Concussion and physiotherapy

A bunch of balls smashing into each other.

Concussion and physiotherapy

A bunch of balls smashing into each other.

Sport-related concussion is a widely publicised and hotly debated topic. Mainstream and social media carry news reports of high-profile athletes sustaining concussion and the commentary surrounding the incidents.

While this has highlighted the issue and the need to be vigilant, the stories don’t often provide the full scope of different aspects of concussion recognition, management and long-term consequences.

These questions often fall to primary healthcare practitioners, including physiotherapists.

Physiotherapists are frequently a port of call for information about concussion.

This may be in hospitals, private practices or on the sidelines at sporting events—and physiotherapists need to be able to answer the questions from concerned stakeholders.

In this series of articles, concussion researchers and physiotherapists Prashant Jhala, Shreya McLeod and Byron Field discuss some of the aspects of the concussion debate.

These articles provide research-informed perspectives on some of the many issues surrounding sport- related concussions. This field of research is constantly growing, and
physiotherapists should stay informed about the ongoing discussions.

In October this year, the 6th International Consensus Conference on Concussion in Sport was held. Several reviews were conducted to inform the discussion, providing up-to-date evidence that will form part of the consensus statement due in 2023.

Long-term impacts of concussion

Sport-related concussion (SRC) has been a hot topic for decades. The most significant question debated in peer-reviewed literature and the media is around the long-term consequences of repetitive SRCs and subconcussive head acceleration events.

News articles often deliver selective interpretations of the research, particularly following the early retirements of players from the AFL (eg, Brad Sheppard in 2021 and Jack Frost in 2018) and the premature deaths of several Australian contact sport athletes (eg, AFL player Shane Tuck in 2020 and NRL player Paul Green in 2022).

The increasing media attention has improved public awareness of concussion but has caused much confusion and concern.

Following the release of several international consensus statements, all major sporting codes in Australia have released SRC guidelines; however, these vary substantially (Gunasakeran et al 2019, du Preez et al 2022).

As primary healthcare professionals who are commonly present at sporting events in amateur and professional settings, physiotherapists are often quizzed on their knowledge about the media speculation involving concussion and long-term consequences.

In this article, we aim to identify some of the main issues debated in the literature. We will highlight some key questions in the debate surrounding concussion and long-term neurological consequences and provide a brief historical overview to illuminate aspects of the debate.

Autopsy findings versus clinical presentations

Repetitive head trauma has been linked most commonly to neuropathological changes identified in autopsied brains and known as chronic traumatic encephalopathy (CTE-NC).

The most recent consensus statement has characterised the autopsy features of CTE-NC as accumulation of phosphorylated tau depositions in neurons at the depth of the cortical sulcus (Bieniek et al 2021).

Much of the debate has surrounded whether these autopsy findings have a clinical presentation that is the result of this neuropathological change.

In 2014, Montenigro et al (2014) proposed the new term ‘traumatic encephalopathy syndrome’ (TES) for the cluster of potential clinical features that may be attributed to autopsy features of CTE-NC. The authors recommended that the term TES should be used in vivo, as opposed to CTE (referred to as CTE-NC in this article).

As we will discuss, CTE-NC has been seen in a variety of populations. The key questions that are being debated include:

1.    Do repetitive head acceleration events (concussive or subconcussive) result in long-term neuropathological changes in the brain?
2.    If so, what is the clinical manifestation of the changes found during autopsy?

The debate about CTE-NC has been split between two opposing views (LoBue et al 2020)—either it is a specific and progressive degenerative neuropathological disease with neurobehavioral features or it is a neuropathological condition unrelated to a clinical syndrome or degenerative process.

History of long-term neuropathological change post-mortem

The history of sport-related neurological pathology extends back to the early twentieth century.

Martland initially noted disturbances in neurological functioning, including gait dysfunction, dysarthria, tremors and cognitive impairments (Martland 1928, Iverson et al 2015), in a
series of professional boxers.

In the 1930s, a neuropsychiatric syndrome characterised by obvious neurological and neurobehavioral problems was termed ‘traumatic encephalopathy’ and ‘dementia pugilistica’ and in 1949,

Critchley coined the term ‘chronic traumatic encephalopathy’ (Parker 1934, Millspaugh 1937, Critchley 1949).

In 1969, Roberts analysed a sample of 224 retired professional boxers in England whose careers spanned from 1929 to 1955 and found 17 per cent had a form of the syndrome ‘chronic traumatic encephalopathy’ (Roberts 1969).

In 1973, Corsellis et al described a variable clinical syndrome in 15 boxers, each of whom had more than 300 fights under their belt. The presentation of these athletes included features ranging from mild clumsiness to memory issues and dysarthria.

Following the description of the microscopic neuropathological changes found on autopsy, the authors concluded that the clinical presentations of the boxers’ symptoms may have been attributed to the novel pattern of cerebral damage they described (Corsellis et al 1973).

In 1990, Roberts et al re-examined the 15 brains from the Corsellis study and found extensive beta-amyloid deposition, similar to that seen in Alzheimer’s disease (Roberts et al 1990a, 1990b).

An early review of chronic traumatic brain injury (TBI) found that clinical presentations varied widely and it was unclear whether there was fixed neurological injury that was made worse by the aging process or if this was a progressive neurodegenerative disease (Jordan 2000).

In 2005, Omalu et al published the first description of CTE-NC in a retired NFL athlete and subsequent findings in a further 16 cases (Omalu et al 2005, Omalu et al 2006, Omalu et al 2010, Omalu et al 2011).

A large case series of 68 patients against 17 controls was published in 2011 (Mckee et al 2011).

Of the 61 subjects who were only athletes (eg, no background in other activities such as military service), 14 demonstrated other pathologies such as Lewy bodies, frontotemporal lobar degeneration, Parkinson’s disease or Alzheimer’s disease and 15 had nosigns of CTE-NC (Mckee et al 2011).

Out of the 68 cases, 43 cases had pathology described to be consistent with CTE-NC (according to the definition at the time), without other coexisting pathology.

A review in 2014 identified 158 cases of CTE-NC in the literature (Gardner et al 2014).

In the review the authors found that of the 85 cases only performed on athletes, 20 per cent demonstrated CTE-NC without any other neuropathology and 23.5 per cent demonstrated no other neuropathology at all.

However, of the remaining cases, 51.8 per cent demonstrated CTE-NC along with other neuropathology and 4.7 per cent demonstrated neuropathology without CTE-NC (Gardner et al 2014).

Since 2015, there has been a substantial increase in published cases and population-based studies investigating CTE-NC post-mortem, including several large case series.

Binniek et al (2015) investigated the brains of 66 men with a history of contact sport and found that 45 (68 per cent) had no signs of CTE-NC and 21 (32 per cent) had cortical tau deposition consistent with CTE-NC (according to the definition at the time).

Out of the 198 control subjects, no brains demonstrated CTE-NC pathology, including 33 controls with documented head trauma (Binniek et al 2015).

In a large post-mortem histopathology case series of 532 consecutive from the general population, Postupna et al (2021) found only 0.3 per cent of the cohort demonstrated pure CTE-NC.

In the subset of patients with a history of TBI, they found increased levels of phosphorylated tau depositions.

In the largest study to date, McCann et al (2022) investigated 636 consecutive post-mortem patients for the presence of CTE-NC, finding that only five (0.79 per cent) among the population studied demonstrated CTE-NC, three of whom had a history of TBI.

Several studies have found links between repetitive head injury and other pathologies, both in the presence and absence of CTE-NC, including Lewy body pathology (Adams et al 2018), cerebral amyloid angiopathy (Standring et al 2019) and progressive supranulear palsy (Ling et al 2015).

The clinical history of many of the subjects in the above studies is either unknown, derived from medical records or, most commonly, based on the recollections of family members post-mortem.

This makes linking CTE-NC findings to a specific set of clinical features challenging.

Prashant Jhala.

Furthermore, research has suffered from many methodological shortcomings and has been heavily reliant on descriptive observations rather than the statistical analysis required for scientific validation (Brett et al 2019, LoBue et al 2020).

As demonstrated, the autopsy research has potentially over-represented pure CTE-NC diagnosed only post-mortem, in the presence of other well-documented neuropathology (Iverson et al 2020, LoBue et al 2020).

Without a process to differentiate the exposure of cases to head acceleration events (concussive or subconcussive), it is difficult to determine if such events definitely led to neuropathological changes in the brain.

Additionally, without prospectively collected clinical histories and serial neurological and neuropsychological evaluation, it is difficult to know if there is a clinical syndrome linked to either SRC or CTE-NC.

The emergence of TES

In addition to the definitions of TES outlined by Montenigro et al (2014), a further four sets of clinical criteria have been published to distinguish ‘possible’ or ‘probable’ TES.

Each set of criteria has included broad clusters of symptoms (eg, cognitive impairment, behavioural or mood symptoms, motor dysfunction, physical neurological symptoms and suicidality), combinations of which meet the diagnostic criteria for TES, in the absence of other medical or psychiatric conditions (LoBue et al 2022).

Each set of clinical criteria has been based on retrospective recollections of patients’ kin rather than longitudinal clinical data (LoBue et al 2022).

The attempts to refine the diagnostic criteria have been the result of criticism that the initially proposed criteria were extremely broad (Iverson et al 2015), having demonstrated extremely high sensitivity (>97 per cent), but very low specificity (<25 per cent) (Metz et al 2021).

Previous studies have demonstrated that substantial numbers of the general population with other diagnosed disorders met the first consensus diagnostic criteria for TES, including depression, chronic pain and people who have experienced suicidality andanger control problems (Iverson and Gardner 2019, 2020, 2021, Iverson et al 2020).

In 2021, the latest set of diagnostic criteria for TES was determined by a panel on behalf of the American National Institute of Neurological Disorders and Stroke and the American National Institute of Biomedical Imaging and Bioengineering (Katz et al 2021).

Four key criteria were identified for diagnosis:

•    substantial repetitive head trauma
•    clinical features of cognitive impairment and/or neurobehavioural dysregulation
•    [the] progress course of the disease
•    [the fact that it is] unexplained by any other neurological, psychiatric or medical conditions (Katz et al 2021, Cullum et al 2021).

The panel did state that the criteria for TES are meant ‘primarily for research purposes and should be used cautiously in clinical settings [avoiding] the equivalence with the
diagnosis of CTE’, referred to as CTE- NC in this article (Katz et al 2021).

Even though the new definition has removed previous criteria that may have contributed to the low specificity, the new criteria pose several challenges to researchers, clinicians
and stakeholders in the public health debate.

The panel defined TES based on its link with CTE-NC, assuming there was a specific set of physical signs and symptoms associated with the condition (Katz et al 2021).

This has not been determined and asymptomatic individuals or individuals with no known history of head trauma have been identified with CTE-NC on autopsy (Iverson et al 2020, McCann et al 2022, Harmon et al 2018).

Additionally, even with more specific criteria, features used for diagnosis are still vague and it is conceivable they will overlap with other pathology, as was the case for previously published TES diagnostic criteria.

Directions and considerations for physiotherapists

Research investigating TBI and long-term neuropathology is still in the very early stages and there are more questions than conclusions that can be drawn.

While concussions have been identified as a risk factor for future post-mortem neuropathology, there is no accepted understanding of how this manifests clinically (Harmon et al 2018). And our understanding of how much exposure from TBI or the minimum threshold for repetitive head impacts is also not yet known.

Although subconcussive blows have also been researched, recent reviews have shown minimal or inconclusive clinical and physiological changes following exposure (Tayebi et al 2021, Joyce et al 2022, Walter et al 2022).

Consequently, exposure rates that result in either clinical features or post-mortem CTE-NC are widely unknown.

The development of CTE-NC and any clinically related symptoms may be related to duration of playing career, number of exposures, recovery from exposures, underlying genetic factors, lifestyle behaviours (eg, drug and alcohol abuse), general health, psychiatric disease and several other factors (Harmon et al 2017).

It is important to note the impact of historical practices on pathological findings.

The mean age at death of individuals in the largest case series ranges from the mid 60s to early 80s, which implies that the peak sporting exposure would have occurred approximately 30–50 years prior to death.

As recently as the late 1990s, athletes were allowed to return to play on the same day if their symptoms had resolved (American Academy of Neurology 1997).

Therefore, the true effect of updated recognition and recovery management protocols is yet to be fully realised. It will be some years before the impact of this practice change is fully understood.

Large, well-designed prospective control studies are needed to investigate the impact of different injury exposures over a sporting career and then to understand the histopathological changes following death.

Physiotherapists will often be asked for their advice about reducing exposure, changing sports or the possible long-term consequences of sustaining one or more concussions.

The simple answer right now is that we don’t have enough scientific evidence to make any definitive conclusions.

Given this, perhaps a cautionary approach is advisable while the research progressively evolves.

Physiotherapists should continue to encourage physical activity, make individualised judgements about patient risk based on their risk factors and work with medical teams and other healthcare professionals on a case-by-case basis.

>> Prashant Jhala is an APA Sports and Exercise Physiotherapist, a senior lecturer in the Faculty of Medicine and Health at the University of New South Wales, a consultant physiotherapist in private practice and a PhD candidate at the University of Newcastle. 


1.    Adams JW, Alvarez VE, Mez J, et al. Lewy body pathology and chronic traumatic encephalopathy associated with contact sports. Journal of Neuropathology & Experimental Neurology. 2018;77(9):757-768. 
2.    Bieniek KF, Cairns NJ, Crary JF, et al. The second NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy. Journal of Neuropathology & Experimental Neurology. 2021;80(3):210-219. 
3.    Bieniek KF, Ross OA, Cormier KA, et al. Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank. Acta neuropathologica. 2015;130(6):877-889. 
4.    Brett BL, Wilmoth K, Cummings P, Solomon GS, McCrea MA, Zuckerman SL. The neuropathological and clinical diagnostic criteria of chronic traumatic encephalopathy: a critical examination in relation to other neurodegenerative diseases. Journal of Alzheimer's disease. 2019;68(2):591-608. 
5.    Corsellis J, Bruton C, Freeman-Browne D. The aftermath of boxing1. Psychological medicine. 1973;3(3):270-303. 
6.    Critchley M. Punch-drunk syndromes: the chronic traumatic encephalopathy of boxers. Hommage a Clovis Vincent. 1949:131-141. 
7.    Cullum CM, LoBue C. Defining traumatic encephalopathy syndrome—advances and challenges. Nature Reviews Neurology. 2021;17(6):331-332. 
8.    du Preez J, Jhala P, Lystad RP. Availability and content of concussion guidelines in Australian combat sports. Journal of science and medicine in sport. 2022;25(10):800-804. 
9.    Gunasekaran P, Hodge C, Pearce A, King D, Fraser C. A review of concussion diagnosis and management in Australian professional sporting codes. The Physician and sportsmedicine. 2020;48(1):1-7. 
10.    Harmon KG, Clugston JR, Dec K, et al. American Medical Society for Sports Medicine position statement on concussion in sport. British journal of sports medicine. 2019;53(4):213-225. 
11.    Iverson GL, Gardner AJ. Risk for misdiagnosing chronic traumatic encephalopathy in men with anger control problems. Frontiers in neurology. 2020;11:739. 
12.    Iverson GL, Gardner AJ. Risk of misdiagnosing chronic traumatic encephalopathy in men with depression. The Journal of neuropsychiatry and clinical neurosciences. 2020;32(2):139-146. 
13.    Iverson GL, Gardner AJ, McCrory P, Zafonte R, Castellani RJ. A critical review of chronic traumatic encephalopathy. Neuroscience & Biobehavioral Reviews. 2015;56:276-293. 
14.    Iverson GL, Keene CD, Perry G, Castellani RJ. The need to separate chronic traumatic encephalopathy neuropathology from clinical features. Journal of Alzheimer's disease. 2018;61(1):17-28. 
15.    Iverson GL, Merz ZC, Terry DP. Examining the research criteria for traumatic encephalopathy syndrome in middle-aged men from the general population who played contact sports in high school. Frontiers in neurology. 2021;12:632618. 
16.    Iverson GL, Terry DP, Luz M, et al. Anger and depression in middle-aged men: implications for a clinical diagnosis of chronic traumatic encephalopathy. The Journal of neuropsychiatry and clinical neurosciences. 2019;31(4):328-336. 
17.    Jordan BD. Chronic traumatic brain injury associated with boxing. Copyright© 2000 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New …; 2000:179-186.
18.    Joyce JM, La PL, Walker R, Harris AD. Magnetic Resonance Spectroscopy of Traumatic Brain Injury and Subconcussive Hits: A Systematic Review and Meta–Analysis. Journal of Neurotrauma. 2022;39(21-22):1455-1476. 
19.    Katz DI, Bernick C, Dodick DW, et al. National Institute of Neurological Disorders and Stroke consensus diagnostic criteria for traumatic encephalopathy syndrome. Neurology. 2021;96(18):848-863. 
20.    Ling H, Holton JL, Shaw K, Davey K, Lashley T, Revesz T. Histological evidence of chronic traumatic encephalopathy in a large series of neurodegenerative diseases. Acta neuropathologica. 2015;130(6):891-893. 
21.    LoBue C, Cullum CM, Hart Jr J. Examination of the Proposed Criteria for Traumatic Encephalopathy Syndrome: Case Report of a Former Professional Football Player. The Journal of Neuropsychiatry and Clinical Neurosciences. 2022:appi. neuropsych. 21090225. 
22.    LoBue C, Schaffert J, Cullum CM. Chronic traumatic encephalopathy: understanding the facts and debate. Current opinion in psychiatry. 2020;33(2):130-135. 
23.    Martland HS. Punch drunk. Journal of the American Medical Association. 1928;91(15):1103-1107. 
24.    McCann H, Bahar AY, Burkhardt K, et al. Prevalence of chronic traumatic encephalopathy in the Sydney Brain Bank. Brain Communications. 2022;4(4):fcac189. 
25.    McKee AC, Stein TD, Nowinski CJ, et al. The spectrum of disease in chronic traumatic encephalopathy. Brain. 2013;136(1):43-64. 
26.    Mez J, Alosco ML, Daneshvar DH, et al. Validity of the 2014 traumatic encephalopathy syndrome criteria for CTE pathology. Alzheimer's & Dementia. 2021;17(10):1709-1724. 
27.    Mez J, Alosco ML, Daneshvar DH, et al. Validity of the 2014 traumatic encephalopathy syndrome criteria for CTE pathology. Alzheimer's & Dementia. 2021;17(10):1709-1724. 
28.    Millspaugh J. Dementia pugilistica. US Naval Med Bull. 1937;35(297):e303. 
29.    Montenigro PH, Baugh CM, Daneshvar DH, et al. Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome. Alzheimer's research & therapy. 2014;6(5):1-17. 
30.    Neurology AAo. Practice parameter: The management of concussion in sports (summary statement): Report of the Standards Subcommittee. Neurology. 1997;48:581-585. 
31.    Omalu B, Bailes J, Hamilton RL, et al. Emerging histomorphologic phenotypes of chronic traumatic encephalopathy in American athletes. Neurosurgery. 2011;69(1):173-183. 
32.    Omalu BI, DeKosky ST, Hamilton RL, et al. Chronic traumatic encephalopathy in a national football league player: part II. Neurosurgery. 2006;59(5):1086-1093. 
33.    Omalu BI, DeKosky ST, Minster RL, Kamboh MI, Hamilton RL, Wecht CH. Chronic traumatic encephalopathy in a National Football League player. Neurosurgery. 2005;57(1):128-134. 
34.    Omalu BI, Hamilton RL, Kamboh MI, DeKosky ST, Bailes J. Chronic traumatic encephalopathy (CTE) in a National Football League Player: Case report and emerging medicolegal practice questions. Journal of forensic nursing. 2010;6(1):40-46. 
35.    Parker HL. Traumatic encephalopathy (punch drunk') of professional pugilists. Journal of Neurology and Psychopathology. 1934;15(57):20. 
36.    Postupna N, Rose SE, Gibbons LE, et al. The delayed neuropathological consequences of traumatic brain injury in a community-based sample. Frontiers in neurology. 2021;12:624696. 
37.    Roberts AH. Brain damage in boxers: a study of the prevalence of traumatic encephalopathy among ex-professional boxers. Pitman Medical & Scientific Publishing Company, Limited; 1969.
38.    Roberts G, Whitwell H, Acland PR, Bruton C. Dementia in a punch-drunk wife. The Lancet. 1990;335(8694):918-919. 
39.    Roberts GW, Allsop D, Bruton C. The occult aftermath of boxing. Journal of Neurology, Neurosurgery & Psychiatry. 1990;53(5):373-378. 
40.    Standring OJ, Friedberg J, Tripodis Y, et al. Contact sport participation and chronic traumatic encephalopathy are associated with altered severity and distribution of cerebral amyloid angiopathy. Acta neuropathologica. 2019;138(3):401-413. 
41.    Tayebi M, Holdsworth SJ, Champagne AA, et al. The role of diffusion tensor imaging in characterizing injury patterns on athletes with concussion and subconcussive injury: a systematic review. Brain injury. 2021;35(6):621-644. 
42.    Walter AE, Wilkes JR, Arnett PA, et al. The accumulation of subconcussive impacts on cognitive, imaging, and biomarker outcomes in child and college-aged athletes: a systematic review. Brain imaging and behavior. 2021:1-15. 




© Copyright 2023 by Australian Physiotherapy Association. All rights reserved.