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Text of the page (random words):
ikipedia the free encyclopedia neurodegenerative disease caused by head injury punch drunk redirects here for other uses see punch drunk disambiguation medical condition chronic traumatic encephalopathy other names traumatic encephalopathy syndrome dementia pugilistica 1 punch drunk syndrome a normal brain left and one with advanced cte right specialty neurology psychiatry sports medicine symptoms behavioral problems mood problems problems with thinking 1 complications brain damage dementia 2 aggression depression suicide 3 usual onset years after initial injuries 2 causes repeated head injuries 1 risk factors contact sports military service repeated banging of the head 1 diagnostic method autopsy 1 differential diagnosis alzheimer s disease parkinson s disease 3 treatment supportive care 3 prognosis worsens over time 2 frequency uncertain 2 chronic traumatic encephalopathy cte is a neurodegenerative disease linked to repeated trauma to the head the encephalopathy symptoms can include behavioral problems mood problems and problems with thinking 1 4 the disease often gets worse over time and can result in dementia 2 most documented cases have occurred in athletes involved in striking based combat sports such as boxing kickboxing and mixed martial arts and contact sports such as rugby union rugby league gridiron football australian rules football professional wrestling and ice hockey it is also an issue in association football but largely as a result of heading the ball rather than player contact 1 5 other risk factors include being in the military combat arms or law enforcement 6 prior domestic violence and repeated injuries to the head 1 the amount of trauma required for the condition to occur is unknown and as of 2026 definitive diagnosis can only occur at autopsy thus it can only be diagnosed postmortem 1 the disease is classified as a tauopathy 1 cte is considered uncommon but significant in the general population with an estimated rate of 0 6 6 7 8 but is highly common among individuals with histories of repetitive head impacts such as contact sports athletes a study of donated post mortem brains of american football players identified cte in 99 of brains from donated nfl players and 87 of all former players 9 the risk of cte is regardless of diagnosed concussions as it is driven by the cumulative total number of repetitive head impacts rhi also known as subconcussive impacts rather than diagnosed concussions 10 exact population rates are unclear 2 the largest study has found cte in 6 of the general population 11 12 7 research in brain damage as a result of repeated head injuries began in the 1920s at which time the condition was known as dementia pugilistica or boxer s dementia boxer s madness or punch drunk syndrome 1 3 it has been proposed that the rules of some sports be changed as a means of prevention 1 there is no specific treatment for the disease 3 with research advancing as of 2020 update 13 signs and symptoms edit symptoms of cte which typically occur in four stages are wide ranging can fluctuate and vary significantly between individuals the variability is due to factors such as genetics injury history and location of damage which mean two people with similar impacts can have vastly different clinical presentations and outcomes 14 there is a delayed onset and it is common for behavioral changes to begin years or decades after the impacts have stopped for athletes symptoms typically appear about 8 14 5 years after retiring from their sport patients who present with psychiatric and behavioral issues tend to have a younger age of onset with a mean age of 35 15 contrary to widespread belief many people with cte never go on to commit violent acts and cte does not always present with speech issues dysarthria motor features such as this including parkinsonism ataxia and dysarthria typically appear in a subset of cases predominantly boxers 16 due to specific rotational and shearing impacts boxing involves frequent powerful punches to the head that cause rapid rotational acceleration these shearing forces are particularly effective at damaging the brainstem and cerebellum the areas responsible for speech production coordination balance and motor control 17 multiple studies have indicated that cte usually presents as one of two distinct forms one form typically appearing in a person s 20s or 30s focuses on behavioral and mood changes such as anxiety irritability impulsivity or mood swings rather than physical symptoms like dizziness or headaches although physical symptoms can still occur with this variant the other form is the cognitive variant which typically appears later in life often in a person s late 50s or 60s while the younger onset form focuses on mood and behavior this second form is characterized by significant trouble with memory and executive function such as difficulty planning organizing and multitasking 18 this variant is much more likely to progress into full blown dementia physical and motor symptoms such as tremors balance issues or parkinsonism are more frequently observed in this later life variant or in the advanced stages of the disease symptoms of both variants can wax and wane often resulting in periods where the person s old self or some form of clarity appears to return before symptoms worsen again while cte is a progressive degenerative disease its symptoms do not always progress in a straight line and can fluctuate in intensity a person may have good days where their original personality is more present fluctuations in symptoms can be influenced by external factors like stress activity levels and adequate rest symptoms can also fluctuate significantly based on the situation often appearing differently in structured environments like work compared to more personal settings like home as the disease reaches advanced stages stages 3 and 4 the old self typically becomes less visible as the pathology spreads and symptoms like profound memory loss paranoia and dementia become more constant 18 general symptoms include anger and irritability memory loss loss of empathy confusion apathy impaired judgment impulse control problems aggression withdrawal or isolation depression and anxiety 19 symptoms generally start to appear eight to ten years after an individual experiences repetitive mild traumatic brain injuries 20 21 they typically follow a pattern of early behavioral issues followed by later cognitive decline 18 stage 1 in the earliest stage many individuals are asymptomatic or experience mild intermittent symptoms that are often dismissed symptoms can include but are not limited to moodiness emotional lability difficulty with attention and concentration hyper vigilance or mild paranoia depression or irritability headaches and occasional dizziness loss of interest in previously enjoyed activities anhedonia and short term memory deficits personality change begins in this stage often noticeable only to those closest to the patient 18 dizziness and headaches while recognized symptoms of cte and sometimes reported in early stages are not required for the diagnoses of traumatic encephalopathy syndrome especially in the behavioral variant physical symptoms like dizziness or balance issues are not required for diagnosis and may never appear as well a small group of patients with predominantly behavioral or mood symptoms can remain stable for years sometimes 11 to 14 years before any other cognitive or physical symptoms progress 18 these subtle changes can be easily missed or attributed to other causes or conditions such as personality disorders mood disorders or attachment styles before progressing 18 in particular among those is an obsessive compulsive personality disorder ocpd pattern of personality traits as ocpd displays high correlation with both traumatic brain injury 22 and parkinsonism and the parkinsonism personality profile 23 parkinsonism and thus its characteristics are highly linked to cte with approximately 25 of patients with cte having traits of parkinsonism 24 stage 2 symptoms become more frequent and impact social or professional life this stage is often defined by explosive emotional shifts symptoms can include loss of empathy executive dysfunction increased aggression or irritability including outbursts or withdrawal poor impulse control and worsening emotional instability in the context of relationships by this stage cte can contribute to a cycle of abuse where the individual has poor impulse control and struggles to regulate anger 25 the disease can manifest in various ways within relationships such as jealousy high conflict personality when attempting to communicate stonewalling grudge holding perseveration sometimes with obsessiveness and paranoia short term memory loss can become more pronounced 18 stage 3 stage three is characterized by significant cognitive decline symptoms can include worsening executive dysfunction and visuospatial difficulties such as getting lost in familiar places significant memory loss and a loss of insight into their own condition anosognosia profound apathy may be present as well as difficulty maintaining focus 18 stage 4 the final stage usually reached around age 50 60 for those with the behavioral variant is characterized by advanced dementia symptoms can include severe memory loss psychotic symptoms including paranoia severe personality changes parkinsonism slurred speech and unsteady gait 18 autonomic symptoms may or may not be present they are similar to those of other tbis and can include abnormal sweating excess or reduced temperature sensitivities abnormally low heart rate bradycardia or high heart rate tachycardia seizures aural seizures or post traumatic epilepsy and neurogenic or psychogenic fevers additional symptoms include dysarthria dysphagia cognitive disorders such as amnesia and ocular abnormalities such as ptosis patients with cte may be prone to inappropriate or explosive behavior and may display pathological jealousy or paranoia 26 cause edit see also chronic traumatic encephalopathy in sports cte is not caused by a single concussion but by repetitive long term hits to the head often occurring over many years most documented cases have occurred in athletes with mild repetitive head impacts rhi over an extended period evidence indicates that repetitive concussive and subconcussive blows to the head cause cte 19 in particular it is associated with contact sports such as boxing american football australian rules football wrestling mixed martial arts ice hockey rugby and association football 1 5 in association football research has since confirmed that heading the ball is the primary mechanism of risk leading countries such as england and scotland to ban heading in youth training as of 2020 27 other potential risk factors include military personnel repeated exposure to explosive charges or large caliber ordnance domestic violence and repeated impact to the head 1 although many military personnel are around blasts and explosions very often it is very rare for these personnel to be diagnosed with cte studies have shown that 4 4 of deceased military veterans have been diagnosed with cte 28 exposure to blasts from explosives can produce symptoms of cte 29 the exact amount of trauma required for the condition to occur is unknown 1 scientists are finding that there isn t a safe specific number of hits but rather a threshold once someone s brain receives a certain amount of force over their lifetime the tau protein starts to misfold and spread even if the hits stop 30 pathology edit the neuropathological appearance of cte is distinguished from other tauopathies such as alzheimer s disease the four clinical stages of observable cte disability have been correlated with tau pathology in brain tissue ranging in severity from focal perivascular epicenters of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions 31 the primary physical manifestations of cte include a reduction in brain weight associated with atrophy of the frontal and temporal cortices and medial temporal lobe the lateral ventricles and the third ventricle are often enlarged with rare instances of dilation of the fourth ventricle 32 other physical manifestations of cte include anterior cavum septi pellucidi and posterior fenestrations pallor of the substantia nigra and locus ceruleus and atrophy of the olfactory bulbs thalamus mammillary bodies brainstem and cerebellum 33 as cte progresses there may be marked atrophy of the hippocampus entorhinal cortex and amygdala 20 on a microscopic scale a pathognomonic cte lesion involves p tau aggregates in neurons with or without thorn shaped astrocytes at the depths of the cortical sulcus around a small blood vessel deep in the parenchyma and not restricted to the subpial and superficial region of the sulcus the pathognomonic lesion must include p tau in neurons to distinguish cte from aging related tau astrogliopathy artag 34 supporting features of cte are superficial neurofibrillary tangles nfts p tau in ca2 and ca4 hippocampus p tau in mammillary bodies hypothalamic nuclei amygdala nucleus accumbens thalamus midbrain tegmentum nucleus basalis of meynert raphe nuclei substantia nigra and locus coeruleus p tau thorn shaped astrocytes tsa in the subpial region p tau dot like neurites 35 purely astrocytic perivascular p tau pathology represents artag and does not meet the criteria for cte 34 a small group of individuals with cte have chronic traumatic encephalomyopathy ctem which is characterized by symptoms of motor neuron disease and which mimics amyotrophic lateral sclerosis als progressive muscle weakness and balance and gait problems problems with walking seem to be early signs of ctem 32 exosome vesicles created by the brain are potential biomarkers of tbi including cte 36 loss of neurons scarring of brain tissue collection of proteinaceous senile plaques hydrocephalus attenuation of the corpus callosum diffuse axonal injury neurofibrillary tangles and damage to the cerebellum are implicated in the syndrome neurofibrillary tangles have been found in the brains of dementia pugilistica patients but not in the same distribution as is usually found in people with alzheimer s 37 one group examined slices of brain from patients having had multiple mild traumatic brain injuries and found changes in the cells cytoskeletons which they suggested might be due to damage to cerebral blood vessels 38 diagnosis edit there is currently no definitive test to prove the presence of cte in a living person in the living possible cte is instead diagnosed as traumatic encephalopathy syndrome using the 2021 ninds consensus criteria 39 traumatic encephalopathy syndrome tes is the clinical diagnosis used to describe the symptoms of a living person suspected of having cte while cte can only be definitively diagnosed after death via brain autopsy tes allows doctors to identify and manage the conditio...