

An increase (spasticity or rigidity) or a decrease in muscle tone

Weakness , particularly which body parts are affected (pattern of weakness)

Loss of dexterity (the ability to use the hands skillfully and nimbly)

The doctor inspects the muscles for size, unusual movements, tone, strength, and dexterity.

Change in muscle size

A muscle wastes away (atrophies) when the muscle or the nerves supplying it are damaged or when the muscle has not been used for months for other reasons (such as being in a cast).

A muscle may increase in size (hypertrophy) because it is working harder to compensate for the weakness of another muscle. Muscles can appear to increase is size when normal muscle tissue is replaced by abnormal tissue, as occurs in amyloidosis and some inherited muscle disorders (such as Duchenne muscular dystrophy ). The abnormal tissue increases the apparent size but not the strength of the muscle.

Involuntary movements

Muscles may move without the person meaning them to (involuntarily). The following are examples of involuntary movements :

Fasciculations are tiny, subtle muscle twitches, which may look ripples under the skin. Fasciculations may indicate nerve damage to the affected muscle.

Myoclonus refers to sudden jerking (contractions) of a muscle or a group of muscles, such as those in the hand, arm, or leg. The muscles move as if the person had just received an electric shock. Myoclonus may occur normally, as when people are falling asleep, or may be caused by a disorder that affects the spinal cord or brain.

Tics are purposeless, repetitive but not rhythmic involuntary movements, such as blinking or jerking the head. Tics often also include involuntary, abrupt, often repetitive sounds and/or words.

Hemiballismus usually involves the sudden involuntary flinging of one arm and/or one leg.

Chorea refers to quick fidgety involuntary movements that start in one part of the body and often move abruptly and unpredictably to another part.

Athetosis refers to continuous slow, writhing involuntary movements.

Dystonia refers to long-lasting (sustained) involuntary muscle contractions that may force people into abnormal, sometimes painful positions.

Involuntary movements may indicate damage in the areas of the brain (basal ganglia) that control motor coordination.

Muscle tone

To evaluate muscle tone, doctors first ask the person to completely relax muscles in a limb. Then doctors move the person’s limb to determine how much the relaxed muscle involuntarily resists being moved—called muscle tone. How muscle tone reacts to being moved suggests possible causes, as follows:

Uneven muscle tone that suddenly increases as the relaxed muscle is moved (spasticity): Possibly due to a stroke or spinal cord injury

Evenly increased muscle tone: Possibly due to a disorder of the basal ganglia, such as Parkinson disease

Severely reduced muscle tone (flaccidity): Possibly due to a disorder of the nerves outside of the brain and spinal cord ( peripheral nerves ), such a polyneuropathy (a disorder that affects many nerves throughout the body)

Flaccidity may be present for a short time after an injury that causes paralysis, such as a spinal cord injury. When flaccidity results from such a spinal cord injury, muscle tone often gradually increases over days to weeks, eventually resulting in spasticity.

If people are afraid or confused during the examination, they may not be able to relax the muscles. In such cases, muscle tone may vary, making it hard for doctors to evaluate.

Muscle strength

Doctors test muscle strength by asking the person to push or pull against resistance or to do maneuvers that require strength, such as walking on the heels and tiptoes or rising from a chair. Doctors then rate muscle strength from 0 (no muscle contraction) to 5 (full strength).

Sometimes muscle weakness is evident when a person uses one limb more than another. For example, a right-handed person may gesture mostly with the left hand during a conversation. A weak arm may swing less while walking or drift downward when the arms are held up and the eyes are closed.

Knowing which body parts are weak (the pattern of weakness) can help doctors identify what the problem is, as in the following cases:

The shoulders and hips are weaker than the hands and feet: The cause may be a disorder that affects muscles (myopathy). Myopathies tend to affect the largest muscles first. People may have difficulty raising their arms to comb their hair, climbing stairs, or getting up from a seated position.

The hands and feet are weaker than the shoulders, arms, and thighs: The problem is often a polyneuropathy (the malfunction of many peripheral nerves throughout the body). Polyneuropathies tend to affect the longest nerves first (those going to the hands and feet). People may have a weak grip and have trouble with fine finger movements (dexterity). People may have difficulty fastening a button, opening a safety pin, or tying their shoes.

Weakness is limited to one side of the body: Doctors suspect a disorder affecting the opposite side of the brain, such as a stroke .

Weakness occurs below a certain level of the body: The cause may be a spinal cord disorder . For example, an injury to the part of the spine in the chest (thoracic spine) causes the legs but not the arms to be paralyzed. An injury in or above the neck causes paralysis of all four limbs.

Muscle weakness may also occur in other patterns, such as the following:

Weakness occurs in only one relatively small area: This type of weakness suggests that only one or a few peripheral nerves are damaged. In such cases, weakness may also impair dexterity.

Weakness becomes apparent only when muscles that are used to do the same activity over and over become weak more quickly than usual. For example, people who once could use a hammer well become weak after hammering for several minutes. Myasthenia gravis can cause this type of weakness.

Weakness accompanied by increased muscle tone (making arms or legs stiff) and exaggerated reflexes suggest a problem in the central nervous system. Weakness accompanied by decreased muscle tone (making arms or legs feel loose or floppy), decreased or absent reflexes, and intermittent twitching in the muscle suggest a problem in the peripheral nervous system.

Sensory Nerves

Sensory nerves carry information from the body to the brain about such things as touch, pain, heat and cold (temperature), vibration, the position of body parts, and the shape of objects. Each of these senses can be tested. Abnormal sensations or reduced perception of sensations may indicate damage to a sensory nerve, the spinal cord, or certain parts of the brain.

Information from specific areas on the body’s surface, called dermatomes , is carried to a specific location (level) in the spinal cord, then to the brain. Thus, doctors may be able to pinpoint the specific level of damage to the spinal cord by identifying the areas where sensation is abnormal or lost.

Sensation in the skin is tested. Usually, doctors concentrate on the area where the person feels numbness, tingling, or pain. The best screening test for loss of sensation involves touching the skin of the face, body, and all four limbs with a pin and a blunt object (such as the head of a safety pin) to see if the person can feel them and tell the difference between sharp and dull. Doctors test both sides of the body. If doctors detect loss of sensation in a specific area, they test nearby areas to estimate the extent of the loss. This approach enables them to determine the abnormality's location in the brain, spinal cord, or peripheral nervous system.

Gentle (light) touch is tested with a cotton wisp.

Temperature sense (the ability to feel hot and cold) is tested with a tuning fork. Both prongs are cold, so the examiner warms one of them slightly by rubbing it. Then each of the prongs is touched to the person's skin.

Vibration sense is also tested with a tuning fork. The fork is lightly tapped to make it vibrate. It is then placed on the joint of a finger to determine whether and how long the person feels the vibration.

To test position sense, doctors move the person’s finger or toe up or down and ask the person to describe its position without looking.

The ability to identify the shape of an object is tested by placing a familiar object, such as a key or safety pin, in a person's hand and asking the person to identify it without looking. Or doctors may trace letters or numbers on the palm of the person's hand and ask the person to identify them. If a person cannot identify them, the cortex of the brain (the outer layer of the cerebrum, the largest part of the brain) may be damaged. This part of the brain integrates and interprets sensory information from different sources.

A reflex is an automatic response to a stimulus. For example, the lower leg jerks when the tendon below the kneecap is gently tapped with a small rubber hammer. The pathway that a reflex follows (reflex arc) does not directly involve the brain. The pathway consists of the sensory nerve to the spinal cord, the nerve connections in the spinal cord, and the motor nerves back to the muscle, causing the knee to jerk.

Doctors test reflexes to determine whether all parts of this pathway are functioning. The reflexes most commonly tested are the knee jerk and similar reflexes at the elbow and ankle.

The plantar reflex may help doctors diagnose abnormalities in the nerve pathways involved in the voluntary control of muscles. It is tested by firmly stroking the outer border of the sole of the foot with a key or other object that causes minor discomfort. Normally, the toes curl downward, except in infants aged 6 months or younger. Having the big toe go upward and the other toes spread out is a sign of an abnormality in the brain or spinal cord.

Testing other reflexes can provide important information. For example, doctors learn the extent of injury in a comatose person by noting the following:

Whether the pupils constrict when light is shined on them (pupillary light reflex)

Whether the eyes blink when the cornea is touched with a wisp of cotton (corneal reflex)

How the eyes move when the person’s head is turned or when water is flushed into the ear canal (caloric testing)

Whether the person gags when the back of the throat is touched, for example, with a tongue depressor (gag reflex)

Doctors also check whether the anus tightens (contracts) when it is lightly touched (called the anal wink). If this reflex is present in a person paralyzed after a spinal cord injury, the injury may be incomplete, and the chance of recovery is better than if the reflex were absent.

Reflex Arc: A No-Brainer

Coordination, balance, and gait.

Coordination and walking (gait) require integration of signals from sensory and motor nerves by the brain and spinal cord.

To test walking, doctors ask a person to walk normally and in a straight line, placing one foot in front of the other. Abnormalities may help identify which part of the nervous system is not functioning normally. For example, if a person takes wide, unsteady steps (called ataxia), the cerebellum may be damaged or malfunctioning. (The cerebellum is the part of the brain that coordinates voluntary movements and controls balance.)

To test coordination, doctors may ask the person to use the forefinger to reach out and touch the doctor’s finger, then the person’s own nose, and then to repeat these actions rapidly. The person may be asked to do these actions first with the eyes open, then with the eyes closed.

The Romberg test is done to test position sense. The person stands still with both feet together as close as possible without losing balance. Then the eyes are closed. If balance is lost, information about position from the legs may not be reaching the brain, usually because the nerves or spinal cord is injured. However, abnormalities may also result from malfunction of the cerebellum or the balance system in the inner ears or its connections with the brain.

Autonomic Nervous System

The autonomic (involuntary) nervous system regulates internal body processes that require no conscious effort, such as blood pressure, heart rate, breathing, and temperature regulation through sweating or shivering. An abnormality of this system may cause problems such as the following:

A fall in blood pressure when a person stands up ( orthostatic hypotension )

Reduction or absence of sweating

Sexual problems such as difficulty initiating or maintaining an erection ( erectile dysfunction )

A pupil that does not widen or narrow in response to changes in light

Doctors may do a variety of tests, such as the following:

Measuring blood pressure and heart rate while the person is lying down, sitting, and standing

Examining the pupils for abnormal responses or lack of response to changes in light

Doing sweat testing

Removing and examining a small sample of skin (skin punch biopsy) to see whether the number of nerve endings has decreased, as occurs in some polyneuropathies that affect small nerves, including autonomic nerves

Blood Flow to the Brain

A severe narrowing of the arteries to the brain reduces blood flow and increases the risk of stroke . The risk is higher for people who are older, who smoke cigarettes, or who have high blood pressure, high cholesterol levels, diabetes, or disorders of the arteries or heart.

The best way to diagnose disorders of the arteries is to do an imaging test such as ultrasonography, magnetic resonance angiography (MRA), computed tomography angiography (CTA), or cerebral angiography .

Blood pressure may be measured in both arms to check for blockages in the large arteries that branch off from the aorta. Such blockages sometimes result in stroke.

• Cookie Preferences

Copyright © 2024 Merck & Co., Inc., Rahway, NJ, USA and its affiliates. All rights reserved.

Free Neurology Essay Examples & Topics

Being a neurologist equates to countless hours of study, research, and work. If you find yourself interested in this field, you have to prepare to face many challenges along the way. Among these challenges are writing neurology essays and choosing what to write about. Thankfully, our experts have prepared an article to help you out.

Neurology and neuroscience are closely related subjects. However, there are distinctions between the two.

Neuroscience is a scientific area. More often than not, neuroscientists spend their days in a laboratory conducting research on the central nervous system.

Neurology is a branch of medicine, concerned with the diseases of the nervous system. People studying neurology are medical students who strive to obtain a medical license. They eventually become practicing doctors. One of the perks of being a neurologist is specialization. These doctors can have a specialty that they work with, such as epilepsy disorders or pediatric neurology.

Below, you will find both neuroscience and neurology essay topics. You will also find advice for writing academic papers. Finally, you can browse through free essay samples provided by students like yourself.

6 Top Tips on Neurologist Essay

To be successful with your neurologist essay, you should adhere to the standard academic style of writing. Here we have collected the tips that will make sure you are on the right path.

1. Brainstorm for ideas. This is one of the essential steps in any academic paper. By this point, you are probably bursting with neurology essay ideas. Putting them all down on paper will help you visualize your process.

2. Pick your topic. When your ideas are outlined in front of you, it is time to choose. Deciding what to go for can be tricky – you need to make sure the topic isn’t too narrow or broad. It is best to go with the area that is the most interesting to you personally. This way, research won’t be a burden, and the writing process will be more exciting.

3. Conduct research. When considering neurological essays, trustworthy sources are essential. Spend an extra hour browsing through books and journal articles. Depending on the scope of your work, you might want to consider interviews with known neurologists. Besides secondary sources, try to obtain primary ones.

4. Come up with a hypothesis. Once you have everything in order, start thinking about your thesis. In other words, draft a solid hypothesis long before writing. This will be the subject that you will discuss throughout your essay. Take your time with it, or let our thesis generator do that for you.

5. Outline your future paper. When you have your hypothesis, outlining your paper should become manageable. Base your introduction, body paragraphs, and conclusion around the thesis statement. Remember that your primary discussion points should be supported by the evidence you gathered in your research.

6. Draft your paper and revise. Most students forget that they can edit their paper as many times as necessary before submission. This can severely influence the quality of your assignment. Proofreading is one of the most fundamental elements of essay writing. Make sure to look over your paper at least once before submitting it.

25 Neurology & Neuroscience Essay Topics

Any essay begins with a carefully chosen topic. Fortunately, you can find hundreds of original ideas related to neuroscience and neurology. We have listed some of them below. Otherwise, you can try our topic generator – it will create more for you.

Feel free to browse through these ideas:

• The effects of Alzheimer’s on the emotional stability of older people.
• Neurosurgery as a cure for depression.
• The link between head injury and physical injury in athletes in professional boxing.
• Is neurology a good field to study human emotions and feelings?
• Brain development after post-traumatic stress.
• The effect of alcoholism on dopamine production in the human brain.
• Clinical neurology and the treatment of Parkinson’s disorder.
• Targeting of specific nerve centers in treatment of chronic pain.
• The impact of mental illness on brain chemistry from a neurosurgeon’s perspective.
• Chronic Fatigue Syndrome and its development in the human brain.
• Why I chose neurology: advantages and disadvantages of clinical neuroscience.
• The formation of irrational phobias and fears.
• The effect of insomnia on the development of cognitive brain functions.
• An analysis of the common methods of treatment for cerebral shaking palsy.
• The causes and cures for schizophrenia in young adults.
• Is brain death completely irreversible? A discussion on the future of neurological theory.
• The link between IQ and brain development in young adults.
• Pros and cons of marijuana use in neurology units in hospitals.
• The interaction of neurons and their impact on mental health.
• The extent of available medicine for neurological disorders.
• The algorithms in brain functions and their link to intelligence in humans.
• A critical examination of treatment for terminal cancer of the brain.
• Frontal lobe and parietal lobe – different impacts on the development of multilingual skills.
• The influence of the Internet on human memory functions.
• Long-time drug use and its effect on human brain development.

We hope that these ideas managed to inspire you. If you need extra guidance, feel free to check out our neurology essay samples below.

Thank you for reading!

326 Best Essay Examples on Neurology

Problem of sleep deprivation.

• Words: 1408

Focused SOAP Note for Neurological Pain and Numbness

• Words: 1224

A Critical Review of “The WJ 4th Edition”

• Words: 1372

Multiple Sclerosis – Definition and Causes

• Words: 1691

Dopamine as a Neurotransmitter

Effects of sleeping disorders on human.

• Words: 1091

Aphasia: Reciprocal Scaffolding Treatment Protocol

Abnormal psychology case study: general anxiety disorder.

• Words: 1031

The Functions of the Human Brain

Meningitis disease: symptoms and treatment.

• Words: 1647

Environmental Adaptation in Occupational Therapy

• Words: 2485

The Autonomic Nervous System

• Words: 1355

Diagnosing Neurological Disorders: Ischemic Stroke

The definitions of insomnia, overview of the cerebral palsy, epilepsy and seizure disorder: a guide for parents, stress reduction among college students, the brain fitness exercises, angelman syndrome and its mechanisms, sleep-disordered breathing and acute ischemic stroke.

• Words: 4135

Caffeine and Its Positive Impacts on Mental Activity

• Words: 1107

Traumatic Brain Injury: Causes, Diagnosis and Treatment

• Words: 1351

The Role of Neurotransmitters

Diagnosis and treatment of epilepsy.

• Words: 2009

Social Work and Speech-Language Pathology

Studying acupuncture, carpal tunnel syndrome: causes and treatment.

• Words: 1749

Stereotypic Movement Disorder, History and Statistics

• Words: 1161

Sleep and Its Implication on Animals

• Words: 1409

Babinski Sign: Pathophysiology and Treatment

Hypoglycaemia management in dementia patients, middle meningeal artery and brain bleeding, dementia care: person-centered approach.

• Words: 1009

Discussion: Concussions in the NFL

The neuroscience of emotions: literature review.

• Words: 2766

Cerebral Palsy and Best Treatment Practices

Migraine, cluster, tension and sinus headaches, alzheimer’s disease: the stem cell therapy, pathophysiological processes after a stroke, alzheimer’s disease: making decisions for patient, characteristics of neurodegenerative disorders, alzheimer’s disease: debilitating neurological ailment.

• Words: 1998

Identification of Enterobacteriaceae from Patient

Rapid eye movement sleep behavior disorder and therapy, dementia: mental health of patients and caregivers, a succinct explanation of autism spectrum disorder, down syndrome’s impact on communication.

• Words: 1296

Hormones in Sexual Behavior: Behavioral Neuroscience

“disorders of early development” by parritz and michael f. troy, sensory compensation: olfactory habituation to food and nonfood odours, the structure and function of the human nervous system, parkinson’s disease: pathogenic mechanisms and treatments, impact of autism disorder on adolescents, native americans: overview of health implications.

• Words: 1226

Risk Factors for Cerebrovascular Strokes

Applied behavior analysis: developmental disorder, possible mechanisms of neurodegenerative disorders.

• Words: 1185

Dopamine Pathways: The Role of Dopamine as a Neurotransmitter in the Human Brain

The frontal lobe and the impact of dementia on it, henry molaison and memory lessons, dementia: non-drug and pharmacological treatment, head injuries and related mental health issues, autism and disability advocacy, neuroplasticity principle interference (melodic intonation therapy).

• Words: 1585

The Spinal Cord Injuries and Nursing Practices

• Words: 1139

Dementia in Older Adults: Effects and Prevention

Hemorrhagic stroke: cholesterol plaques and blood clots, use of neuroleptic drugs: complications, migraine: characterization and diagnosis, the alzheimer’s association dementia care practice, dementia, alzheimer, and delirium in an elderly woman.

• Words: 1766

Cranial Brain Injury Implications for a Football Player

Non- and pharmacological dementia care methods, the development of a child’s brain, cerebral palsy: a neurodegenerative illness.

• Words: 1581

Sensory Processing Disorder: Consequences

Parkinson’s disease: symptoms and predictors.

• Words: 1358

Sensory Processing Disorder (SPD)

Amyotrophic lateral sclerosis: symptoms and effects.

• Words: 1231

Sensory Processing Information: Problems in Children

Attention-deficit hyperactivity disorder in a young girl.

• Words: 1651

Chapters 16-19 of “Aphasia…” by Papathanasiou & Potagas

Children with autism spectrum disorder: the training program for caregivers.

• Words: 2088

Emotional Impacts of Vestibular Disorders

Coping with stress in clinical neuropsychiatry, sensory integration disorders: impact on learning, self-management of epilepsy and mental illness, a sudden incurable neurological injury, resilience and the brain: annotated bibliography, the impact of substance abuse on the brain, multilingual and monolingual children with dyslexia, bilinguals’ cognitive-linguistic abilities and alzheimer’s disease, neuroscience on mental health issues.

• Words: 1476

Aspects of Multiple Sclerosis

• Words: 1939

ASD: Diagnostic and Statistical Manual of Mental Disorders

• Words: 2924

Neurological Alterations: Idiopathic Intracranial Hypertension

• Words: 1276

Peripheral Neuropathy: Symptoms and Treatment

The attention deficit hyperactivity disorder treatment, “neurogenetics and auditory processing in developmental dyslexia” by giraud, alzheimer’s disease: definition, stages, diagnosis, nervous system of organism at proxima centauri, therapy approaches to aphasia and dementia, disorders of consciousness: mechanisms, prognosis, and emerging therapies.

• Words: 1383

Amyotrophic Lateral Sclerosis and Its Features

Neurogenic communication disorders, cerebral palsy: historical and modern perspectives.

• Words: 1503

Neurologic System’s Influence on the Coordination of Muscles

Parkinson’s disease: neurological and musculoskeletal pathophysiologic processes, traumatic brain injury: chronic illness and disability, the spinal cord injury: quality of life, down syndrome in karyotype studies, aphasia among neurogenic communication disorders, alzheimer’s disease in an iranian patient, vascular neurocognitive disorder in a patient, aspects of parkinson’s disease.

• Words: 1652

Multiple Sclerosis: The Risk Factors

Peripheral nervous system and its development.

• Words: 1008

Diagnosis, Treatment, and Prognosis of Naegleria Fowleri Disease

Parkinson’s disease: the main aspects.

• Words: 2248

The Florida Red Tide: Neurological Illnesses

Sample Essays on “Who Am I?” How to guide, with Outlines

Published by gudwriter on November 23, 2017 November 23, 2017

How to Write an Essay About Yourself

Many students, from high school to college level, do not know how to describe themselves. They mix up ideas as they do not really know what they need to include in their writing. The main aim of a who am I essay is to make the reader understand who you are and what you believe in. Remember, the essay doesn’t have to be always about the positive side- you can include your weak points as well in a creative way. You can also write about what makes you unique (unique skills, character, etc). If you need help, college admission essay writing services is available to assist you.

Elevate Your Writing with Our Free Writing Tools!

Did you know that we provide a free essay and speech generator, plagiarism checker, summarizer, paraphraser, and other writing tools for free?

Striking the balance makes your essay realistic and convincing.

Character : What are your character traits? Which habits define you?

Values : What is your value system? Here, you need to include things that inspire you. It is here that you state your beliefs, motivations, principles, and inspirations. The reader expects you to have either staunch stands on certain things and this is the part where you make them know. Do not highlight radical points, though.

Skills : What aptitudes do you have? And, what is the level in each skill? This may include communication, computer, education, languages, leadership, or anything else you find worthy.

Achievements :

Life experiences that influenced your life

Perhaps you would like to read an essay sample on what makes you unique ?

Who Am I Essay Example 1 Outline

Below is a layout you should follow when writing a personal essay to impress your professor.

• Hook – The Question – who am I?
• Brief summary: Well, I know quite much about myself: I am a social, kind, respectful, and principled young man.
• Thesis : I am a kind, friendly, respectful, and principled young person.
• Point : Social
• Illustration : Meeting new friends
• Logic : Makes me dynamic
• Thesis relation: A cheerful, social and accommodative person is how many people know me.
• Point : Respectful and law abiding
• Illustration : Want to get along with everyone- both juniors and seniors. Car seats, polite character
• Explanation : I know the limits
• Thesis relation : Every day, I want to be known as a person who is respectful even to those who least deserve it.
• Point : Hobbies
• Illustrations : Sports, chess, music
• Explanation : Clear my mind, get healthier.
• Thesis relation : Sportsmanship has taught me to be fair other people, diligent and focused.
• Point : I am not perfect- when I don’t hit my targets, obvious opposition from people who don’t love progress. My love for novelty makes me uncomfortable with normal rules.
• Illustrations : My mum says I am selfish and that I always want everything to go my way. Yet, I’m still the person you will find in doing voluntary community work to help people.
• Explanation : I guess my self-esteem is too high for people to put down. This rubs feathers with people who stand my path to success.
• Thesis relation : I’d be a liar to say I am a genius, flawless or immortal- and that’s who I am.
• Restatement of thesis
• Summary of essay
• Signing out

Easily create engaging speeches that will express yourself confidently and fluently, all thanks to our innovative free speech writer generator .

Who Am I Essay Example 1

Who am I? Describing oneself is one of the most complicated tasks. In most cases, we always define ourselves using institutions, other people, or activities. Well, I know quite much about myself: I am a kind, friendly, respectful, and principled young person.

First, I am a sociable person. I love to meet people and make new friends. It’s not that I am an extrovert. However, I always work towards getting along with people. Of course, there are times I enjoy being alone for meditation . However, being around people makes me feel comfortable. I like to utilize every chance I get to make new friends. Interacting with people from different parts of the world makes me a diverse person. I am one of those people who believe that there is richness in human diversity. I am not quite selective of who I socialize with. A cheerful, cordial, and accommodative person is how many people know me.

Second, I am kind and respectful. Well, I appreciate that there is a thin line between being social and respectful. I want to treat everyone – junior or senior- with utmost reverence. In this regard, I am quite a listener. This didn’t start yesterday- I have always loved to give up my seats to elders in the train since I was young. Again, I am firm and at the same time polite. I love to make my points in a way that won’t hurt those around me. I always desire to be respectful even to those who least deserve it. Being respectful does not subtract anything from me after all.

Third, I have a great affection to team play. Well, I probably got this trait from my life as a sportsperson. I have been a school captain in Team Handball and Badminton. Today, I still participate in these games as a coach. I’m adherent to chess and I could become a grandmaster in the next few months. Sports and competitions have trained me to be fair, diligent, hardworking, and focused. As my hobby, chess clears my mind while athletics make me healthy. I’d definitely not tell who I am without mentioning sportsmanship. Actually, sports largely define me.

I am not perfect, though. I can be moody when I don’t hit my targets. My love for novelty makes me uncomfortable with normal rules. My mum says I am selfish and that I always want everything to go my way. Yet, I’m still the person you will find doing voluntary community work to help people. I guess my self-esteem is too high for people to put down. This rubs feathers with anyone who stands on the path to success. I’d be a liar if I said that I am a genius, flawless or immortal- and that’s who I am.

Anyway, it may be a little difficult to explain who I am. However, there are qualities that are an outright depiction of me. Respect, principles, sportsmanship, and leadership are some of them. As a quick learner, I love to change every behavior that doesn’t make me a better person. The desire to be good to everybody has made me who I am today and I intend to keep it that way.

Personal Essay Example 2 Outline

Introduction.

I give a description of myself in relation to my family background, personality, and how I view life.

Paragraph 1:

Family background

• Revolves around strong Christian faith since my parents are staunch Roman Catholic faithful
• I was born in Chicago, Illinois 21 years ago and I am the third born in a family of four children.
• I am a female of African American origin and I am very proud of my cultural background and family values

Paragraph 2:

My personality

• I am outspoken and like socializing and making new friends
• I value respect and believe it is two way
• I am hard working

Paragraph 3:

My view of life

• All humans are equal regardless of their cultural, racial and religious backgrounds as well as gender
• I am liberal in that I am open to learning new things such as new cultures, religions, and even languages
• Divergent views should be tolerated

I can summarize myself as someone who is respectful, accommodating, and open minded. I appreciate that as a human, I need others for my life to be complete. I believe my personality and world views are matching and thus I find life more sociable and interesting.

Personal Essay Example 2

My family background revolves around strong Christian faith since my parents are staunch Roman Catholic faithful. I was born in Chicago, Illinois 21 years ago and I am the third born in a family of four children. I am a female of African-American origin and I am very proud of my cultural background and family values. Like my parents, I have developed the habit and routine of going to church every Sunday in line with Christian doctrines. As a matter of fact, all the members of my family value attending Sunday masses wherever they may find themselves. I grew up in a working-parents family and I have grown to live in harmony with my siblings.

Regarding my personality, I am one person who is outspoken and likes socializing and making new friends. The number of friends I have in college is uncountable because I have no boundaries when it comes to building relationships. That notwithstanding, I value respect and believe it is two way. I expect that anybody I interact with should show me the same level of respect I show them irrespective of their background or status in the society. I am hard working because my parents taught me to loathe laziness since it is the beginning of poverty and miserable life. To me, respect and hard work go hand in hand. Working hard respectfully has opened many doors for me so far in my life.

My view of life is that all humans are equal regardless of their cultural, racial, and religious backgrounds as well as gender. This is why I have friends whose cultural and other backgrounds are diverse. I am also liberal in that I am open to learning new things such as new cultures, religions, and even languages. For instance, I can speak fluent French and Spanish yet I am American. I also believe that divergent views should be tolerated because this is part of enhancing human diversity. My parents had once tried to stop me from being too open minded but I persisted with it. Being open to new things, in my view, amounts to being accommodative to human diversity.

In conclusion, I can summarize myself as someone who is respectful, accommodative, and open minded. I appreciate that as a human, I need others for my life to be complete. When I show that I care for and accommodate different views, I find it easy working with others. I have thus managed to evade suffering any form of racial or cultural profiling because people find me easy to deal with. I believe my personality and world views are matching and thus I find life more sociable and interesting. It is my intention to continue leading this fulfilling life.

Ready to pay to write essay ? We offer a legit service that thousands of students are making use of everyday. Let us do the hard work so you can have some much deserved fun. Order now and receive a quality paper on time.

Personal Essay Sample 3 Outline

I am a faithful Christian who is open-minded, friendly, and action-oriented.

Paragraph1:

In spite of being a staunch Christian, I am open to other people’s ways of worship and generally to other people’s way of life and opinions.

• I can listen to and understand what other people say and treat it as their opinion to which they are entitled whether or not I agree with it.
• I am able to live amongst people of various cultures.
• However, I do not let other people’s views or cultures affect my own.

I am a friendly person who highly values friendship.

• I have the habit of forming strong friendships both in our neighborhood and at school.
• I have quite a number of friends from various backgrounds because I do not choose friends based on their cultural backgrounds.
• I believe in genuine friendship and as soon as I detect that one is not a true friend, I drop them.

I follow my decisions and promises with actions as I believe that it is through actions that one can solve their problems and meet their life goals.

• I keep to my decisions once I make them.
• I have been able to accomplish many of my life’s endeavors especially in my academic life.
• I also know that keeping promises is one of the best ways of keeping relationships alive and healthy.
• I normally do all it takes to keep a promise irrespective of who I make it to.

I am an open-minded Christian who values relationships and I act on my decisions and promises. I am accommodative to diverse views and opinions even when they sharply contrast with mine. I pursue my life goals and keep relationships through action.

Personal Essay Sample 3

As a person, I feel growing over the years has significantly changed who I am. I have had to see and experience many things that I did not get to see in my childhood. I have also met many different people and visited many places. Some of the perspectives I held about people and certain things have certainly changed. In addition, I have undergone significant personal growth which has seen my personality transform as well. I have also become more decisive in my actions and in my relationships with others. I am a faithful Christian who is open-minded, friendly, and action-oriented.

In spite of being a staunch Christian, I am open to other people’s ways of worship and generally to other people’s way of life and opinions. I can listen to and understand what other people say and treat it as their opinion to which they are entitled whether or not I agree with it. This way, I have been able to learn a lot from others and widen my view of life and humanity. I am also able to live amongst people of various cultures. However, I do not let other people’s views or cultures affect my own as much as I may be accommodative to them. This is because I believe that the world has enough space for everyone to practice their own cultures and share their opinions without interfering with others.

I am also a friendly person who highly values friendship. From my childhood, I developed the habit of forming strong friendships both in our neighborhood and at school. I have carried this habit to my adulthood and I have quite a number of friends from various backgrounds because I do not choose friends based on their cultural backgrounds. However, I believe in genuine friendship and as soon as I detect that one is not a true friend, I drop them. To me, a friend should be like family that is always there for one in their better and tough days and moments. Out of this belief, I have helped a number of friends both in and out of school and shared with them some of my innermost secrets. I too have benefited from the loyalty of these friendships.

Further, I follow my decisions and promises with actions as I believe that it is through actions that one can solve their problems and meet their life goals. This virtue has helped me accomplish many of my life’s endeavors especially in my academic life. For example, since my middle school level, I decided that I would not consume television content during examination periods but maximally concentrate on the exams. I have kept to this decision and have thus posted good grades all through because I always have enough time to prepare for exams. I also know that keeping promises is one of the best ways of keeping relationships alive and healthy. I normally do all it takes to keep a promise irrespective of who I make it to. I do keep even as simple a promise as that of sharpening my younger sister’s drawing pencil every morning before she goes to school.

I am an open-minded Christian who values relationships and I act on my decisions and promises. I am accommodative to diverse views and opinions even when they sharply contrast with mine. I pursue my life goals and keep relationships through action. I also have many friends since I believe that genuine friendship is highly beneficial to humans. This personality and values enable me to live a fulfilling life as I am capable of accomplishing my goals and at the same time live harmoniously with others.

Don’t spend hours on the same essay again and again whereas you can us an essay maker tool that will help you create a unique and plagiarism-free essay.

Special offer! Get 20% discount on your first order. Promo code: SAVE20

Related Posts

Free essays and research papers, artificial intelligence argumentative essay – with outline.

Artificial Intelligence Argumentative Essay Outline In recent years, Artificial Intelligence (AI) has become one of the rapidly developing fields and as its capabilities continue to expand, its potential impact on society has become a topic Read more…

Synthesis Essay Example – With Outline

The goal of a synthesis paper is to show that you can handle in-depth research, dissect complex ideas, and present the arguments. Most college or university students have a hard time writing a synthesis essay, Read more…

Examples of Spatial Order – With Outline

A spatial order is an organizational style that helps in the presentation of ideas or things as is in their locations. Most students struggle to understand the meaning of spatial order in writing and have Read more…

EBN - European Board of Neurology Examination

General information.

The European Board Examination in Neurology is considered to be a tool for the assessment of neurological training and for boosting its standards. It is an important step towards further harmonisation in European neurology.

Successful candidates from all over the world are conferred the title "Fellow of the European Board of Neurology (FEBN)"

The exam is unified based on European Training Requirements in Neurology and EAN Guidelines . It consists of a step 1 written part testing (handling) knowledge, and a step 2 oral part testing other competencies from the CanMEDS roles.

The exam was held in 2009 for the very first time and since then 850 candidates passed the exam.

Joint Education Board

The European Board Examination in Neurology is a joint assignment of both EAN and UEMS SN/EBN via the Joint Education Board (JEB) . Since establishing the JEB, cooperation in this regard is conducted via the board and has a designed framework.

EBN Exam 2024

16th European Board Examination in Neurology 2024

The EBN Exam exists of two partial exams (written and oral) and both will be held  ONLINE  only.

Oral exam : 31 May & 1 June 2024  (Friday/Saturday) Written exam: 7 June 2024  (Friday)

Deadlines: Early bird application deadline: January 15, 2024 Final application deadline: March 01, 2024 Deadline for submitting workpieces (CAT, Essay) for the oral examination: March 5, 2024

Please find more information about the EBN Exam and the Application Process on the Website of UEMS-SN:  UEMS Section of Neurology - European Board Examination (uems-neuroboard.org)

Discounts and Funding

EAN RRFS, Full and Corresponding members, who participate in the exam, receive 20% discount on their congress registration.

All other exam participants and examiners receive a 10% discount off their congress registration fee.

JEB Examination Committee

In order to effectively organise the continually thriving exam, the Examination Committee has been established. This committee is a working group of the Joint Education Board that will coordinate and conduct all activities concerning the exam, from collecting and supervising questions to management of the examination on-site. The nomination is for at least two years.

Composition of the Examination Committee:

Dr. david garcía azorín (uems-sn/ebn) , valladolid, spain   , prof. pablo irimia-sieira (ean), pamplona, spain  , dr francesco di lorenzo (ean), rome, italy  , prof. massimiliano filosto (ean), gussago brescia, italy  , prof. jan b.m. kuks (uems-sn/ebn), groningen, the netherlands, dr. deborah mcintyre (uems-sn/ebn), luxembourg, louxembourg  , dr. tim counihan (uems-sn/ebn), galway, ireland  , ean eqtf representative, hana brozova, prague, czech republic, fellows of the ebn exam.

Find out more

Cramming for an exam isn’t the best way to learn – but if you have to do it, here’s how

Senior Teaching Fellow in Education, University of Strathclyde

Disclosure statement

Jonathan Firth does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

University of Strathclyde provides funding as a member of The Conversation UK.

View all partners

Around the country, school and university students are hitting the books in preparation for exams. If you are in this position, you may find yourself trying to memorise information that you first learned a long time ago and have completely forgotten – or that you didn’t actually learn effectively in the first place.

Unfortunately, cramming is a very inefficient way to properly learn. But sometimes it’s necessary to pass an exam. And you can incorporate what we know about how learning works into your revision to make it more effective.

Read more: Exams: seven tips for coping with revision stress

A great deal of research evidence on how memory works over time shows that we forget new information very quickly at first, after which the process of forgetting slows down.

In practice, this means that very compressed study schedules lead to a catastrophic amount of forgetting.

A better option is to space out learning a particular topic more gradually and over a longer period. This is called the “spacing effect” and it leads to skills and knowledge being retained better, and for longer.

Research has found that we remember information better when we leave a gap of time between first studying something and revisiting it, rather than doing so straight away. This even works for short timescales – a delay of a few seconds when trying to learn a small piece of information, such as a pair of words, for instance. And it also works when the delay between study sessions is much longer .

In the classroom , spacing out practice could mean reviewing and practising material the next day, or delaying homework by a couple of weeks, rather than revisiting it as soon as possible. As a rule, psychologists have suggested that the best time to re-study material is when it is on the verge of being forgotten – not before, but also not after.

But this isn’t how things are learned across the school year. When students get to exam time, they have forgotten much of what was previously studied.

Better cramming

When it comes to actually learning – being able to remember information over the long term and apply it to new situations – cramming doesn’t work. We can hardly call it “learning” if information is forgotten a month later. But if you need to pass an exam, cramming can lead to a boost in temporary performance. What’s more, you can incorporate the spacing effect into your cramming to make it more efficient.

It’s better to space practising knowledge of a particular topic out over weeks, so if you have that long before a key exam, plan your revision schedule so you cover topics more than once. Rather than allocating one block of two hours for a particular topic, study it for one hour this week and then for another hour in a week or so’s time.

If you don’t have that much time, it’s still worth incorporating smaller gaps between practice sessions. If your exam is tomorrow, practice key topics in the morning today and then again in the evening.

Learning is also more effective if you actively retrieve information from your memory, rather than re-reading or underlining your notes. A good way to do this, incorporating the spacing effect, is to take practice tests. Revise a topic from your notes or textbook, take a half-hour break, and then take a practice test without help from your books.

An even simpler technique is a “brain dump” . After studying and taking a break, write down everything you can remember about the topic on a blank sheet of paper without checking your notes.

Change the way we teach

A shift in teaching practices may be needed to avoid students having to cram material they only half-remember before exams.

But my research suggests that teachers tend to agree with the idea that consolidation of a topic should happen as soon as possible, rather than spacing out practice in ways that would actually be more effective.

Teachers are overburdened and make heroic efforts with the time they have. But incorporating the spacing effect into teaching needn’t require radical changes to how teachers operate. Often, it’s as simple as doing the same thing on a different schedule .

Research has shown the most effective way to combine practice testing and the spacing effect is to engage in practice testing in the initial class, followed by at least three practice opportunities at widely spaced intervals. This is quite possible within the typical pattern of the school year.

For example, after the initial class, further practice could come via a homework task after a few days’ delay, then some kind of test or mock exam after a further gap of time. The revision period before exams would then be the third opportunity for consolidation.

Building effective self-testing and delayed practice into education would spell less stress and less ineffective cramming. Exam time would be for consolidation, rather than re-learning things that have been forgotten. The outcome would be better long-term retention of important knowledge and skills. As a bonus, school students would also gain a better insight into how to study effectively.

• Motivate me

Want to write?

Write an article and join a growing community of more than 184,400 academics and researchers from 4,972 institutions.

Register now