Chronic traumatic encephalopathy

This article or area is currently under construction and may only be partially complete. Please come back soon to see the finished work! (26/11/2021)

Original Editor - Gareth Geoffreys

Top Contributors - Gareth Geoffreys  

Introduction[edit | edit source]

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder caused by repetitive blunt force[1] and the transfer of acceleration-deceleration forces to the brain. CTE was originally classified as "punch drunk" syndrome due to its prevalence in boxers. Although 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[2].

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 subconcussive and concussive level[3].

Epidimiology[edit | edit source]

Annually worldwide an estimated 100-300 per 100,000 people seek medical attention for mild traumatic brain injury (MTBI)[4]. However, as a large number of people with MTBI may not seek medical attention[5], it is suspected that the global population incidence of MTBI exceeds 600 per 100,000 people annually[6]. If this reserved value is to be taken, then an estimated 42 million people suffer a MTBI or concussion each year[6].

Neuropathology[edit | edit source]

CTE is a tauopathy that results from the culmination of repetitive MTBI[6] . 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[1]. Like other neurodegenerative disorders, CTE is characterized by the accumulation of abnormal tau proteins.

Symptoms[edit | edit source]

Symptoms of CTE can manifest in any of the four main clinical domains[7]:

  • Behavioural:
    • 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[1]. With Age CTE is often found to develope into more serious forms of neurological disorders, such as Motor Neurone Disease, Alzheimer's Disease and Lewy Body Disease.

Clinical subtypes of chronic traumatic encephalopathy[7]
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[edit | edit source]

Single incidences of head trauma such as concussion will very rarely result in the development of CTE. However, repeated brain trauma sustained at the subconcussive and concussive level has been found to be a strong predictor of CTE Development[1].

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)[7] suggest five criteria:

  1. 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)
  2. No other neurological disorder (including residual effects from a single TBI or persistent post-concussion syndrome) that could likely account for any clinical features.
  3. 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.
  4. 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)
  5. Two or more supportive features must be present:
    1. 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.
    2. Anxiety:
      • History of anxious mood
      • agitation
      • excessive fears
      • obsessive or compulsive behaviour (or both)
    3. Apathy:
      • Loss of interest in usual activities
      • loss of motivation and emotions
      • reduction of voluntary, goal-directed behaviours
    4. Paranoia:
      • Delusional beliefs of suspicion
      • persecution
      • unwarranted jealousy
    5. Suicidal thoughts/behaviour:
      • History of suicidal thoughts or attempts
    6. Headache:
      • Significant and chronic headache with at least one episode per month for a minimum of 6 months
    7. Motor signs:
      • Dysarthria
      • Dysgraphia
      • Bradykinesia
      • Tremor
      • Rigidity
      • Gait disturbance
    8. Documented decline:
      • Progressive decline in function and/or a progression in symptoms and/or signs
Assessing severity of MTBI[edit | edit source]

when assessing the gravity of an MTBI, the Centers for Disease control and prevention (CDC) suggests the following procedure[8]:

  1. Assess for on or more of the following:
    • 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, seizure, and intracranial lesion not requiring surgery
  2. Glasgow Coma Scale score of 13–15 after 30 min post-injury or later upon presentation for healthcare
  3. 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).

Glasgow Coma Scale assessment


Combination of assessment techniques:[edit | edit source]

As mentioned previously, the strongest predictor of CTE likelihood is the total amount of brain trauma sustained at the subconcussive and concussive level[3]. It is therefore vital to do frequent and detailed 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[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 the 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, 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[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[3].

Management[edit | edit source]

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

Exercise[edit | edit source]

Although the precise mechanisms are not fully understood, exercise (specifically aerobic exercise) can increase neurogenesis and neuroplasticity[10]. As little as 30 minutes of light to moderate intesity exercise five days a week can greatly slow down the onset of neurological disorder[11].

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[12]. 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[12]. 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[13].

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. 1.0 1.1 1.2 1.3 McKee A, Stein T, Kiernan P, Alvarez V. The Neuropathology of Chronic Traumatic Encephalopathy. Brain Pathology. 2015;25(3):350-364.
  2. Omalu B, DeKosky S, Minster R, Kamboh M, Hamilton R, Wecht C. Chronic Traumatic Encephalopathy in a National Football League Player. Neurosurgery. 2006;:E1003.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Cantu R, Budson A. Management of chronic traumatic encephalopathy. Expert Review of Neurotherapeutics. 2019;19(10):1015-1023.
  4. Cassidy J, Carroll L, Peloso P, Borg J, von Holst H, Holm L et al. 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;36(0):28-60.
  5. Setnik L, Bazarian J. The characteristics of patients who do not seek medical treatment for traumatic brain injury. Brain Injury. 2007;21(1):1-9.
  6. 6.0 6.1 6.2 Gardner R, Yaffe K. Epidemiology of mild traumatic brain injury and neurodegenerative disease. Molecular and Cellular Neuroscience. 2015;66:75-80.
  7. 7.0 7.1 7.2 Montenigro P, Baugh C, Daneshvar D, Mez J, Budson A, Au R 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(5-8).
  8. Carroll L, Cassidy J, Peloso P, Borg J, von Holst H, Holm L et al. Prognosis for mild traumatic brain injury: results of the who collaborating centre task force on mild traumatic brain injury. Journal of Rehabilitation Medicine. 2004;36(0):84-105.
  9. GCS at 40. Glasgow Coma Scale at 40 | The new approach to Glasgow Coma Scale assessment. Available from:
  10. Kimhy D, Vakhrusheva J, Bartels M, Armstrong H, Ballon J, Khan S et al. 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;41(4):859-868.
  11. Müllers P, Taubert M, Müller N. Physical Exercise as Personalized Medicine for Dementia Prevention?. Frontiers in Physiology. 2019;10.
  12. 12.0 12.1 Koehler R, Wilhelm E, Shoulson I. Cognitive rehabilitation therapy for traumatic brain injury. Washington, D.C.: National Academies Press; 2011.
  13. Gupta S, Mishra C, Katyayan P, Joshi N. Assistive Technology for Neurological Disorders. SSRN Electronic Journal. 2018;.