Chronic Traumatic Encephalopathy: Difference between revisions

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# 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
# 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
#




when assessing the gravity of an MTBI, the Centers for Disease control and prevention (CDC) suggests the following procedure:
when assessing the gravity of an MTBI, the Centers for Disease control and prevention (CDC) suggests the following procedure<ref>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.</ref>:


# Assess for on or more of the following:
# Assess for on or more of the following:
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#* loss of consciousness for 30 min or less  
#* loss of consciousness for 30 min or less  
#* post traumatic amnesia for less that 24h
#* post traumatic amnesia for less that 24h
#* and/or other transient 93 neurological abnormalities such as focal signs, seizure, and intracra94 nial lesion not requiring surgery
#* and/or other transient 93 neurological abnormalities such as focal signs, 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
# 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.
# 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.

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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

Epidimiology[edit | edit source]

Every year an estimated 42 million people suffer a mild traumatic brain injury (MTBI) or concussion[3].

Neuropathology[edit | edit source]

CTE is a tauopathy that results from the culmination of repetitive MTBI[3] .

Symptoms[edit | edit source]

Symptoms of CTE can manifest in any of the four main clinical domains[4]:

  • 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 neuromuscular diseases, such as Motor Neurone Disease, Alzheimer's Disease and Lewy Body Disease.

Clinical subtypes of chronic traumatic encephalopathy[4]
Behavioral 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)[4] 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


when assessing the gravity of an MTBI, the Centers for Disease control and prevention (CDC) suggests the following procedure[5]:

  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 93 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

[6]

Management[edit | edit source]

Resources[edit | edit source]

  • bulleted list
  • x

or

  1. numbered list
  2. x

References[edit | edit source]

  1. 1.0 1.1 1.2 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 Gardner R, Yaffe K. Epidemiology of mild traumatic brain injury and neurodegenerative disease. Molecular and Cellular Neuroscience. 2015;66:75-80.
  4. 4.0 4.1 4.2 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).
  5. 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.
  6. GCS at 40. Glasgow Coma Scale at 40 | The new approach to Glasgow Coma Scale assessment. Available from: https://youtu.be/v6qpEQxJQO4