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Traumatic Encephalopathy (CTE) in Hyderabad: The Long-Term Brain Consequences of a Life of Head Impacts — Honest Assessment for Athletes and Veterans at KIMS
TES clinical assessment, cognitive testing, advanced MRI, biomarkers, and honest evidence-based counselling at KIMS Neuroscience, Secunderabad, Hyderabad.
CTE is a progressive neurodegenerative disease strongly associated with repetitive head impacts — including sub-concussive impacts that do not cause overt concussion — though causation has not been definitively established and post-mortem case series carry selection bias. It is characterised pathologically by perivascular accumulation of hyperphosphorylated tau protein at the depths of cerebral sulci. CTE can only be definitively diagnosed after death at neuropathology. The clinical diagnosis of Traumatic Encephalopathy Syndrome (TES) is used during life and encompasses progressive cognitive impairment, mood and behavioural changes, and sometimes motor dysfunction in individuals with a documented history of repetitive head exposure (contact sport athletes, military veterans). There is currently no approved disease-modifying treatment; symptom-targeted care and prevention of further head impact exposure are the priorities. At KIMS, assessment integrates a detailed head-impact history, neuropsychological testing, MRI brain (with attention to septum pellucidum and volumetric analysis), and mood/behavioural evaluation — with honest counselling about diagnostic uncertainty.
- TES — the living clinical diagnosis
- CTE can only be confirmed at neuropathology after death. The clinical diagnosis during life is Traumatic Encephalopathy Syndrome (TES): progressive cognitive, mood, or behavioural changes in someone with a documented history of repetitive head exposure (contact sport athletes, military veterans).
- Sub-concussive impacts — associated, but individual risk not established
- American football linemen without any diagnosed concussion in their career can have CTE at autopsy. Sub-concussive impacts have been associated with CTE pathology in some studies, but the individual risk, dose-response relationship, and minimum exposure threshold that produces CTE have not been definitively established. Reducing head impact exposure across a sport remains sensible — the association is well supported even where causation is not proven.
- Ascertainment bias in NFL studies
- The widely-quoted "99% CTE in NFL brains" figure is based on a severely biased sample: families of players with symptoms donated brains; asymptomatic former players did not. The realistic prevalence of CTE in the general contact-sport population is significant but far from universal, and unknown from these studies.
- APOE e4 — a modulating genetic factor
- APOE e4 is associated with worse outcomes after head injury and may modulate CTE risk in those with repetitive head exposure. Genotype does not determine fate but adds context to individual risk discussion at KIMS.
- Septum pellucidum cavum / fenestration
- Cavum septi pellucidi or septal fenestration is seen in ~70–80% of CTE autopsy cases — a structural marker visible on MRI that, with the right exposure history, supports a TES diagnosis during life.
- India context — kabaddi, kushti, boxing, cricket
- CTE is no longer just an NFL story. Kabaddi players, kushti wrestlers, boxers, and cricket fielders sustain repetitive head impacts over careers. KIMS provides cognitive assessment, mood evaluation, and head-impact-reduction counselling for current and retired Indian contact sport athletes.
- Honest uncertainty
- There is no approved disease-modifying treatment for CTE/TES. Symptom-targeted care (SSRIs for mood, cognitive rehab, behavioural strategies, family support) is the standard at KIMS. The most effective intervention is prevention — head impact reduction in current athletes.
| Fact | Details |
|---|---|
| Definition | Progressive neurodegenerative disease strongly associated with repetitive head impacts (concussive + sub-concussive); causation not definitively established · Hyperphosphorylated tau at the depths of cerebral sulci, perivascular · Definitive diagnosis only at neuropathology after death · No validated in-vivo biomarker |
| TES (clinical diagnosis) | Used during life · Progressive cognitive, mood, or behavioural changes + documented repetitive head impact history · Allows assessment, support, and counselling without overstating diagnostic certainty |
| Risk profile | Total head impact exposure (years × intensity × sub-concussive load) is the strongest associated factor, though no dose-response threshold is established · Many heavily exposed athletes never develop CTE · APOE e4 modulates risk · Septum pellucidum cavum/fenestration in 70–80% of CTE cases |
| Ascertainment bias | "99% of NFL brains" reflects donation bias, not population prevalence · True CTE rate in contact-sport athletes is unknown but real · Honest, evidence-based counselling at KIMS, not media-amplified worst case |
| India context | Kabaddi · Wrestling/kushti · Boxing · Cricket (fielders, batters hit by ball) · Underreported and under-counselled · KIMS provides athlete-specific assessment |
| Treatment | No approved disease-modifying treatment · Symptom-targeted: SSRIs/mood stabilisers for emotional dysregulation, cognitive rehab, behavioural strategies, family education · Prevention is the most effective intervention |
| Differential diagnosis | Frontotemporal dementia · Alzheimer's disease · Mood disorders · Substance use · Sleep disorders · Neuropsychological testing + MRI + history clarify the picture at KIMS |
About This Condition
The Former Kabaddi Player
A 52-year-old man in Hyderabad played professional kabaddi for 18 years. He retired 8 years ago. For the past 4 years, his wife has been concerned: he forgets conversations from the previous day; he has become short-tempered and has explosive rages that are out of character for a man who was calm and thoughtful throughout his career; he has been depressed and withdrawn; and he sometimes gets disoriented in familiar surroundings. He has seen two psychiatrists and is on antidepressants with partial benefit. His family wonders if this is early dementia.
At KIMS, his history of 18 years of professional kabaddi — a full-contact sport involving repeated tackles, falls, and impacts — is immediately flagged as a significant head impact history. His symptom complex — progressive memory decline, impulse dyscontrol with explosive rage, and depression in a former contact sport athlete — is consistent with Traumatic Encephalopathy Syndrome (TES). Neuropsychological assessment documents: memory impairment (encoding and retrieval); reduced processing speed; executive dysfunction (impaired planning and flexibility); and preserved language. MRI brain shows mild cortical atrophy and, on FLAIR sequences, some white matter signal change in the frontal lobes. CSF tau/phospho-tau: mildly elevated.
The assessment at KIMS is honest. He does not have a confirmed CTE diagnosis — that requires neuropathology and is only possible after death. He has TES: clinical features consistent with CTE in a person with significant head impact history. The differential diagnoses are considered and investigated: early Alzheimer's disease (amyloid PET negative, reducing this likelihood); frontotemporal dementia (the tau pathology of CTE and FTD overlap); and depression-related cognitive impairment (the SSRI has been inadequately dosed — this is optimised). He is offered: cognitive rehabilitation; pharmacological support for depression and impulse dyscontrol; counselling for him and his wife; referral to a TES support group; and the option of volunteering for brain bank research so that his diagnosis can be confirmed post-mortem.
Book a Consultation
Speak directly with our TES/CTE specialist team. Multidisciplinary assessment for athletes, veterans, and their families. Monday to Saturday.
040-44885000Emergency line: 040-46324365Quick Facts about CTE and TES
The essential context: what CTE is, why TES is the right term in living patients, who is at risk, and what is genuinely uncertain in the current evidence.
What it is
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease characterised by the pathological accumulation of hyperphosphorylated tau protein in the brain, occurring in a distinctive perivascular distribution at the depths of cerebral sulci (the folds of the brain). Repetitive head impacts — not just concussions, but also the sub-concussive impacts that occur in much larger numbers throughout a contact sport career — are strongly associated with this tau pathology, but causation has not been definitively established. Post-mortem studies carry selection bias, because brains are donated by families who already suspected CTE, which inflates observed prevalence. Not all individuals with extensive exposure to repetitive head impacts develop CTE, suggesting that additional factors including genetic susceptibility contribute to individual risk. CTE can only be definitively diagnosed after death through neuropathological examination of the brain, and the relationship between CTE pathology and clinical symptoms is not fully established — some individuals with CTE pathology had no apparent clinical syndrome during life.
TES — the clinical diagnosis during life
Because CTE requires post-mortem diagnosis, the term Traumatic Encephalopathy Syndrome (TES) is used for the clinical presentation in living individuals. TES is defined by: a history of repetitive head impact exposure (contact sport, military combat); specific progressive clinical features (cognitive impairment — particularly memory and executive function; mood and behavioural changes — depression, explosive rage, emotional dysregulation; and sometimes motor features — tremor, Parkinsonism, or ataxia); and supportive biomarker findings (neuroimaging, tau-PET in research settings). TES is a clinical research diagnosis, not a well-established clinical entity with validated diagnostic criteria.
Who is at risk
Any individual with a history of multiple concussions or prolonged exposure to repetitive sub-concussive head impacts: professional and amateur contact sport athletes (boxing, American football, rugby, ice hockey; and in India: kabaddi, wrestling/kushti, boxing, cricket in fielding positions); military veterans with blast exposure; and individuals with a history of domestic violence with repeated head impacts. Sub-concussive exposure matters: American football linemen who have never had a diagnosed concussion in their career can have CTE at autopsy. The cumulative burden of impacts, rather than the presence of diagnosed concussions alone, appears to carry the association — though the individual risk and the exposure threshold involved are not established, and many heavily exposed athletes never develop CTE pathology.
Honest uncertainty
CTE is surrounded by considerable scientific uncertainty and media sensationalism. The prevalence of CTE in the general contact sport population is unknown — the brain bank studies that found CTE in 99% of donated NFL brains are severely biased by selection (families of players with symptoms donated brains, not families of asymptomatic players). The causal relationship between head impacts and CTE is strong but not absolute. Not every contact sport athlete develops CTE; many factors including genetics (APOE e4 carrier status) and overall health may modulate risk. At KIMS, TES assessment is honest about what is known, what is not, and what can be done.
The Four Clinical Domains of TES
TES is not one symptom — it is a constellation across four domains. Recognising the pattern is what triggers the assessment.
Cognitive impairment — the most consistent feature
Memory problems: difficulty encoding new information and retrieving recently learned material. This is different from the word-finding difficulties that characterise early Alzheimer's disease in some patients. Executive dysfunction: difficulty with planning, organisation, and mental flexibility. Processing speed slowing: the cognitive fatigue and slowing that many former athletes notice in their late career and after retirement, attributed to 'ageing' but worsening progressively. Visuospatial difficulties in some. At KIMS, neuropsychological assessment provides an objective profile of these domains and tracks progression over time.
Mood and behavioural changes — often the most socially disabling
Depression is present in approximately 60–70% of people with TES. The depression of TES has a specific quality: it is often accompanied by profound hopelessness and anhedonia (inability to feel pleasure) that is resistant to the antidepressants that work well for depression without neurological underpinning. Emotional dysregulation and explosive rage (dysthymia punctuated by sudden anger episodes disproportionate to the trigger) is one of the most diagnostically specific features of TES. Impulsivity: acting without considering consequences. Apathy: loss of motivation and initiative (distinct from depression). These behavioural features cause relationship breakdown, job loss, and social isolation, compounding the underlying neurological disease.
Motor features — in some patients
Some TES patients develop motor features: Parkinsonism (resting tremor, bradykinesia, masked facies, shuffling gait — overlapping with the CTE Parkinson's variant, or PD itself, which is more common in contact sport athletes); cerebellar ataxia (unsteadiness, limb incoordination, dysarthria); and dysarthria (slurred speech without tongue weakness). These motor features appear later in the disease course and are less consistent than the cognitive and mood features.
The sub-concussive impact problem — why 'I never had a concussion' is not reassuring
A significant proportion of CTE cases at neuropathology occur in athletes who, by self-report, never had a diagnosed concussion during their careers. The mechanism: while a single concussion requires biomechanical forces sufficient to produce transient neurological dysfunction, sub-concussive impacts — head impacts below the concussion threshold that are asymptomatic — still transmit inflammatory and axonal injury signals. A professional kabaddi player or wrestler who trains and competes 300 days per year may sustain thousands of sub-concussive head impacts per career. Sub-concussive impacts have been associated with CTE pathology in some studies, but the individual risk, the dose-response relationship, and the minimum exposure threshold that produces CTE have not been definitively established — so no athlete can be told what their personal risk is from a given exposure. The association is nonetheless strong enough to support sport-wide head impact reduction policies, not just concussion management after the fact.
Diagnosis at KIMS
Assessment at KIMS
The TES assessment integrates head impact history, formal neuropsychological testing, structural and advanced MRI, and CSF and blood biomarkers — providing the most rigorous clinical-research-grade workup possible during life.
Structured head impact history
A detailed account of the sports or combat history: years played, position, estimated number of concussions (formally diagnosed and undiagnosed), return-to-play practices, and the specific mechanics of head impact in the sport. Kabaddi: tackles involving head contact; wrestling: throws, takedowns with head impact; cricket: batting without adequate helmet use historically; boxing: sparring and bout impacts cumulative over years.
Neuropsychological assessment
A formal battery covering memory (immediate recall, delayed recall, recognition), processing speed (symbol search, coding), executive function (trail making, verbal fluency, Stroop), attention (digit span, CPT), and visuospatial function. The neuropsychological profile in TES typically shows relatively spared language and naming with impaired episodic memory, processing speed, and executive function — a profile different from early Alzheimer's and useful in differential diagnosis.
MRI brain — structural and advanced sequences
Standard MRI: cortical atrophy (global or frontal-predominant); septum pellucidum cavum or fenestration (a marker of repetitive head trauma, seen in approximately 70–80% of CTE cases at autopsy); white matter signal change. Advanced sequences: susceptibility-weighted imaging (SWI) for microhaemorrhages from prior impacts; diffusion tensor imaging (DTI) for white matter tract integrity. At KIMS, the MRI is reviewed with specific attention to these TES-associated findings, not just as a routine structural study.
CSF and blood biomarkers
CSF tau and phospho-tau: elevated in CTE/TES compared to healthy controls, though with significant overlap with Alzheimer's disease. CSF amyloid-beta: used to distinguish CTE (typically beta-amyloid normal or mildly reduced) from Alzheimer's disease (significantly reduced amyloid-beta in CSF). Plasma NfL (neurofilament light chain): elevated in active neurodegeneration; useful for monitoring progression. Tau-PET imaging (where available in research settings) shows tau accumulation in a specific perisylvian distribution in CTE.
Treatment
Management at KIMS
There is currently no approved disease-modifying treatment for CTE. Management focuses on symptom control, family support, and — most importantly — preventing further head impact exposure.
Treating the Symptoms
Depression: SSRIs (sertraline, escitalopram) at adequate dose; augmentation with mirtazapine or venlafaxine if incomplete response.
Explosive rage and emotional dysregulation: SSRIs plus, in some patients, mood stabilisers (valproate, lamotrigine) or low-dose quetiapine.
Impulsivity: methylphenidate or atomoxetine in some patients (with careful monitoring).
Apathy: occasionally responds to stimulants or dopaminergic agents.
Parkinsonism: levodopa where motor features warrant treatment.
Cognitive rehabilitation: Memory aids (notebooks, phone reminders), structured daily routines, simplification of complex tasks, and compensatory strategies for executive dysfunction.
Sleep optimisation: Sleep disturbance is near-universal in TES and significantly worsens cognitive and mood symptoms. Sleep hygiene, melatonin, and treatment of obstructive sleep apnoea (common in former athletes).
Family counselling: The behavioural features of TES — rage, impulsivity, paranoia — destroy relationships. Partners and children need to understand that these are neurological symptoms, not choices.
Suicide risk monitoring: Suicidality is significantly elevated in TES. Impulsivity combined with depression and hopelessness is a dangerous combination. Every patient with suspected TES undergoes depression and suicidality screening at every visit.
The Most Effective Treatment
The most important intervention in CTE is preventing the head impacts that cause it. KIMS specifically advocates for:
Helmet standards in Indian sport: ISI-marked helmets for cricket; proper headgear for kabaddi and wrestling in school and club sport.
Concussion recognition and management: Athletes removed from play after any concussion; no same-day return; structured return-to-play protocol (SCAT6).
Reducing sub-concussive exposure in training: Reducing the number of full-contact practice sessions; head impact threshold monitoring (head impact sensor technology in research settings).
Rule changes in sport: Advocating for rule modifications that reduce the incidence of high-impact head contact (e.g., head-high contact penalties in kabaddi).
Related Conditions
Traumatic encephalopathy belongs to the family of traumatic neurological conditions managed at KIMS:
FAQs
Frequently Asked Questions
The former kabaddi player whose wife says he has changed. The boxer who can't remember conversations from yesterday. The cricket captain whose family has noticed explosive anger for the first time.
Traumatic Encephalopathy Syndrome is assessed at KIMS Neuroscience, Secunderabad, Hyderabad with neuropsychological testing, advanced MRI, biomarkers, and honest evidence-based counselling. There is no cure today — but there are treatments for the symptoms, support for the family, and the knowledge that comes from knowing what is happening. Call 040-44885000.
International enquiries: info@kimsneurosciences.com