Chronic Traumatic Encephalopathy: Difference between revisions

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== Introduction ==
== Introduction ==
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder caused by repetitive blunt force<ref name=":0">McKee AC, Stein TD, Kiernan PT, Alvarez VE. [https://onlinelibrary.wiley.com/doi/abs/10.1111/bpa.12248 The neuropathology of chronic traumatic encephalopathy.] Brain pathology. 2015 May;25(3):350-64.</ref> and the transfer of acceleration-deceleration forces to the [[Brain Anatomy|brain]]. CTE was originally classified as "punch drunk" syndrome due to its prevalence in boxers. Although [[Traumatic Brain Injury|Brain trauma]] like CTE has been a recognized neurological condition in boxing for almost a century now, its prevalence in other contact sports, such as rugby, hockey and American football has only recently been brought to light<ref>Omalu B, DeKosky S, Minster R, Kamboh M, Hamilton R, Wecht C. Chronic Traumatic Encephalopathy in a National Football League Player. Neurosurgery. 2006;:E1003.</ref>.     
[[File:Boxing fighter.jpeg|thumb|Boxing injury]]
Chronic Traumatic Encephalopathy (CTE) is a progressive, neurodegenerative [[tauopathy]] disorder associated with a history of repetitive brain trauma. It is characterised by the accumulation of tau protein within the brain, which leads to cognitive, behavioural, and physical impairments over time. While the condition was initially recognised in individuals involved in high-contact professions such as professional boxing, it's now understood that CTE can affect a wide range of individuals who've experienced repeated head injuries, including those from other contact sports like football, rugby, and hockey, as well as military personnel and others subject to repeated concussive and sub-concussive blows<ref>Omalu B, DeKosky S, Minster R, Kamboh M, Hamilton R, Wecht C. Chronic Traumatic Encephalopathy in a National Football League Player. Neurosurgery. 2006;:E1003.</ref><ref name=":5">Radiopedia CTE Available: https://radiopaedia.org/articles/chronic-traumatic-encephalopathy?lang=us<nowiki/>(accessed 18.3.2022)</ref>.     


CTE is a neurological disorder that can only be confirmed in a post-mortem Autopsy. However, tracking a patients history of neurological trauma and creating baselines of neurological behaviour can give warning signs of the onset of a neurodegenerative disorder. The strongest predictor of CTE likelihood is the total amount of brain trauma sustained at the sub-concussive and concussive level<ref name=":3">Cantu R, Budson A. [https://www.tandfonline.com/doi/abs/10.1080/14737175.2019.1633916 Management of chronic traumatic encephalopathy.] Expert Review of Neurotherapeutics. 2019 Oct 3;19(10):1015-23.</ref>.    
* CTE is a [[Neurodegenerative Disease|neurodegenerative disorder]] that can only be confirmed in a post-mortem autopsy<ref name=":3">Cantu R, Budson A. [https://www.tandfonline.com/doi/abs/10.1080/14737175.2019.1633916 Management of chronic traumatic encephalopathy.] Expert Review of Neurotherapeutics. 2019 Oct 3;19(10):1015-23.</ref>.
* Unfortunately, there is currently no treatment for CTE. Prevention, therefore, is of great importance.<ref name=":1">Very well health CTE Available: https://www.verywellhealth.com/chronic-traumatic-encephalopathy-2488875<nowiki/>(accessed 18.3.2022)</ref>


== Epidemiology ==
== Epidemiology ==
Annually worldwide an estimated 100-300 per 100,000 people seek medical attention for mild traumatic brain injury (MTBI)<ref>Cassidy JD, Carroll L, Peloso P, Borg J, Von Holst H, Holm L, Kraus J, Coronado V. [https://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.453.3575&rep=rep1&type=pdf Incidence, risk factors and prevention of mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury.] Journal of rehabilitation medicine. 2004 Feb 1;36(0):28-60.</ref>. However, as a large number of people with MTBI may not seek medical attention<ref>Setnik L, Bazarian JJ. [https://www.tandfonline.com/doi/abs/10.1080/02699050601111419 The characteristics of patients who do not seek medical treatment for traumatic brain injury.] Brain injury. 2007 Jan 1;21(1):1-9.</ref>, it is suspected that the global population incidence of MTBI exceeds 600 per 100,000 people annually<ref name=":2">Gardner RC, Yaffe K. [https://www.sciencedirect.com/science/article/pii/S1044743115000305 Epidemiology of mild traumatic brain injury and neurodegenerative disease.] Molecular and Cellular Neuroscience. 2015 May 1;66:75-80.</ref>. If this reserved value is to be taken, then an estimated 42 million people suffer a  MTBI or concussion each year<ref name=":2" />.
[[File:Boxing Championship.jpeg|right|frameless]]
The exact incidence and prevalence of CTE is unknown. Most commonly it is seen in amateur and professional sports players where head contact is common (e.g. boxing, American football, rugby, ice hockey), as well as in military personnel exposed to explosive blasts.<ref name=":5" />  


== Neuropathology ==
== Neuropathology ==
CTE is a tauopathy that results from the culmination of repetitive MTBI<ref name=":2" /> . Postmortem analyses have indicated that the symptoms of CTE are associated with neuropathological changes in the brain such as atrophy of certain brain structures and degeneration of myelinated neurons<ref name=":0" />. Like other [[Neurodegenerative Disease|neurodegenerative]] disorders, CTE is characterized by the accumulation of abnormal tau proteins.   
CTE is a [[tauopathy]] that arises from the accumulation of repetitive mild traumatic brain injuries (MTBI)<ref name=":2">Gardner RC, Yaffe K. [https://www.sciencedirect.com/science/article/pii/S1044743115000305 Epidemiology of mild traumatic brain injury and neurodegenerative disease.] Molecular and Cellular Neuroscience. 2015 May 1;66:75-80.</ref>. Post-mortem analyses have revealed that the symptoms of CTE are associated with neuropathological changes in the brain, such as atrophy of certain brain structures and degeneration of myelinated [[Neurone|neurones]].<ref name=":0">McKee AC, Stein TD, Kiernan PT, Alvarez VE. [https://onlinelibrary.wiley.com/doi/abs/10.1111/bpa.12248 The neuropathology of chronic traumatic encephalopathy.] Brain pathology. 2015 May;25(3):350-64.</ref> Like other [[Neurodegenerative Disease|neurodegenerative]] disorders, CTE is characterised by the accumulation of abnormal tau proteins.   
[[File:Atrophy caused by CTE.png|thumb|600x600px|alt=|none]]


== Symptoms ==
Historically, CTE was first recognised in boxers under the term "[[Dementia Pugilistica]]," also known as "punch-drunk" syndrome. Today, we understand that Dementia Pugilistica can be considered a subtype or precursor to our broader understanding of CTE. It's important to note that CTE encompasses a wider range of potential causes and manifestations, not restricted to professional boxing.<ref name=":5" />
Symptoms of CTE can manifest in any of the four main clinical domains<ref name=":1">Montenigro PH, Baugh CM, Daneshvar DH, Mez J, Budson AE, Au R, Katz DI, Cantu RC, Stern RA. [https://alzres.biomedcentral.com/articles/10.1186/s13195-014-0068-z Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome.] Alzheimer's research & therapy. 2014 Oct;6(5):1-7.</ref>:


* Behavioural:
Other conditions associated with repetitive MTBI and similar neuropathological changes include [[Alzheimer's Disease|Alzheimers]], [[Parkinson's|Parkinsons]], and, in some cases, [[Amyotrophic Lateral Sclerosis (ALS): A Case Study|Amyotrophic Lateral Sclerosis (ALS)]]. Each of these conditions, while distinct in their clinical presentation and progression, share a common thread of neurodegeneration, which is likely influenced by a combination of genetic, environmental, and lifestyle factors.<ref>Gardner RC, Yaffe K. Epidemiology of mild traumatic brain injury and neurodegenerative disease. Molecular and Cellular Neuroscience. 2015 May 1;66:75-80.</ref>
** Verbal or physical violence
** Explosivity
** Loss of control/short fuse
* Cognitive:
** Impairment of memory
** Executive dysfunction
** Reduced attention span
* Mood:
** [[Depression]]
** Helplessness
* Motor:


Motor dysfunction only occurs at later stages of Neurodegeneration and is strongly correlated with age<ref name=":0" />. With Age, CTE is often found to develop into more serious forms of [[Neurological Disorders|neurological disorders]], such as [[Motor Neurone Disease MND|Motor Neurone Disease]], [[Alzheimer's Disease]] and [[Lewy Body Disease]].
== Symptoms ==
{| class="wikitable"
Symptoms have an insidious onset, most often years after the initial injuries, with loss of normal attention, concentration, impaired judgement, aggression, depression and memory loss. This can progress, in some cases in 2-3 years, to include motor symptoms such as impaired gait, impaired, executive function, lack of insight and poor judgment<ref name=":5" />
!Clinical subtypes of chronic traumatic encephalopathy<ref name=":1" />
{| class="wikitable"
!Behavioural features
!Mood features
!Cognitive features
!Motor features
|-
|Explosivity
|Depression
|Dementia
|Ataxia
|-
|Loss of control
|Hopelessness
|Memory impairment
|Dysarthria
|-
|Short fuse
|Suicidality
|Executive dysfunction
|Parkinsonism
|-
|Impulsivity
|Anxiety
|Lack of insight
|Gait Disturbance
|-
|Aggression
|Fearfulness
|Perseveration
|Tremor
|-
|Rage
|Irritability
|Impaired attention and
|Masked facies
|-
|Physical violence
|Labile emotions
|concentration
|Rigidity
|-
|Verbal violence
|Apathy
|Language difficulties
|Muscle weakness
|-
|Inappropriate speech
|Loss of interest
|Dysgraphia
|Spasticity
|-
|Boastfulness
|Fatigue
|Alogia
|Clonus
|}
|}
 
== Clinical Assessment ==
Single incidences of head trauma such as concussion will very rarely result in the development of CTE. However, repeated brain trauma sustained at the sub-concussive and concussive level has been found to be a strong predictor of CTE Development<ref name=":0" />.  
 
CTE is a neurological disorder that can only be confirmed in a post-mortem Autopsy. Therefore, a general consensus on the best way to clinically assess CTE is lacking. however, some have tried to create frameworks from which you can more accurately judge the likelihood of CTE being present. '''When assessing the clinical presentation of CTE, Montenigro et al. (2014)<ref name=":1" /> suggest five criteria:'''


# History of multiple impacts, 2 moderate or severe TBI’s, 4 concussions, or 6 years of sub-concussive trauma (e.g. contact sports, military service, domestic abuse)
* Motor dysfunction only occurs at later stages of Neurodegeneration and is strongly correlated with age<ref name=":0" />.  
# No other neurological disorder (including residual effects from a single TBI or persistent [[Post-concussion Syndrome|post-concussion syndrome]]) that could likely account for any clinical features.
* With Age, CTE is often found to develop into more serious forms of [[Neurological Disorders|neurological disorders]], such as [[Motor Neurone Disease MND|Motor Neurone Disease]], [[Alzheimer's Disease]] and [[Lewy Body Disease]].
# Clinical features must be present for a minimum of 12 months. However, if treatment (for example, ‘antidepressant’ medication) results in an improvement in select symptoms, the clinician should use her or his best judgment to decide whether the symptoms would have persisted or progressed if treatment had not been initiated.
# At least one of the core clinical features must be present and should be considered a change from baseline functioning:
#* Cognitive (defined as 1.5 standard deviation below normal on standardized cognitive neuropsychological test)
#* Behavioral (described as explosive, short fuse, out of control, physical or verbally violent or intermittent explosive disorder
#* Mood (feeling overly sad, depressed, hopeless or diagnosis of major or persistence depressive disorder)
# Two or more supportive features must be present:
## Impulsivity:
##* Impaired impulse control, as demonstrated by new behaviours, such as excessive gambling, increased or unusual sexual activity, substance abuse, excessive shopping or unusual purchases, or similar activities.
## [[Generalized Anxiety Disorder|Anxiety]]:
##* History of anxious mood
##* agitation
##* excessive fears
##* obsessive or compulsive behaviour (or both)
## Apathy:
##* Loss of interest in usual activities
##* loss of motivation and emotions
##* reduction of voluntary, goal-directed behaviours
## [[Paranoia]]:
##* Delusional beliefs of suspicion
##* persecution
##* unwarranted jealousy
## Suicidal thoughts/behaviour:
##* History of suicidal thoughts or attempts
## [[Headache]]:
##* Significant and chronic headache with at least one episode per month for a minimum of 6 months
## Motor signs:
##* [[Dysarthria]]
##* [[Dysgraphia]]
##* [[Bradykinesia]]
##* Tremor
##* [[Rigidity]]
##* [[Gait Disturbances|Gait disturbance]]
## Documented decline:
##* Progressive decline in function and/or a progression in symptoms and/or signs


#
== Diagnosis ==
[[File:Atrophy caused by CTE.png|thumb|600x600px|alt=|Atrophy caused by CTE]]Single incidences of head trauma such as concussion will very rarely result in the development of CTE. However, repeated brain trauma sustained at the sub-concussive and concussive level has been found to be a strong predictor of CTE Development<ref name=":0" />.


=== Assessing severity of MTBI ===
The core diagnostic features present in more than 70% of confirmed CTE cases without comorbidities falls into the three domains: 


'''when assessing the gravity of an MTBI, the Center for Disease control and prevention (CDC) suggests the following procedure<ref>Carroll L, Cassidy JD, Peloso P, Borg J, Von Holst H, Holm L, Paniak C, Pépin M. [http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.473.6862&rep=rep1&type=pdf Prognosis for mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury.] Journal of rehabilitation medicine. 2004 Feb 1;36(0):84-105.</ref>:'''
# Cognitive symptoms include impairments in memory and executive functioning. 
# Behavioral symptoms include verbal and physical violent behavior, explosivity, and impulsivity.
# Mood symptoms often include depression.


# Assess for on or more of the following:
Differentiation of these various manifestations of CTE from other forms of TBI like post-concussive syndrome, remains difficult.<ref>Pierre K, Dyson K, Dagra A, Williams E, Porche K, Lucke-Wold B. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8069746/ Chronic Traumatic Encephalopathy: Update on Current Clinical Diagnosis and Management.] Biomedicines. 2021 Apr;9(4):415.Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8069746/<nowiki/>(accessed 18.3.2022)</ref>
#* Confusion or disorientation
#* loss of consciousness for 30 min or less
#* post traumatic [[amnesia]] for less that 24h
#* and/or other transient neurological abnormalities such as focal signs, [[Epilepsy|seizure]], and intracranial lesion not requiring surgery
# [[Glasgow Coma Scale]] score of 13–15 after 30 min post-injury or later upon presentation for healthcare
# These manifestations of MTBI must not be due to drugs, alcohol, medications, caused by other injuries or treatment for other injuries (e.g., psychological trauma, language barrier or coexisting medical conditions) or caused by penetrating craniocerebral injury).
#


'''<u>[[Glasgow Coma Scale|Glasgow Coma Scale assessment]]</u>'''{{#ev:youtube|v6qpEQxJQO4}}<ref>GCS at 40. Glasgow Coma Scale at 40 | The new approach to Glasgow Coma Scale assessment. Available from: https://youtu.be/v6qpEQxJQO4</ref>
There are several brain findings of CTE on autopsy. Notably, there is accumulation in various areas of the brain of certain proteins eg as tau (distinct from Alzheimer’s disease, which shows beta-amyloid plaques). In addition there is: reduced brain weight; thinning of the [[Corpus Callosum|corpus callosum]]; frequent atrophy of the [[Frontal Lobe|frontal lobes]].  Other affected areas of the brain include the mammillary bodies, [[hippocampus]], and medial [[Temporal Lobe|temporal lobe]], which are involved with [[memory]], as well as the substantia nigra, which is involved with movement.<ref name=":1" />  
 
=== Combination of Assessment Techniques ===
As mentioned previously, the strongest predictor of CTE likelihood is the total amount of brain trauma sustained at the subconcussive and [[Concussion|concussive]] level<ref name=":3" />. It is therefore vital to do frequent and detailed [[Concussion Assessment|concussion assessments]]. Each concussion should be assessed for a number of symptoms, severity of symptoms, and duration of symptoms as can first be remembered. While the number of concussions is relevant, the proximity of concussions – especially within weeks or months and severity as determined by duration of signs and symptoms – is felt to be even more important<ref name=":3" />. Once the quantity and severity of MTBI reaches levels of concern (Montenigro at al. 2014; Criteria 1) the appropriate checks should be made for any additional signs of CTE.  
 
If additional signs do emerge, there are several tests for biomarkers that may help to back up an evaluation. An elevated circulation of total tau protein the [[CSF Cerebrospinal Fluid|spinal fluid]] can indicate some type of brain injury. Although, the presence of tau isn't specific to CTE it can give an indication that symptoms aren't solely due to other factors (post-concussive syndrome or depression).
 
Additionally, the use of Structural brain imaging can look for signs of brain atrophy. Again, this isn't specific to CTE, however, it can indicate at what stage of CTE the patient is at. Only quite advanced stages of CTE would show atrophy in the [[hippocampus]] and the multiple cortical regions of the brain<ref name=":3" />.  
 
Finally, fluorodeoxyglucose (FDG) positron emission tomography (PET) and technetium-99 single photon emission computed tomography (SPECT) scans can detect the reduction in metabolic rates in certain parts of the brain that occurs in CTE patients years before atrophy can be detected<ref name=":3" />.
 
== Differential Diagnosis ==
 
# ''Corticobasal degeneration (CBD) -'' the presence of cerebellar symptoms can help rule out this condition.
# ''[[Frontotemporal Dementia|Frontotemporal dementia]] (FTD) -''  core clinical features and  diagnostic criteria for FTD differ with respect to CTE.
# ''[[Multiple System Atrophy]] (MSA) -''  additional symptoms of dysautonomy and marked cerebellar atrophy, as occurs in MSA, can be used to differentiate from CTE.<ref>Wenning GK, Colosimo C. [https://www.sciencedirect.com/science/article/pii/S0035378710003309 Diagnostic criteria for multiple system atrophy and progressive supranuclear palsy.] Revue neurologique. 2010 Oct 1;166(10):829-33.</ref>
# ''Neurosyphilis -''  this diagnosis can be ruled out by normal VDRL.
# ''[[Vitamin B12 Deficiency|B12]] deficiency -'' this diagnosis was ruled out by normal vitamin B12.
# ''[[Alzheimer’s Disease in a Semi-Professional Pianist: A Case Study|Alzheimer’s]] Disease -''  changes that are not usually involved in this pathology, such as parkinsonism, subcortical and cerebellar manifestations can help rule out this condition.<ref>Caixeta L, Dangoni Filho I, Sousa RD, Soares PP, Mendonça AC. [https://www.scielo.br/j/dn/a/FY8F9bDhBT5Y79DvGVXZwqs/abstract/?lang=en Extending the range of differential diagnosis of chronic traumatic encephalopathy of the boxer: Insights from a case report.] Dementia & Neuropsychologia. 2018 Jan;12:92-6.</ref>


== Management ==
== Management ==
The development of CTE is specific to each patient, therefore, a case by case therapeutic intervention should be applied.  
The development of CTE is specific to each patient, therefore, a case by case therapeutic intervention should be applied.  


=== Exercise ===
* There is no treatment available for CTE once it has developed. As is usually the case, prevention is the best medicine.
* The need for a safe culture in sports and the rest of life is becoming increasingly emphasized.
 
=== Physiotherapy ===
Although the precise mechanisms are not fully understood, exercise (specifically [[Aerobic Exercise|aerobic]] exercise) can increase neurogenesis and [[neuroplasticity]]<ref>Kimhy D, Vakhrusheva J, Bartels MN, Armstrong HF, Ballon JS, Khan S, Chang RW, Hansen MC, Ayanruoh L, Lister A, Castrén E. [https://academic.oup.com/schizophreniabulletin/article-abstract/41/4/859/2338141 The impact of aerobic exercise on brain-derived neurotrophic factor and neurocognition in individuals with schizophrenia: a single-blind, randomized clinical trial]. Schizophrenia bulletin. 2015 Jul 1;41(4):859-68.</ref>. As little as 30 minutes of light to moderate intensity exercise five days a week can greatly slow down the onset of neurological disorder<ref>Müllers P, Taubert M, Müller NG. [https://www.frontiersin.org/articles/10.3389/fphys.2019.00672/full Physical exercise as personalized medicine for dementia prevention?]. Frontiers in Physiology. 2019 May 29;10:672.</ref>.   
Although the precise mechanisms are not fully understood, exercise (specifically [[Aerobic Exercise|aerobic]] exercise) can increase neurogenesis and [[neuroplasticity]]<ref>Kimhy D, Vakhrusheva J, Bartels MN, Armstrong HF, Ballon JS, Khan S, Chang RW, Hansen MC, Ayanruoh L, Lister A, Castrén E. [https://academic.oup.com/schizophreniabulletin/article-abstract/41/4/859/2338141 The impact of aerobic exercise on brain-derived neurotrophic factor and neurocognition in individuals with schizophrenia: a single-blind, randomized clinical trial]. Schizophrenia bulletin. 2015 Jul 1;41(4):859-68.</ref>. As little as 30 minutes of light to moderate intensity exercise five days a week can greatly slow down the onset of neurological disorder<ref>Müllers P, Taubert M, Müller NG. [https://www.frontiersin.org/articles/10.3389/fphys.2019.00672/full Physical exercise as personalized medicine for dementia prevention?]. Frontiers in Physiology. 2019 May 29;10:672.</ref>.   


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=== Cognitive Rehabilitation ===
=== Cognitive Rehabilitation ===
Implementing [[Cognitive Rehabilitation|cognitive rehabilitation]] at the early stages of cognitive impairment has a greater chance of positively effecting the quality of life of the individual as they age<ref name=":3" />. Cognitive rehabilitation can be divided into components: restorative and compensatory<ref name=":4">Shoulson I, Wilhelm EE, Koehler R, editors. [https://books.google.com/books?hl=en&lr=&id=tOueOgVhb0sC&oi=fnd&pg=PR1&dq=Koehler+R,+Wilhelm+E,+Shoulson+I.+&ots=KvoBDEC6ju&sig=AGAyrWbypJhS_GavA2txG1ENc0I Cognitive rehabilitation therapy for traumatic brain injury: evaluating the evidence.] National Academies Press; 2012 Jan 28.</ref>. The restorative approach aims at restoring impaired skills by carrying out repeated exercise of standardized cognitive tests. These tests should aim to increase in difficulty and should target specific cognitive domains appropriate to the patients needs. Compensatory approach teaches ways of bypassing or compensating for the impaired function<ref name=":4" />. [[Assistive Technology: Cognition Products|Assistive technology]], such as prospective memory aids (PMAs) and retrospective memory aids (RMAs) are used in compensatory interventions. these are context-aware aids that make use of artificial intelligence to determine if a particular guidance is necessary or not at the moment, thus help to remember future intentions<ref>Gupta S, Mishra C, Katyayan P, Joshi N. [https://www.researchgate.net/profile/Pragya-Katyayan/publication/325187950_Assistive_Technology_for_Neurological_Disorders/links/5b08f3e1a6fdcc8c25301858/Assistive-Technology-for-Neurological-Disorders.pdf Assistive Technology for Neurological Disorders]. InProceedings of 3rd International Conference on Internet of Things and Connected Technologies (ICIoTCT) 2018 Apr 20 (pp. 26-27).</ref>.  
Implementing [[Cognitive Stimulation Therapy|cognitive rehabilitation]] at the early stages of [[Cognitive Impairments|cognitive impairment]] has a greater chance of positively effecting the quality of life of the individual as they age<ref name=":3" />. Cognitive rehabilitation can be divided into components: restorative and compensatory<ref name=":4">Shoulson I, Wilhelm EE, Koehler R, editors. [https://books.google.com/books?hl=en&lr=&id=tOueOgVhb0sC&oi=fnd&pg=PR1&dq=Koehler+R,+Wilhelm+E,+Shoulson+I.+&ots=KvoBDEC6ju&sig=AGAyrWbypJhS_GavA2txG1ENc0I Cognitive rehabilitation therapy for traumatic brain injury: evaluating the evidence.] National Academies Press; 2012 Jan 28.</ref>. The restorative approach aims at restoring impaired skills by carrying out repeated exercise of standardized cognitive tests. These tests should aim to increase in difficulty and should target specific cognitive domains appropriate to the patients needs. Compensatory approach teaches ways of bypassing or compensating for the impaired function<ref name=":4" />. [[Assistive Technology: Cognition Products|Assistive technology]], such as prospective memory aids (PMAs) and retrospective memory aids (RMAs) are used in compensatory interventions. these are context-aware aids that make use of artificial intelligence to determine if a particular guidance is necessary or not at the moment, thus help to remember future intentions<ref>Gupta S, Mishra C, Katyayan P, Joshi N. [https://www.researchgate.net/profile/Pragya-Katyayan/publication/325187950_Assistive_Technology_for_Neurological_Disorders/links/5b08f3e1a6fdcc8c25301858/Assistive-Technology-for-Neurological-Disorders.pdf Assistive Technology for Neurological Disorders]. InProceedings of 3rd International Conference on Internet of Things and Connected Technologies (ICIoTCT) 2018 Apr 20 (pp. 26-27).</ref>.  


=== Mood/Behaviour therapy ===
=== Mood/Behaviour therapy ===
For patients with prominent mood (depression, hopelessness, and anxiety) and behavioral (explosivity, impulsivity, short fuse) symptoms, psychological therapy/counseling by a clinical psychologist, neuropsychologist, or psychiatrist is recommended<ref name=":3" />.
For patients with prominent mood ([[depression]], hopelessness, and anxiety) and behavioral (explosivity, impulsivity, short fuse) symptoms, psychological therapy/counseling by a clinical psychologist, neuropsychologist, or psychiatrist is recommended<ref name=":3" />.


== References  ==
== References  ==

Latest revision as of 19:17, 27 June 2023

Original Editor - Gareth Geoffreys

Top Contributors - Gareth Geoffreys, Lucinda hampton, Kim Jackson, Rucha Gadgil, Aminat Abolade and Carina Therese Magtibay  

Introduction[edit | edit source]

Boxing injury

Chronic Traumatic Encephalopathy (CTE) is a progressive, neurodegenerative tauopathy disorder associated with a history of repetitive brain trauma. It is characterised by the accumulation of tau protein within the brain, which leads to cognitive, behavioural, and physical impairments over time. While the condition was initially recognised in individuals involved in high-contact professions such as professional boxing, it's now understood that CTE can affect a wide range of individuals who've experienced repeated head injuries, including those from other contact sports like football, rugby, and hockey, as well as military personnel and others subject to repeated concussive and sub-concussive blows[1][2].

  • CTE is a neurodegenerative disorder that can only be confirmed in a post-mortem autopsy[3].
  • Unfortunately, there is currently no treatment for CTE. Prevention, therefore, is of great importance.[4]

Epidemiology[edit | edit source]

Boxing Championship.jpeg

The exact incidence and prevalence of CTE is unknown. Most commonly it is seen in amateur and professional sports players where head contact is common (e.g. boxing, American football, rugby, ice hockey), as well as in military personnel exposed to explosive blasts.[2]

Neuropathology[edit | edit source]

CTE is a tauopathy that arises from the accumulation of repetitive mild traumatic brain injuries (MTBI)[5]. Post-mortem analyses have revealed that the symptoms of CTE are associated with neuropathological changes in the brain, such as atrophy of certain brain structures and degeneration of myelinated neurones.[6] Like other neurodegenerative disorders, CTE is characterised by the accumulation of abnormal tau proteins.

Historically, CTE was first recognised in boxers under the term "Dementia Pugilistica," also known as "punch-drunk" syndrome. Today, we understand that Dementia Pugilistica can be considered a subtype or precursor to our broader understanding of CTE. It's important to note that CTE encompasses a wider range of potential causes and manifestations, not restricted to professional boxing.[2]

Other conditions associated with repetitive MTBI and similar neuropathological changes include Alzheimers, Parkinsons, and, in some cases, Amyotrophic Lateral Sclerosis (ALS). Each of these conditions, while distinct in their clinical presentation and progression, share a common thread of neurodegeneration, which is likely influenced by a combination of genetic, environmental, and lifestyle factors.[7]

Symptoms[edit | edit source]

Symptoms have an insidious onset, most often years after the initial injuries, with loss of normal attention, concentration, impaired judgement, aggression, depression and memory loss. This can progress, in some cases in 2-3 years, to include motor symptoms such as impaired gait, impaired, executive function, lack of insight and poor judgment[2]

Diagnosis[edit | edit source]

Atrophy caused by CTE

Single incidences of head trauma such as concussion will very rarely result in the development of CTE. However, repeated brain trauma sustained at the sub-concussive and concussive level has been found to be a strong predictor of CTE Development[6].

The core diagnostic features present in more than 70% of confirmed CTE cases without comorbidities falls into the three domains:

  1. Cognitive symptoms include impairments in memory and executive functioning.
  2. Behavioral symptoms include verbal and physical violent behavior, explosivity, and impulsivity.
  3. Mood symptoms often include depression.

Differentiation of these various manifestations of CTE from other forms of TBI like post-concussive syndrome, remains difficult.[8]

There are several brain findings of CTE on autopsy. Notably, there is accumulation in various areas of the brain of certain proteins eg as tau (distinct from Alzheimer’s disease, which shows beta-amyloid plaques). In addition there is: reduced brain weight; thinning of the corpus callosum; frequent atrophy of the frontal lobes. Other affected areas of the brain include the mammillary bodies, hippocampus, and medial temporal lobe, which are involved with memory, as well as the substantia nigra, which is involved with movement.[4]

Management[edit | edit source]

The development of CTE is specific to each patient, therefore, a case by case therapeutic intervention should be applied.

  • There is no treatment available for CTE once it has developed. As is usually the case, prevention is the best medicine.
  • The need for a safe culture in sports and the rest of life is becoming increasingly emphasized.

Physiotherapy[edit | edit source]

Although the precise mechanisms are not fully understood, exercise (specifically aerobic exercise) can increase neurogenesis and neuroplasticity[9]. As little as 30 minutes of light to moderate intensity exercise five days a week can greatly slow down the onset of neurological disorder[10].

More information regarding the role exercise has in the regulation of neurological conditions can be found here.

Cognitive Rehabilitation[edit | edit source]

Implementing cognitive rehabilitation at the early stages of cognitive impairment has a greater chance of positively effecting the quality of life of the individual as they age[3]. Cognitive rehabilitation can be divided into components: restorative and compensatory[11]. The restorative approach aims at restoring impaired skills by carrying out repeated exercise of standardized cognitive tests. These tests should aim to increase in difficulty and should target specific cognitive domains appropriate to the patients needs. Compensatory approach teaches ways of bypassing or compensating for the impaired function[11]. Assistive technology, such as prospective memory aids (PMAs) and retrospective memory aids (RMAs) are used in compensatory interventions. these are context-aware aids that make use of artificial intelligence to determine if a particular guidance is necessary or not at the moment, thus help to remember future intentions[12].

Mood/Behaviour therapy[edit | edit source]

For patients with prominent mood (depression, hopelessness, and anxiety) and behavioral (explosivity, impulsivity, short fuse) symptoms, psychological therapy/counseling by a clinical psychologist, neuropsychologist, or psychiatrist is recommended[3].

References[edit | edit source]

  1. ↑ Omalu B, DeKosky S, Minster R, Kamboh M, Hamilton R, Wecht C. Chronic Traumatic Encephalopathy in a National Football League Player. Neurosurgery. 2006;:E1003.
  2. ↑ 2.0 2.1 2.2 2.3 Radiopedia CTE Available: https://radiopaedia.org/articles/chronic-traumatic-encephalopathy?lang=us(accessed 18.3.2022)
  3. ↑ 3.0 3.1 3.2 Cantu R, Budson A. Management of chronic traumatic encephalopathy. Expert Review of Neurotherapeutics. 2019 Oct 3;19(10):1015-23.
  4. ↑ 4.0 4.1 Very well health CTE Available: https://www.verywellhealth.com/chronic-traumatic-encephalopathy-2488875(accessed 18.3.2022)
  5. ↑ Gardner RC, Yaffe K. Epidemiology of mild traumatic brain injury and neurodegenerative disease. Molecular and Cellular Neuroscience. 2015 May 1;66:75-80.
  6. ↑ 6.0 6.1 6.2 McKee AC, Stein TD, Kiernan PT, Alvarez VE. The neuropathology of chronic traumatic encephalopathy. Brain pathology. 2015 May;25(3):350-64.
  7. ↑ Gardner RC, Yaffe K. Epidemiology of mild traumatic brain injury and neurodegenerative disease. Molecular and Cellular Neuroscience. 2015 May 1;66:75-80.
  8. ↑ Pierre K, Dyson K, Dagra A, Williams E, Porche K, Lucke-Wold B. Chronic Traumatic Encephalopathy: Update on Current Clinical Diagnosis and Management. Biomedicines. 2021 Apr;9(4):415.Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8069746/(accessed 18.3.2022)
  9. ↑ Kimhy D, Vakhrusheva J, Bartels MN, Armstrong HF, Ballon JS, Khan S, Chang RW, Hansen MC, Ayanruoh L, Lister A, Castrén E. The impact of aerobic exercise on brain-derived neurotrophic factor and neurocognition in individuals with schizophrenia: a single-blind, randomized clinical trial. Schizophrenia bulletin. 2015 Jul 1;41(4):859-68.
  10. ↑ Müllers P, Taubert M, Müller NG. Physical exercise as personalized medicine for dementia prevention?. Frontiers in Physiology. 2019 May 29;10:672.
  11. ↑ 11.0 11.1 Shoulson I, Wilhelm EE, Koehler R, editors. Cognitive rehabilitation therapy for traumatic brain injury: evaluating the evidence. National Academies Press; 2012 Jan 28.
  12. ↑ Gupta S, Mishra C, Katyayan P, Joshi N. Assistive Technology for Neurological Disorders. InProceedings of 3rd International Conference on Internet of Things and Connected Technologies (ICIoTCT) 2018 Apr 20 (pp. 26-27).
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