nursing research articles on head trauma

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Improving Traumatic Brain Injury Care and Research : A Report From the National Academies of Sciences, Engineering, and Medicine

• 1 National Academies of Sciences, Engineering, and Medicine, Washington, DC
• 2 Institute for Healthcare Improvement, Boston, Massachusetts
• JAMA Insights Mild Traumatic Brain Injury in 2019-2020 Noah D. Silverberg, PhD; Ann-Christine Duhaime, MD; Mary Alexis Iaccarino, MD JAMA
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• Review Pharmacological Interventions and Symptom Reduction for Mild Traumatic Brain Injury Charles Feinberg, BA; Catherine Carr, MLIS; Roger Zemek, MD; Keith Owen Yeates, PhD; Christina Master, PhD; Kathryn Schneider, PT, PhD; Michael J. Bell, MD; Stephen Wisniewski, PhD; Rebekah Mannix, MD, MPH JAMA Neurology

Traumatic brain injury (TBI) takes a substantial toll on health and health care costs in the US. Yet TBI is often unrecognized, misclassified, undertreated (especially in its longer-term manifestations), and, in proportion to its public health consequences, underresearched. Despite the dedication of an increasing number of professionals, disciplines, and organizations devoted to TBI care and research, including innovative programs for military service members and veterans, care often fails to meet the needs of affected individuals, families, and communities. The US lacks consolidated leadership for achieving improvements in TBI care and outcomes, and, partly as a result, it lacks a strategic plan for fostering change and overseeing progress. With stronger leadership and proper redesign, the health care system could reduce the morbidity and disability associated with TBI, while enhancing the effectiveness of TBI care.

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Bowman K , Matney C , Berwick DM. Improving Traumatic Brain Injury Care and Research : A Report From the National Academies of Sciences, Engineering, and Medicine . JAMA. 2022;327(5):419–420. doi:10.1001/jama.2022.0089

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‘Let’s hear it for the midwives and everything they do’

STEVE FORD, EDITOR

• You are here: Accident and emergency

Trauma nursing 3: assessing and managing head injury

19 December, 2022 By Nuala Oughton and Peachiammal Subramanian

This third article in our trauma series explores causes, types and treatment of traumatic brain injuries

Head injury is a major cause of hospital admission for trauma patients. This third article in our series on trauma nursing explores causes and types of head injuries, and the assessment and management of traumatic brain injury. As well as a focus on acute care, topics also discussed are rehabilitation and long-term support.

Citation: Oughton N, Subramanian P (2023) Trauma nursing 3: assessing and managing head injury. Nursing Times [online]; 119: 1.

Authors: Nuala Oughton and Peachiammal Subramanian are both senior sisters in practice development, Adult Critical Care Unit, Barts Health NHS Trust, and honorary lecturers, City, University of London.

• This article has been double-blind peer reviewed
• Scroll down to read the article or download a print-friendly PDF here (if the PDF fails to fully download please try again using a different browser)
• Click here to see other articles in this series

Introduction

Head injury (HI) is defined by the National Institute for Health and Care Excellence (NICE) (2014) as “any trauma to the head other than superficial injuries to the face”; this may or may not involve brain injury. Although the overall incidence of death from HI is low at six to ten people per 100,000 annually, HI is the most common cause of death or disability in people aged 1 year to 40 years in the UK (NICE, 2014).

In the UK, around 20% of people with HI require hospital admission, but only 2% of people attending the emergency department with HI die (NICE, 2014). Most fatal outcomes involve people who have sustained moderate-to-severe HIs. This article, the third in a series about trauma, explores how HIs are assessed and managed, including how to identify the few patients who will go on to develop serious acute intracranial complications.

“A blunt brain injury is usually caused by a fall, blunt assault or road traffic collision”

Traumatic brain injury

Traumatic brain injury (TBI) is defined as injury to brain function, or the indication of brain pathology, caused by an external force (Khellaf et al 2019). The worldwide yearly incidence of TBI is estimated at 50 million; severe TBI can cause significant physical, psychosocial and social deficits and, in up to 60% of cases, has mortality rates of 30–40% (Khellaf et al, 2019).

TBI is the largest contributor to the global burden of disability and costs the international economy around US$400bn annually, amounting to approximately 0.5% of the entire annual global economic output (Maas et al, 2017). Timely intervention and structured follow-up for this patient cohort could, therefore, reduce this burden (Maas et al, 2017). TBI might also be a major risk factor for late neurodegenerative disorders, such as dementia and Parkinson’s disease , contributing to the view that TBI can evolve into a progressive, lifelong illness (Maas et al, 2017).

The epidemiology of TBI is changing. In high-income countries, the number of older people sustaining TBIs is increasing, primarily due to falls; in lower-income countries, the number of TBIs caused by road traffic collisions is increasing (Maas et al, 2017). Small regional studies reported a decrease in TBI during Covid-19 lockdowns, reflecting decreased mobility, sports and recreational activity, and possibly a reluctance to seek medical help for milder injuries (Mass et al, 2022).

Primary and secondary brain injury

Primary brain injury occurs at the moment of impact and is irreversible. Primary brain injuries can be:

• Penetrating;

A penetrating brain injury involves an open wound to the head from a foreign object, for example, during a shooting or stabbing. It is typically evident due to focal damage occurring along the route through which the object has travelled in the brain; this includes fractured skull, torn meninges (layers that protect the brain), and damage to the brain tissue.

A blunt brain injury is usually caused by a fall, blunt assault or road traffic collision (American College of Surgeons (ACS), 2018).

Secondary brain injuries can:

• Evolve from primary damage;
• Be a result of insult from highly preventable and treatable causes, such as hypotension and hypoxia.

Intracranial injuries can be further classified according to the location of damage (Table 1).

Assessing HI

All trauma patients and clinical emergencies must receive a thorough and systematic ABCDE assessment, which checks:

• Circulation;
• Disability;
• Exposure (ACS, 2018).

Additionally, TBI severity is assessed by the Glasgow Coma Scale (GCS) and further determined by the duration of post-traumatic amnesia (Tenovuo et al, 2021).

The GCS is a practical, structured assessment method that determines impaired consciousness in response to defined stimuli. It supports, but does not replace, clinical decision making (Royal College of Physicians and Surgeons of Glasgow, nd). The GCS scores a patient’s best motor, verbal and eye-opening responses (Table 2). This information is used to classify a TBI’s clinical severity as mild (concussion), moderate or severe. However, the GCS is limited due to there being other causes for a reduced score in trauma , such as alcohol consumption, sedation or seizure.

The minimum required neurological observations for patients admitted to hospital with HI are:

• Pupil size and reactivity;
• Limb movements;
• Respiratory rate ;
• Heart rate ;
• Blood pressure;
• Temperature;
• Blood–oxygen saturation (NICE, 2014).

These should be documented.

NICE (2014) guidelines state that all patients with HI taking anticoagulants must receive a CT scan. CT is a fast and precise method of imaging in acute craniocerebral trauma, allowing quick diagnosis of TBI (Kumar et al, 2019). The patterns of damage that a CT scan detects can be:

• Focal (localised);
• Diffuse (widespread).

However, the two types often coexist (Haydel and Lauro, 2021). Table 3 lists features of each type.

CT assessment of primary brain injuries, combined with clinical assessment using the GCS, helps determine HI severity and helps in the planning of treatment (Kumar et al, 2019). Fractures occur in 5% of patients with mild TBI and in up to 50% of those with severe TBI (Haydel and Lauro, 2021).

Intracranial pressure (ICP) can increase quickly in the limited space of the skull and if the brain’s blood supply is interrupted for just a few minutes, brain tissue dies; TBI is, therefore, a time-critical injury (Fairley, 2017).

Pre-hospital management

Pre-hospital management of patients includes initial resuscitation and interventions to stabilise them at the scene of injury and when they are on the way to hospital. This assessment and management should focus on preventing secondary brain injury and follow the Advanced Trauma Life Support course (NICE, 2014).

To avoid hypoxia, patients should be intubated, and ventilation should be started if they have:

• Severe HI and a GCS score of ≤8;
• Facial fractures;
• Injuries that compromise oxygenation and ventilation (ACS, 2018).

Hypotension (systolic blood pressure of <90mmHg) has the highest correlation with increased morbidity and mortality (Vella et al, 2017). The Brain Trauma Foundation (BTF) (2016) guidelines recommend maintaining a mean arterial pressure (MAP) of around 90mmHg.

Intravenous access should be established, and volume resuscitation with isotonic fluids is recommended (McNair, 2019). Cervical spine immobilisation must be maintained until full clinical assessment and imaging are completed. Effective pain management is important to reduce the ICP, and GCS and pupil response should be continuously assessed for any abnormalities. Immediate transport to the nearest trauma centre to further evaluate and manage the HI is essential.

Hospital management

The goals of the intensive care unit (ICU) care are to:

• Maintain adequate cerebral oxygen delivery;
• Manage and treat intracranial hypertension;
• Prevent secondary brain injury;
• Prevent or manage potential complications.

On arrival at the emergency department, the patient’s history, mechanism of injury and previous treatment must be clarified. When that has been done, health professionals should:

• Attach the patient to continuous monitoring equipment;
• Establish adequate vascular access;
• Insert an indwelling urinary catheter;
• Continue resuscitation and stabilisation;
• Conduct relevant diagnostic tests (NICE, 2014).

CT scanning without contrast will help to diagnose most intracranial injuries, such as depressed skull fracture, extradural haematoma, subdural haematoma, intracerebral haemorrhage and contusion (Table 1). Cerebral angiograms are needed to exclude any vascular injury that is secondary to trauma (McNair, 2019).

Management in the emergency department is directed at resuscitation, stabilisation and diagnosis. When these steps have been completed, surgical intervention for life-threatening injuries can be carried out, or the patient can be transferred to the ICU or ward for medical management.

Patient monitoring should be tailored to the clinical presentation. As a minimum, it is essential to monitor:

• Electrocardiography;
• Oxygen saturation;
• Central venous pressure;
• Arterial pressure;
• Urine output.

Cardiac-output monitoring should be used to guide fluid and inotrope requirements (Khellaf et al, 2019).

ICP monitoring is essential if the therapy is targeted to maintain cerebral perfusion pressure (CPP). CPP refers to the blood-pressure gradient across the brain and is calculated as follows:

MAP-ICP = CPP

Raised ICP reduces cerebral perfusion, which results in cerebral ischaemia (Khellaf et al, 2019). The BTF’s (2016) guidelines recommend maintaining ICP at 20-25mmHg and CPP at >60mmHg. Criteria for patients who need ICP monitoring are outlined in Table 1. Maintaining a CPP of >60mmHg is achieved by increasing the MAP and decreasing the ICP. Hypotension and prolonged increases in ICP of >20mmHg are associated with poorer patient outcomes (Rosner et al, 1995).

Patients with HI require ICP monitoring if they have a GCS score of ≤8 and either an abnormal CT scan or a normal CT scan and two or more of the following:

• Aged >40 years;
• Motor posturing;
• Systolic blood pressure of <90mmHg (BTF, 2016).

Respiratory management

Tracheal intubation remains the gold standard for airway management for patients with a GCS of ≤8. Careful preparation and pre-oxygenation are mandatory. Adequate sedation and muscle relaxation reduce cerebral metabolic oxygen requirements and optimise ventilation (Dinsmore, 2013).

Hypoxia is defined as a lack of oxygen supply or excessive oxygen consumption resulting in insufficient oxygen levels to maintain normal cellular function (Bhutta et al 2022). Oxygenation should be monitored, and hypoxia or oxygen saturation of <90% avoided. Blood–oxygen content regulates the cerebral blood flow; Nathanson et al (2020) have recommended maintaining the partial pressure of oxygen (PaO2) at >13kPa. Hypoxia causes vasodilation and impairs cerebral autoregulation, resulting in increased ICP.

Maintaining the normal partial pressure of carbon dioxide (PaCO2) value of 4.5-5kPa in a patient with TBI is fundamental. Hypercapnia or too much carbon dioxide in the blood (PaCO2 of >6kPa) is a potent vasodilator, which increases cerebral blood flow and results in increased ICP (Dinsmore, 2013).

Endotracheal suctioning increases the ICP and so health practitioners should hyper oxygenate patients with 100% oxygen for 60 seconds, before suctioning for less than 15 minutes (Mestecky, 2007). Mild-to-moderate hyperventilation is recommended when other medical interventions fail to reduce the ICP: BTF (2016) guidelines suggest using hyperventilation to achieve a PaCO2 of 4-4.5kPa as a temporary measure to reduce the ICP.

“Enteral feeding must be started as soon as possible to meet patients’ nutritional requirements”

Nursing activities

Nursing interventions – such as positioning, personal care, linen changing and endotracheal suctioning – can increase ICP if carried out in sequence, so clustering nursing activities should be avoided (Mestecky, 2007). If the patient is receiving ICP monitoring, the nurse must assess their individual response to these interventions and adjust their care accordingly. Noxious stimuli must be avoided, and nursing interventions that reduce the patient’s ICP must be used. Ensure everything is ready before repositioning the patient to avoid a prolonged period of increased ICP.

The optimal head position for a patient with HI is 30 degrees because it promotes venous drainage; the neck should be kept in alignment to avoid interrupting venous drainage. Endotracheal ties around the neck should fit properly and care should be taken to avoid obstructing venous return. Extreme hip flexion should also be avoided as it increases the intra-abdominal pressure, resulting in increased ICP (McNair, 2019).

Adequate sedation is essential to help ventilation and prevent coughing and gagging on the endotracheal tube. Coughing increases intrathoracic pressure and impairs cerebral venous drainage. Sedation reduces cerebral metabolic rate and demand, cerebral blood flow and the ICP (Dinsmore, 2013).

Flower and Hellings (2012) recommended using the sedative propofol, due to its neuroprotective properties and short duration of action, which allows the patients to be formally neurologically assessed. However, a common side-effect of propofol is hypotension, which is important to avoid. Fluids and inotropes should be administered to minimise the effect on the MAP and CPP.

Analgesics such as morphine and fentanyl are often used to manage pain and reduce anaesthetic requirements. Fentanyl is commonly used in neurosurgical units due to its reduced half-life and accumulation properties when compared with other opioids (Flower and Hellings, 2012). Barbiturates are recommended over other medical and surgical treatments when the ICP remains high (Mestecky, 2007).

Patients with HI have high energy and protein requirements due to hypermetabolic and hypercatabolic responses to HI. Enteral feeding must be started as soon as possible to meet the patient’s nutritional requirements (Kurtz and Rocha, 2020). Carney et al (2017) highlighted the importance of avoiding hypoglycaemia (<80mg/dL or ≤4.4mmol/L) and hyperglycaemia (>180mg/dL or ≥10mmol/L).

Hyperglycaemia increases the cerebral metabolism and hypoglycaemia causes cerebral ischemia. Dextrose-containing solutions should be avoided because they reduce the plasma osmolality, which, in turn, increases the water content in the brain (McNair, 2019).

Surgical interventions

Surgical evacuation should be considered for patients with acute subdural haematoma, extradural haematoma or compound fractures with associated mass effect (Vella et al, 2017).

Decompressive craniectomy is a surgical procedure in which a large area of the skull is removed to make additional space for the swollen brain. This procedure is used for patients with refractory ICP that is not responding to medical management. However, the practice remains controversial and evidence of its benefits is insufficient to make it a level 1 BTF recommendation (BTF, 2016).

Supporting psychological issues and personality changes

HI can result in a vast array of psychological effects. Common issues include:

• Depression;
• Cognitive issues;
• Problems regulating behaviour.

These develop due to damage to the areas of the brain responsible for managing emotions, or the patient’s inability to do the activities they previously did. Some patients may experience post-traumatic stress disorder. This is a severe psychological reaction to trauma, involving persistent re-experiencing of the event, avoidance of stimuli triggering memories of it and a numbing of emotional response (Vasterling et al, 2018). The emotional problems associated with brain injury depend on an individual’s personality, coping skills and the personal and professional support available to them.

HI is also a source of acute stress for a patient’s close family members, due to:

• The shock of the initial injury;
• The recovery;
• Adjusting to the patient’s personality changes (Barman et al, 2016).

Psychological services help patients with HI and their families throughout the course of recovery, including through acute care, rehabilitation and long-term support. Most regional neurosurgical centres and neurorehabilitation services have access to specialist neuropsychological services. Services that are available at these centres are:

• Early cognitive assessment;
• Cognitive rehabilitation;
• Behavioural management;
• Social skills training;
• Psychological counselling;
• Psychotherapy;
• Family therapy (Barman et al, 2016).

The recovery period is varied and patients can show marked improvement and make successful adjustments to disabilities that remain. Headway (headway.org.uk) is a UK-wide charity that aims to improve life after HI by providing support and information services. It has a range of factsheets on all aspects of brain injury, books and publications about the effects of injury, emergency funds for patients and a directory of approved residential homes and rehabilitation units specialising in HI.

Clinical management of patients with HI starts with an ABCDE assessment, and interventions depend on the degree of patient risk according to the intracranial injury symptoms. Prompt treatment can prevent secondary brain injury and improve patient outcomes. Acute care management based on best-evidence guidelines and recommendations should be provided from the initial injury onwards. This requires a sound knowledge of pathophysiology and best practice for the effective management of HI.

• Traumatic brain injury is a significant cause of morbidity and mortality worldwide
• Head injuries should be assessed using the ABCDE (airway, breathing, circulation, disability, exposure) assessment and the Glasgow Coma Scale
• Initial management should focus on preventing secondary brain injury
• Intracranial pressure can increase quickly, so head injuries are time critical
• Head injuries can cause psychological problems in patients and their families

Also in this series

• Trauma nursing 1: an overview of major trauma and the care pathway
• Trauma nursing 2: management of patients with rib fractures
• Trauma nursing 4: recognising and managing haemorrhage in trauma
• Trauma nursing 5: identifying and assessing patients who self-harm

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The Journal of Trauma Nursing is released six times a year - four printed issues are mailed to subscribers, and two issues are distributed as online editions.

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Trauma nursing research: a description and means of evaluation

• PMID: 7946199

This article describes and discusses trends in trauma nursing research from 1988 to 1993, and provides a basis for evaluating this type of research. Trauma nursing research is divided into several topics: trauma prevention, prehospital care, acute care, outcome and rehabilitation, trauma systems and health policy, and trauma nursing education and administration. Variables specific to trauma, such as the trauma score, are identified and described. The contents of a research article and a means of evaluating each section of such literature are discussed.

Publication types

• Research Support, Non-U.S. Gov't
• Education, Nursing
• Multiple Trauma / nursing*
• Nursing Research / classification
• Nursing Research / methods*
• Nursing Research / standards
• Nursing, Supervisory

REVIEW article

Repurposing development genes for axonal regeneration following injury: examining the roles of wnt signaling provisionally accepted.

• 1 Leonard M. Miller School of Medicine, University of Miami, United States

The final, formatted version of the article will be published soon.

In this review, we explore the connections between developmental embryology and axonal regeneration. Genes that regulate embryogenesis and central nervous system (CNS) development are discussed for their therapeutic potential to induce axonal and cellular regeneration in adult tissues after neuronal injury. Despite substantial differences in the tissue environment in the developing CNS compared with the injured CNS, recent studies have identified multiple molecular pathways that promote axonal growth in both scenarios. We describe various molecular cues and signaling pathways involved in neural development, with an emphasis on the versatile Wnt signaling pathway. We discuss the capacity of developmental factors to initiate axonal regrowth in adult neural tissue within the challenging environment of the injured CNS.Our discussion explores the roles of Wnt signaling and also examines the potential of other embryonic genes including Pax, BMP, Ephrin, SOX, CNTF, PTEN, mTOR and STAT3 to contribute to axonal regeneration in various CNS injury model systems, including spinal cord and optic crush injuries in mice, Xenopus and zebrafish. Additionally, we describe potential contributions of Müller glia redifferentiation to neuronal regeneration after injury. Therefore, this review provides a comprehensive summary of the state of the field, and highlights promising research directions for the potential therapeutic applications of specific embryologic molecular pathways in axonal regeneration in adults.

Keywords: axon regeneration, Embryonic Development, Wnt signaling, Müller glia, Retina, Spinal Cord, Brain

Received: 16 Apr 2024; Accepted: 13 May 2024.

Copyright: © 2024 Albano and Hackam. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Abigail S. Hackam, Leonard M. Miller School of Medicine, University of Miami, Miami, 33136, Florida, United States

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A fragment of human brain, mapped in exquisite detail

A cubic millimeter of brain tissue may not sound like much. But considering that tiny square contains 57,000 cells, 230 millimeters of blood vessels, and 150 million synapses, all amounting to 1,400 terabytes of data, Harvard and Google researchers have just accomplished something enormous.   

A Harvard team led by Jeff Lichtman, the Jeremy R. Knowles Professor of Molecular and Cellular Biology and newly appointed dean of science , has co-created with Google researchers the largest synaptic-resolution, 3D reconstruction of a piece of human brain to date, showing in vivid detail each cell and its web of neural connections in a piece of human temporal cortex about half the size of a rice grain.

The feat, published in Science, is the latest in a nearly 10-year collaboration with scientists at Google Research, who combine Lichtman’s electron microscopy imaging with AI algorithms to color-code and reconstruct the extremely complex wiring of mammal brains. The paper’s three co-first authors are former Harvard postdoctoral researcher Alexander Shapson-Coe; Micha? Januszewski of Google Research, and Harvard postdoctoral researcher Daniel Berger.

The collaboration’s ultimate goal, supported by the National Institutes of Health BRAIN Initiative , is to create a high-resolution map of a whole mouse brain’s neural wiring, which would entail about 1,000 times the amount of data they just produced from the 1-cubic-millimeter fragment of human cortex.  

“The word ‘fragment’ is ironic,” Lichtman said. “A terabyte is, for most people, gigantic, yet a fragment of a human brain – just a miniscule, teeny-weeny little bit of human brain – is still thousands of terabytes.”  

The latest map in Science contains never-before-seen details of brain structure, including a rare but powerful set of axons connected by up to 50 synapses. The team also noted oddities in the tissue, such as a small number of axons that formed extensive whorls. Since their sample was taken from a patient with epilepsy, they’re unsure if such unusual formations are pathological or simply rare.

Lichtman’s field is “connectomics,” which, analogous to genomics, seeks to create comprehensive catalogues of brain structure, down to individual cells and wiring. Such completed maps would light the way toward new insights into brain function and disease, about which scientists still know very little.

Google’s state-of-the-art AI algorithms allow for reconstruction and mapping of brain tissue in three dimensions. The team has also developed a suite of publicly available tools researchers can use to examine and annotate the connectome.

“Given the enormous investment put into this project, it was important to present the results in a way that anybody else can now go and benefit from them,” said Google Research collaborator Viren Jain.

Next the team will tackle the mouse hippocampal formation, which is important to neuroscience for its role in memory and neurological disease.

• Brain-Computer Interfaces
• Brain Injury
• Neuroscience
• Intelligence
• Disorders and Syndromes
• Mad Cow Disease
• Bitemporal hemianopsia
• Anchoring bias in decision-making
• Neural network

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Materials provided by Harvard University . Original written by Anne J. Manning. Note: Content may be edited for style and length.

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Unlocking the mysteries of CTE: Inside New Zealand’s brain bank

Alex Powell

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• Top scientist Dr Helen Murray recommends introducing high-contact sports at older ages to minimise head-injury risks.
• The Centre for Brain Research collaborates globally to study Chronic Traumatic Encephalopathy (CTE), aiming for a diagnostic test within a decade.
• Two New Zealand athletes, including former rugby player Billy Guyton, were diagnosed with CTE this year.
• New Zealand Rugby acknowledges the need for more research on rugby and CTE.

As she sits down with the Herald to discuss the important work of studying brain injuries, Dr Helen Murray – one of New Zealand’s top neuroscientists – sports a fresh bruise under her right eye, which she believes she picked up playing ice hockey.

With her two passions at times overlapping, Murray is more qualified than most to understand the link between Chronic Traumatic Encephalopathy (CTE) and contact sport.

Aside from her years of work studying the human brain, she was also captain of New Zealand’s national ice hockey team, the Ice Fernz.

CTE is a neurological condition linked to repeated head trauma, where a patient’s brain deteriorates over time. Symptoms include memory deficits, mood changes and movement issues, among others.

As society becomes more aware of CTE and its relationship with contact sports, the work of the New Zealand Brain Bank is more important than ever.

This year, former Tasman, Blues, and Māori All Blacks halfback Billy Guyton was confirmed to have died with CTE. He was the first New Zealand athlete to be found with the condition.

This month, a former Kiwis international – for now unnamed – was confirmed as the first known case of a national representative with CTE.

In 2021, former All Blacks prop Carl Hayman revealed he’d been diagnosed with early onset dementia, as a result of numerous head injuries he sustained over his playing career.

While most research on CTE and sport originated from the United States, and concerns the NFL , New Zealand is playing its part.

In the early 1990s, the Neurological Foundation’s Human Brain Bank was established, allowing for research to be carried out in Aotearoa, with donations from families.

More than 700 brains have been stored in the bank since its opening, with nine different neurological conditions including Alzheimer’s, Parkinson’s, and CTE, stored at -80C.

Since 2009, the Centre for Brain Research (CBR) has studied numerous neurological conditions, including CTE, in collaboration with other brain banks of its kind around the world. In 2019, a specialised unit for sport was opened, allowing former athletes’ brains to be donated after they had died. The brains would be researched to better understand the link to head trauma.

But as much as we already know about CTE, there is still so much more to learn and understand.

“This is an ongoing story,” CBR director Sir Richard Faull told the Herald . “This is not the conclusion. We’re just beginning on the journey of trying to unravel the science.

“The outcome from such a study is going to be gradual over years.

“Getting a real scientific profile is the real problem. How much head injury is too much? Is any too much?”

For Murray, none of these cases come as a surprise. Given the national significance of contact sport, and rugby in particular, there will be thousands of cases in athletes that have gone undiagnosed for years.

Now, though, with the condition coming into mainstream focus, it’s hoped more and more affected people can come forward.

“It reflects what we probably already knew,” Murray said. “New Zealanders are affected by CTE.

“Just because there hadn’t been a case reported in New Zealand prior to our sports brain bank doesn’t mean it didn’t exist.

“The other reaction is it reflects there’s a raised awareness, these head injuries can have a long-term implication. That’s been a good thing, that people aren’t dismissing it.

“Also, a lot of these cases make me think of how we think of dementia and cognitive decline as being an ‘older person’s condition’. This is a situation where we’ve got relatively young people experiencing cognitive changes.

“It is a little bit scary. That’s what makes this quite different to some of the other things we study here.”

At present, one of the biggest problems around CTE is the fact that it can’t be diagnosed in living people. Both Guyton and the unnamed player’s cases were discovered after their deaths.

It’s hoped that within the next decade - possibly in five years - there will be a way to test for the condition in living people.

For now, thought, it’s important to understand the difference between concussion and CTE.

“Concussion is the symptoms you experience after a head injury,” Murray explained. “You can have heaps of these impacts during trainings, games where you feel absolutely fine. Asymptomatic things.

“We know that a lot of those sharp acceleration, deceleration twisting forces are building up over time. That’s the risk factor for CTE.

“It’s more about the exposure, accumulative number of impacts and the force of impacts over a long period of time.

“That’s the risk factor for CTE, as opposed to the number of concussions.

“The number one priority when I talk to people is diagnosis, and getting that right. If we can diagnose, we can get some idea of how many people are affected.”

New Zealand’s two biggest at-risk codes are taking steps to minimalism the risk of repeated head injuries.

Professional rugby requires players who fail head injury assessments (HIAs) to observe a 12-day stand down period before they are allowed to return to play in any capacity.

That window extends to 21 days at the amateur level, taking into account the lack of professional support, without access to the same resources.

In the NRL, an 11-day stand down is in place for the same reason, before any return is allowed to occur.

While Murray does commend the sports for having something in place to reduce risk for players, having a set time period to allow for recovery isn’t as simple as just putting a number of days on it.

“Every injury and every individual is going to be different,” she said. “For some people, that’s going to be nowhere near long enough. For others, it might be fine.

“It’s just so hard to put a blanket number and say ‘this is what’s safe’.

“You’re basing it on how someone’s feeling, whether their symptoms are gone. But we don’t have many measures where we can take an image, or a blood test and say ‘actually, your brain is still showing signs of damage, you should sit out for longer’.

“As guidelines, it’s hard to say what is enough time. My mindset is people should be super cautious. If you have any symptoms, irrespective of a stand down, you should listen to your body.”

That overlap hasn’t gone unnoticed either, with teammates and fellow players consistently coming to her with concerns over potential head injury worries.

And naturally, her two passions overlapping has affected the way Murray competes.

“I was always a cautious player,” she admits.

“I’m never the type of player who’d run head-first into a collision with someone way bigger than me. I’m injury adverse. I haven’t had many head injuries because of the way I play.

“I’m way more aware now of impacts I would have dismissed before. Sometimes even the smaller impacts or what I think is a small impact can have a consequence for my long-term health.

“I’m just way more aware of it.”

In 2023, New Zealand Rugby moved to reject the link between repeated head injuries and CTE. When asked by the Herald for its current position, NZR said it believes more research is required to ascertain the full understanding of the link between its own sport and the condition.

“NZR acknowledges that there is an association between repeated head impacts and chronic traumatic encephalopathy neuropathologic change (CTE-NC), as identified in the autopsies of contact sport athletes. More rigorous research designs are required, including cohort studies which allow those involved in contact sports to be properly compared with those who have not played.

“NZR is actively contributing to understanding this area more with the largest study of its kind ever undertaken.

“Whilst there is debate about CTE-NC and scientific research associated with it, what can’t be disagreed with is that repeated head impacts are a safety risk in contact sports like rugby. NZR continues to prioritise reducing and mitigating that risk to participants at all levels of the game.

“Player welfare is one of NZR’s major priorities and we are absolutely focused on doing everything we can to keep players as safe as possible from the risks of concussion.

“We believe that we are world-leading in our approach, including providing ongoing care and concern to players through our work with the New Zealand Rugby Players Association, the New Zealand Rugby Foundation, and World Rugby.”

The risk of permanent injury, be it neurological or otherwise, has always been part of sport. But now more than ever, that risk is front and centre.

While it would perhaps be easy within the scientific community to find those willing to draw a line through participation in contact sport at any level, Murray and Sir Richard Faull are different.

Instead, Murray advises minimising risk through later participation in high-contact sport, introducing participation at later ages to allow for the brain to further develop before its placed at risk.

What’s more, the window of opportunity for head knocks to be suffered would also diminish, by reducing the number of years any player is exposed to contact.

However, at no point will exclusion from contact sport, or getting rid of it altogether be put forward by New Zealand’s experts.

“You’ve got to maintain perspective,” she said. “Not everyone who plays a contact sport is going to develop a neurodegenerative condition.

“In fact, the vast majority won’t. Part of the research is trying to figure out why some people do and some people don’t.

“We need to be careful. Diagnosis of dementia or cognitive decline is a life-changing thing, for the person, for their family. We don’t want to get it wrong. That weighs on me a lot.

“We don’t want to incite fear. Sport has so many positive benefits to our lives. I don’t think we should forget that.

“As someone who plays a contact sport, and loves my contact sport, I’d never tell someone that they shouldn’t do something they’re passionate about.

“We just have to look really honestly at the sports we play and ask where there is risk that doesn’t need to be there?

“I’ve thought about this so much. I don’t think I’d ever stop my kids from doing something they’re passionate about.

“I’m not anti-sport at all. There’s risk in everything we do in life, but there is stuff we can do to make it as safe as we can.”

While the CBR continues to make strides in research of the brain and CTE in particular, it is limited in resources.

Funding will always be needed for research, but most significantly, so are brains.

People worried about damage or cognitive change in their loved ones are always welcomed to donate brains.

Anyone who has played contact sport for at least six years with an extended history of head injury in particular is what’s wanted.

However, control brains without any damage are also equally important, as control subjects to compare to those being studied.

That’s not just limited to men either; the rapid growth in the popularity of women’s sport will also see the same issues arise further down the track.

With more research, will come greater understanding. And most importantly for Kiwis, it’s hoped that understanding will pave the way for science to plot the best possible course for treatment and management of a condition that threatens to impact so many lives.

“You don’t have to be a rocket scientist to work out a hit to the head isn’t good for you,” Sir Richard said. “We need to put that into perspective for Aotearoa New Zealand. That’s where we can add to it.

“Ultimately, the outcome we want is to see how much of a problem we really do have. It’s probably going to take 10 years for that.

“But then [we have to] make sure we feed this on in a non-emotional way to influence the future of how we look after ourselves, make sure sport is being played as safely as we can, but not taking the fun out of it.”

Alex Powell is an Online Sports Editor for the NZ Herald . He has been a sports journalist since 2016, and previously worked for both Newshub and 1News.

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Covid Vaccine Side Effects: 4 Takeaways From Our Investigation

Thousands of Americans believe they experienced rare but serious side effects. But confirming a link is a difficult task.

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By Apoorva Mandavilli

Apoorva Mandavilli spent more than a year talking to dozens of experts in vaccine science, policymakers and people who said they had experienced serious side effects after receiving a Covid-19 vaccine.

Soon after their arrival in late December 2020, the Covid-19 vaccines turned the pandemic around and opened a path back to normalcy. They prevented about 14.4 million deaths worldwide, according to one estimate .

In a small percentage of people, they also produced side effects.

Over the course of more than a year, The New York Times talked to 30 people who said they had been harmed by Covid vaccines. Their symptoms may turn out to be unrelated to the shots. But they — along with more than a dozen experts — felt federal officials are not doing enough to investigate their complaints.

All vaccines carry some risk of side effects. More than 270 million Americans received about 677 million doses of the Covid vaccines, and even rare side effects — occurring, say, in just 0.001 percent of patients — might mean thousands of recipients were affected.

Indeed, more than 13,000 have submitted claims to a government fund that compensates people for Covid vaccine injuries. So far, however, only a dozen people have been compensated, nearly all of them for a heart problem caused by the vaccines.

Here are four takeaways from our investigation.

For most people, the benefits of Covid vaccines outweigh any risks.

Even the best vaccines and drugs have some side effects. That does not negate their benefits, nor does it suggest that people should stop taking them.

The rotavirus vaccine, for example, is an unmitigated success, but it can lead to intussusception — a life-threatening condition in which the intestine folds in on itself — in about 0.02 percent of children who are vaccinated.

Some side effects caused by the Covid vaccines may be equally rare. Researchers in Hong Kong analyzed that country’s health records and found that about seven of every million doses of Pfizer-BioNTech vaccine triggered a bout of shingles serious enough to require hospitalization.

Other side effects are slightly more common. The Covid vaccines may lead to myocarditis, or inflammation of the heart, in one of every 10,000 adolescent males. (Myocarditis is one of the four serious side effects acknowledged by federal health officials.)

Deaths from the vaccines are vanishingly rare , despite claims from some conspiracy theorists that vaccines have led to a spike in mortality rates.

More intensive analysis may indicate that in some groups, like young men, the benefit of Covid shots may no longer outweigh the risks. But for the majority of Americans, the vaccines continue to be far safer than contracting Covid itself.

Federal surveillance has found some side effects but may miss others.

To detect problems with vaccines, federal agencies rely on multiple databases. The largest, the Vaccine Adverse Event Reporting System, is useful for generating hypotheses, but contains unverified accounts of harms. Other databases combine electronic health records and insurance claims.

These systems spotted blood-clotting problems associated with the Johnson & Johnson vaccine and a potential risk of stroke after mRNA immunizations, which is still under investigation. But federal researchers trailed Israeli scientists in picking up myocarditis as a problem among young men.

The American health care system is fragmented, with medical records stored by multiple companies that do not collaborate. Electronic health records do not all describe symptoms the same way, making comparisons difficult. Insurance claims databases may have no record of shots administered at mass vaccination sites.

Federal systems may also miss symptoms that defy easy description or diagnosis.

Proving vaccination led to an illness is complicated.

Among the hundreds of millions of Americans who were immunized against Covid, there were deaths, heart attacks, strokes, miscarriages and autoimmune illnesses. How to distinguish illnesses caused by the vaccine from those that would have happened anyway?

The rarer the condition, the harder it is to answer this question.

Merely judging by the timing — the appearance of a particular problem after vaccination — can be misleading. Most famously, childhood vaccines were mistakenly linked to autism because the first noticeable features often coincided with the immunization schedule.

Serious side effects may first turn up in animal studies of vaccines. But few such studies were possible given the nation’s desperate timeline in 2020. Clinical trials of the vaccines were intended to test their effectiveness, but they were far from big enough to detect side effects that may occur only in a few people per million doses.

Most independent studies of side effects have not been large enough to detect rare events, nor to exclude their possibility; others have looked only for a preset list of symptoms and might have missed the rare outliers.

An expert panel convened by the National Academies concluded in April that for most side effects, there was not enough data to accept or reject a link to Covid vaccination.

Understanding the full range of side effects may take years.

Federal health officials acknowledge four major side effects of Covid vaccines — not including the temporary injection site pain, fever and malaise that may accompany the shots.

But in federal databases, thousands of Americans have reported that Covid vaccines caused ringing in the ears, dizziness, brain fog, sharp fluctuations in blood pressure and heart rate, new or relapsed autoimmune conditions , hives , vision problems , kidney disorders, tingling , numbness and a loss of motor skills.

Some studies have examined reports of side effects and largely concluded that there was no link . Closer scrutiny may reveal that many, perhaps most, of the other reported side effects are unrelated to immunization. Most of them are also associated with Covid , and may be the result of undiagnosed infections. But without in-depth studies, it is impossible to be sure, experts said.

Apoorva Mandavilli is a reporter focused on science and global health. She was a part of the team that won the 2021 Pulitzer Prize for Public Service for coverage of the pandemic. More about Apoorva Mandavilli

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Plants can communicate and respond to touch. Does that mean they're intelligent?

Tonya Mosley

"The primary way plants communicate with each other is through a language, so to speak, of chemical gasses," journalist Zoë Schlanger says. Mohd Rasfan/AFP via Getty Images hide caption

"The primary way plants communicate with each other is through a language, so to speak, of chemical gasses," journalist Zoë Schlanger says.

In the 1960s and '70s, a series of questionable experiments claimed to prove that plants could behave like humans, that they had feelings, responded to music and could even take a polygraph test .

Though most of those claims have since been debunked, climate journalist Zoë Schlanger says a new wave of research suggests that plants are indeed "intelligent" in complex ways that challenge our understanding of agency and consciousness.

"Agency is this effect of having ... an active stake in the outcome of your life," Schlanger says. "And when I was looking at plants and speaking to botanists, it became very clear to me that plants have this."

In her new book, The Light Eaters: How the Unseen World of Plant Intelligence Offers a New Understanding of Life on Earth , Schlanger, a staff reporter at The Atlantic, writes about how plants use information from the environment, and from the past, to make "choices" for the future.

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Schlanger notes that some tomato plants, when being eaten by caterpillars, fill their leaves with a chemical that makes them so unappetizing that the caterpillars start eating each other instead. Corn plants have been known to sample the saliva of predator caterpillars — and then use that information to emit a chemical to attract a parasitic wasp that will attack the caterpillar.

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Schlanger acknowledges that our understanding of plants is still developing — as are the definitions of "intelligence" and "consciousness." "Science is there [for] observation and to experiment, but it can't answer questions about this ineffable, squishy concept of intelligence and consciousness," she says.

But, she adds, "part of me feels like it almost doesn't matter, because what we see plants doing — what we now understand they can do — simply brings them into this realm of alert, active processing beings, which is a huge step from how many of us were raised to view them, which is more like ornaments in our world or this decorative backdrop for our our lives."

Interview highlights

On the concept of plant "intelligence"

Intelligence is this thing that's loaded with so much human meaning. It's too muddled up sometimes with academic notions of intelligence. ... Is this even something we want to layer on to plants? And that's something that I hear a lot of plant scientists talk about. They recognize more than anyone that plants are not little humans. They don't want their subjects to be reduced in a way to human tropes or human standards of either of those things.

On the debate over if plants have nervous systems

I was able to go to a lab in Wisconsin where there [were] plants that had ... been engineered to glow, but only to glow when they've been touched. So I used tweezers to pinch a plant on its vein, ... the kind of mid-rib of a leaf. And I got to watch this glowing green signal emanate from the point where I pinch the plant out to the whole rest of the plant. Within two minutes, the whole plant had received a signal of my touch, of my "assault," so to speak, with these tweezers. And research like that is leading people within the plant sciences, but also people who work on neurobiology in people to question whether or not it's time to expand the notion of a nervous system.

On if plants feel pain

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We have nothing at the moment to suggest that plants feel pain, but do they sense being touched, or sense being eaten, and respond with a flurry of defensive chemicals that suggest that they really want to prevent whatever's going on from continuing? Absolutely. So this is where we get into tricky territory. Do we ascribe human concepts like pain ... to a plant, even though it has no brain? And we can't ask it if it feels pain. We have not found pain receptors in a plant. But then again, I mean, the devil's advocate view here is that we only found the mechanoreceptors for pain in humans, like, fairly recently. But we do know plants are receiving inputs all the time. They know when a caterpillar is chewing on them, and they will respond with aggressive defensiveness. They will do wild things to keep that caterpillar from destroying them further.

On how plants communicate with each other

Zoë Schlanger is a staff writer at The Atlantic. Heather Sten/Harper Collins hide caption

Zoë Schlanger is a staff writer at The Atlantic.

The primary way plants communicate with each other is through a language, so to speak, of chemical gasses. ... And there's little pores on plants that are microscopic. And under the microscope, they look like little fish lips. ... And they open to release these gasses. And those gasses contain information. So when a plant is being eaten or knocked over by an animal or hit by wind too hard, it will release an alarm call that other plants in the area can pick up on. And this alarm call can travel pretty long distances, and the plants that receive it will prime their immune systems and their defense systems to be ready for this invasion, for this group of chewing animals before they even arrive. So it's a way of saving themselves, and it makes evolutionary sense. If you're a plant, you don't want to be standing out in a field alone, so to speak. It's not good for reproductive fitness. It's not good for attracting pollinators. It's often in the interest of plants to warn their neighbors of attacks like this.

On plant "memory"

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There's one concept that I think is very beautiful, called the "memory of winter." And that's this thing where many plants, most of our fruit trees, for example, have to have the "memory," so to speak, of a certain number of days of cold in the winter in order to bloom in the spring. It's not enough that the warm weather comes. They have to get this profound cold period as well, which means to some extent they're counting. They're counting the elapsed days of cold and then the elapsed days of warmth to make sure they're also not necessarily emerging in a freak warm spell in February. This does sometimes happen, of course. We hear stories about farmers losing their crops to freak warm spells. But there is evidence to suggest there's parts of plants physiology that helps them record this information. But much like in people, we don't quite know the substrate of that memory. We can't quite locate where or how it's possibly being recorded.

On not anthropomorphizing plants

What's interesting is that scientists and botany journals will do somersaults to avoid using human language for plants. And I totally get why. But when you go meet them in their labs, they are willing to anthropomorphize the heck out of their study subjects. They'll say things like, "Oh, the plants hate when I do that." Or, "They really like this when I do this or they like this treatment." I once heard a scientist talk about, "We're going to go torture the plant again." So they're perfectly willing to do that in private. And the reason for that is not because they're holding some secret about how plants are actually just little humans. It's that they've already resolved that complexity in their mind. They trust themselves to not be reducing their subjects to human, simplistic human tropes. And that's going to be a task for all of us to somehow come to that place.

It's a real challenge for me. So much of what I was learning while doing research for this book was super intangible. You can't see a plant communicating, you can't watch a plant priming its immune system or manipulating an insect. A lot of these things are happening in invisible ways. ... Now when I go into a park, I feel totally surrounded by little aliens. I know that there is immense plant drama happening all over the place around me.

Sam Briger and Susan Nyakundi produced and edited this interview for broadcast. Bridget Bentz and Molly Seavy-Nesper adapted it for the web.