TBI/Trauma

Research on TBI has linked it to the following mental health and related outcomes:

• Depression, including after mild TBI Ogonah, M.G.T., Botchway, S., Yu, R., Schofield, P.W. and Fazel, S. (2025) ‘An umbrella review of health outcomes following traumatic brain injury’, Nature Mental Health, 3(1), pp. 83–91.
• Anxiety, most commonly generalised anxiety disorder Dehbozorgi, M., Maghsoudi, M.R., Mohammadi, I., Firouzabadi, S.R., Mohammaditabar, M., Oraee, S. et al. (2024) ‘Incidence of anxiety after traumatic brain injury: a systematic review and meta-analysis’, BMC Neurology, 24(1), article 293.
• Post-traumatic stress disorder (PTSD) and other trauma-related symptoms Ogonah, M.G.T., Botchway, S., Yu, R., Schofield, P.W. and Fazel, S. (2025) ‘An umbrella review of health outcomes following traumatic brain injury’, Nature Mental Health, 3(1), pp. 83–91. Toccalino, D., Moore, A.M., Cripps, E., Gutierrez, S.C., Colantonio, A., Wickens, C.M. et al. (2023) ‘Exploring the intersection of brain injury and mental health in survivors of intimate partner violence: a scoping review’, Frontiers in Public Health, 11, article 1100549.
• Psychosis, particularly after childhood TBI Ogonah, M.G.T., Botchway, S., Yu, R., Schofield, P.W. and Fazel, S. (2025) ‘An umbrella review of health outcomes following traumatic brain injury’, Nature Mental Health, 3(1), pp. 83–91.
• Suicidal thoughts, plans, attempts and suicide Liao, M., Hu, E. and Liu, K. (2025) ‘Risk of suicidal behaviors following sport-related and non-sport-related concussion: a systematic review and meta-analysis’, BMC Psychiatry, 25(1), article 1072. 
• Attention-deficit/hyperactivity disorder (ADHD) after severe childhood TBI Ogonah, M.G.T., Botchway, S., Yu, R., Schofield, P.W. and Fazel, S. (2025) ‘An umbrella review of health outcomes following traumatic brain injury’, Nature Mental Health, 3(1), pp. 83–91.
• Cognitive decline and dementia in later life Ogonah, M.G.T., Botchway, S., Yu, R., Schofield, P.W. and Fazel, S. (2025) ‘An umbrella review of health outcomes following traumatic brain injury’, Nature Mental Health, 3(1), pp. 83–91. Livingston, G., Huntley, J., Liu, K.Y., Costafreda, S.G., Selbæk, G., Alladi, S. et al. (2024) ‘Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission’, The Lancet, 404(10452), pp. 572–628.
• A loss of drive and pleasure (anhedonia) linked to changes in dopamine signalling Mata-Bermúdez, A., Trejo-Chávez, R., Martínez-Vargas, M., Pérez-Arredondo, A., Martínez-Cárdenas, M.L.Á., Díaz-Ruiz, A., Ríos, C. and Navarro, L. (2024) ‘Dysregulation of the dopaminergic system secondary to traumatic brain injury: implications for mood and anxiety disorders’, Frontiers in Neuroscience, 18, article 1447688.
• Irritability, personality change and difficulty regulating emotions, which are commonly reported by patients and families alike

Mild TBI roughly doubles the risk of depression, and childhood TBI is linked to a higher risk of psychosis and, after severe injury, ADHD. Increased suicide risk has been documented in veterans, and TBI is also linked to a higher risk of dementia, motor neurone disease and epilepsy. Ogonah, M.G.T., Botchway, S., Yu, R., Schofield, P.W. and Fazel, S. (2025) ‘An umbrella review of health outcomes following traumatic brain injury’, Nature Mental Health, 3(1), pp. 83–91. These are group-level findings, and most people who have a TBI, especially a mild one, recover well, but the risks are high enough that it is worth taking any change in mood or thinking seriously after a head injury.

Depression after brain injury does not follow a single course. Most people recover and stay well, but a minority go on to develop persistent or worsening symptoms, and depression can emerge or intensify years after the injury, sometimes with no obvious trigger. Sex, age, injury severity, education and a psychiatric history before the injury all appear to influence the course symptoms take. Prince, P., Naragon-Gainey, K., Becerra Parra, R.G., Weinborn, M. and Pestell, C. (2025) ‘Characterising long-term depressive symptoms post-brain injury: a systematic review of symptom trajectory groups and their predictors’, Neuropsychology Review. This is one reason why ongoing monitoring, rather than a single check soon after injury, is important, and why a new episode of depression, even long after a head injury, is worth mentioning to a doctor alongside that history.

People with TBI are considerably more likely to develop anxiety than those without, most commonly generalised anxiety disorder, characterised by persistent, excessive worry. This risk does not appear to depend on how severe the original injury was, meaning even a mild concussion can be followed by significant anxiety. Dehbozorgi, M., Maghsoudi, M.R., Mohammadi, I., Firouzabadi, S.R., Mohammaditabar, M., Oraee, S. et al. (2024) ‘Incidence of anxiety after traumatic brain injury: a systematic review and meta-analysis’, BMC Neurology, 24(1), article 293.

Some people continue to have symptoms for months after a mild TBI or concussion, including headache, difficulty thinking, dizziness and balance problems, visual disturbance, low mood and fatigue, a pattern often called post-concussion syndrome. Brain-imaging research points to the salience network, which includes the anterior insula and dorsal anterior cingulate cortex and helps the brain decide what is important and switch between tasks, as a core network involved in these persisting post-concussive symptoms. Mollica, A., Cash, R.F.H., Leochico, C.F.D., Giacobbe, P., Sewell, I.J., Zalesky, A. et al. (2025) ‘The network-based underpinnings of persisting symptoms after concussion: a multimodal neuroimaging meta-analysis’, Nature Mental Health, 3(10), pp. 1276–1290. This gives a biological explanation for symptoms that are sometimes dismissed as “just in someone’s head” once initial scans come back clear.

Sleep disturbance is very common after brain injury, with insomnia affecting a large proportion of people, sometimes persisting for years after the original injury. Evening melatonin, the hormone that signals night-time to the body, is often reduced after TBI, although the evidence for melatonin supplementation as a treatment is still mixed. Bell, A.P., Hewins, B., Bishop, C., Fortin, A., Wang, J., Creamer, J., Collen, J. and Werner, J.K. (2023) ‘Traumatic brain injury, sleep, and melatonin—intrinsic changes with therapeutic potential’, Clocks & Sleep, 5(2), pp. 177–203. Poor sleep and low mood often go together and can worsen each other, so sleep is worth raising with a doctor after a head injury rather than being treated as a separate, lower-priority issue.

Concussion is linked to a higher risk of suicidal thoughts, making a suicide plan, attempting suicide and dying by suicide, with the risk comparable after sport-related and non-sport-related concussion. Liao, M., Hu, E. and Liu, K. (2025) ‘Risk of suicidal behaviors following sport-related and non-sport-related concussion: a systematic review and meta-analysis’, BMC Psychiatry, 25(1), article 1072. Most people who have a concussion do not develop suicidal thoughts, but these findings underline the importance of checking on mood, not just physical recovery, after any head injury.

Brain injury is a hidden but frequent consequence of intimate partner violence, and is often overlooked in survivors because it may not involve loss of consciousness or an obvious visible injury. A large proportion of survivors have experienced a head injury or TBI, often involving strangulation or loss of consciousness, and survivors with brain injury show significantly higher rates of depression, post-traumatic stress and anxiety than those without. Toccalino, D., Moore, A.M., Cripps, E., Gutierrez, S.C., Colantonio, A., Wickens, C.M. et al. (2023) ‘Exploring the intersection of brain injury and mental health in survivors of intimate partner violence: a scoping review’, Frontiers in Public Health, 11, article 1100549. Anyone supporting a survivor of domestic violence should be aware that brain injury may be an unrecognised contributor to their mental health symptoms.

Repeated blows to the head, as in some contact sports, can be harmful even when no single blow is severe enough to cause a diagnosed concussion. Chronic traumatic encephalopathy (CTE) is a brain disease diagnosed after death, defined by a build-up of abnormal tau protein in the brain. The great majority of published CTE cases have occurred in people with known repetitive head impact exposure, and the risk rises with the number of years played. McKee, A.C., Stein, T.D., Huber, B.R., Crary, J.F., Bieniek, K.F., Dickson, D.W. et al. (2023) ‘Chronic traumatic encephalopathy (CTE): criteria for neuropathological diagnosis and relationship to repetitive head impacts’, Acta Neuropathologica, 145(4), pp. 371–394. CTE can only be confirmed after death, and the clinical symptoms, which can include mood changes, impulsivity and memory problems, cannot be confirmed with certainty during life. McKee, A.C., Stein, T.D., Huber, B.R., Crary, J.F., Bieniek, K.F., Dickson, D.W. et al. (2023) ‘Chronic traumatic encephalopathy (CTE): criteria for neuropathological diagnosis and relationship to repetitive head impacts’, Acta Neuropathologica, 145(4), pp. 371–394.

Brain-tissue research shows that repeated head impacts can cause nerve-cell loss and provoke inflammation earlier than was previously understood, and before any build-up of tau protein. Butler, M.L.M.D., Pervaiz, N., Breen, K. et al. (2025) ‘Repeated head trauma causes neuron loss and inflammation in young athletes’, Nature, 647(8088), pp. 228–237. Former contact-sport athletes also show a substantially higher likelihood of a diagnosed mental health disorder and higher PTSD symptom scores in midlife than those from non-contact sports. Buddenbaum, C.V., Recht, G.O., Rodriguez, A.K., Newman, S.D. and Kawata, K. (2024) ‘Associations between repetitive head impact exposure and midlife mental health wellbeing in former amateur athletes’, Frontiers in Psychiatry, 15, article 1383614.  This has prompted growing efforts across many sports to better detect and manage head impacts at every level of play.

Brain injury involves two phases. Primary injury is the irreversible tissue damage that occurs at the moment of impact. Secondary injury is a cascade of processes that unfolds over minutes to days afterwards, affecting even previously uninjured regions of the brain through reduced blood supply, inflammation and cell dysfunction. Freire, M.A.M., Rocha, G.S., Bittencourt, L.O., Falcão, D., Lima, R.R. and Cavalcanti, J.R.L.P. (2023) ‘Cellular and molecular pathophysiology of traumatic brain injury: what have we learned so far?’, Biology, 12(8), article 1139. Because secondary injury evolves over time, it is the phase most open to treatment, and the phase in which many of the biochemical changes relevant to mental health arise. This is part of why early, appropriate care after a head injury can make a real difference to longer-term outcomes.

After TBI, excessive glutamate (the brain’s main excitatory messenger) overstimulates nerve-cell receptors and floods cells with calcium. This activates enzymes that break down proteins and fats and can lead to cell death, establishing damaging feedback loops.Freire, M.A.M., Rocha, G.S., Bittencourt, L.O., Falcão, D., Lima, R.R. and Cavalcanti, J.R.L.P. (2023) ‘Cellular and molecular pathophysiology of traumatic brain injury: what have we learned so far?’, Biology, 12(8), article 1139. Uncontrolled calcium entry also disrupts the mitochondria, the cell’s energy-producing structures. Olatona, O.A., Sterben, S.P., Kansakar, S.B.S., Symes, A.J. and Liaudanskaya, V. (2025) ‘Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration’, Frontiers in Cellular Neuroscience, 19, article 1570596.

Calcium overload triggers a programmed cell-death cascade in the mitochondria, and injured mitochondria produce much more of the reactive molecules known as reactive oxygen species, impairing production of ATP, the cell’s energy currency. Freire, M.A.M., Rocha, G.S., Bittencourt, L.O., Falcão, D., Lima, R.R. and Cavalcanti, J.R.L.P. (2023) ‘Cellular and molecular pathophysiology of traumatic brain injury: what have we learned so far?’, Biology, 12(8), article 1139. Damage to the mitochondria also forces brain cells toward less efficient energy production, and injured mitochondria release their own DNA, which activates microglia and sustains neuroinflammation — creating a vicious cycle of mitochondrial dysfunction, oxidative damage, inflammation and neurodegeneration. Olatona, O.A., Sterben, S.P., Kansakar, S.B.S., Symes, A.J. and Liaudanskaya, V. (2025) ‘Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration’, Frontiers in Cellular Neuroscience, 19, article 1570596.. This energy shortfall may help explain the profound fatigue and cognitive fog that many people experience after a significant head injury. See our page on Mitochondrial dysfunction.

Oxidative stress arises when reactive oxygen and nitrogen species overwhelm the body’s antioxidant defences. After TBI, these reactive molecules damage fats, proteins and DNA, and the body’s antioxidant defences become depleted, worsening the injury.Freire, M.A.M., Rocha, G.S., Bittencourt, L.O., Falcão, D., Lima, R.R. and Cavalcanti, J.R.L.P. (2023) ‘Cellular and molecular pathophysiology of traumatic brain injury: what have we learned so far?’, Biology, 12(8), article 1139.

Activated microglia and astrocytes release pro-inflammatory messengers, chemokines and proteases after TBI. This “wound amplification” can be more damaging than the primary injury itself, and the blood–brain barrier is disrupted, allowing swelling and immune cells to enter the brain. Freire, M.A.M., Rocha, G.S., Bittencourt, L.O., Falcão, D., Lima, R.R. and Cavalcanti, J.R.L.P. (2023) ‘Cellular and molecular pathophysiology of traumatic brain injury: what have we learned so far?’, Biology, 12(8), article 1139.. Levels of key inflammatory messengers rise in the first week after mild TBI and are linked to poorer clinical outcomes. Malik, S., Alnaji, O., Malik, M., Gambale, T., Farrokhyar, F. and Rathbone, M.P. (2023) ‘Inflammatory cytokines associated with mild traumatic brain injury and clinical outcomes: a systematic review and meta-analysis’, Frontiers in Neurology, 14, article 1123407.. See our page on Inflammation.

Microglia can also become “primed” by injury, so that they over-respond to later challenges, and raised inflammatory activity has been detected many years after injury. Immune cells from the bloodstream can enter the brain, and autoantibodies against brain proteins have also been found, along with changes in immune-cell function that may raise susceptibility to infection. Abikenari, M., Ha, J.H., Liu, J., Ren, A., Cho, K.B., Lim, J., Kim, L.H., Medikonda, R., Choi, J. and Lim, M. (2025) ‘The immunological landscape of traumatic brain injury: insights from pathophysiology to experimental models’, Frontiers in Neurology, 16, article 1668480.. This raises the possibility of a two-way link between brain injury and infection; see our Infections page.

Post-traumatic stress disorder and TBI frequently occur together, for example in people injured in combat or accidents, and the two conditions can be difficult to tell apart because their symptoms overlap so much. Interleukin-6, an inflammatory messenger, is the most consistently raised blood marker in people with both conditions, and neurofilament light chain, a marker of nerve-cell damage, is also raised. Cowansage, K.K., Nair, R., Lara-Ruiz, J., Berman, D.E., Boyd, C., Milligan, T. et al. (2025) ‘Genetic and peripheral biomarkers of comorbid posttraumatic stress disorder and traumatic brain injury: a systematic review’, Frontiers in Neurology, 16, article 1500667.. Researchers hope that markers like these will eventually help distinguish the biological contribution of the two conditions and guide treatment.

TBI can disturb dopamine circuits throughout the brain, producing a “hypodopaminergic”, or underactive, state. Damage to different dopamine pathways may contribute to different symptoms: disruption of the pathway involved in reward and motivation may lead to anhedonia, a core symptom of depression, while disruption of the pathway involved in executive function may affect emotional regulation and decision-making. Mata-Bermúdez, A., Trejo-Chávez, R., Martínez-Vargas, M., Pérez-Arredondo, A., Martínez-Cárdenas, M.L.Á., Díaz-Ruiz, A., Ríos, C. and Navarro, L. (2024) ‘Dysregulation of the dopaminergic system secondary to traumatic brain injury: implications for mood and anxiety disorders’, Frontiers in Neuroscience, 18, article 1447688. Serotonin, inflammation and stress-hormone changes are also involved alongside dopamine. See our page on Neurotransmitter imbalances.

The pituitary gland, which sits at the base of the brain and directs much of the hormone system, can be damaged by head injury. Around a third of people develop dysfunction of at least one pituitary hormone axis after TBI, most commonly growth hormone deficiency, followed by deficiency of sex hormones, cortisol-related hormones and thyroid hormone. Aljboor, G.S.R., Tulemat, A., Alsaedi, A.J., Rădoi, M.P., Toader, C. and Papacocea, T. (2024) ‘Acute and chronic hypopituitarism following traumatic brain injury: a systematic review and meta-analysis’, Neurosurgical Review, 47(1), article 841.. Hormone deficiencies can themselves affect mood and energy, which makes this an important and often overlooked area to consider when mood or energy problems persist after a head injury. See our pages on Stress hormone imbalances, Sex hormone imbalances and Thyroid hormone imbalances.

Injury can also disturb whole-body metabolism. TBI is linked to stress-induced high blood sugar and glucose intolerance, and changes in blood lipid profiles, with plasma insulin levels carrying prognostic significance for complications after severe TBI. Kursancew, A.C.S., Faller, C.J., Piva-Uchida, E.M., Benedet, I.B., Maciel, P.M., de Figueredo, S.M., Petronilho, F., Ceretta, L.B., Streck, E.L. and Generoso, J.S. (2025) ‘Metabolic disorders after traumatic brain injury: a narrative review of systemic consequences’, Metabolic Brain Disease, 40(1), article 93. Our Metabolism page and our Insulin hormone imbalances page look at these processes in more depth.

Early research suggests infection and injury may interact. In concussed athletes, those who carried cytomegalovirus (CMV) show greater structural brain changes on imaging than those who did not, and neuroinflammation after brain injury may trigger CMV to reactivate, contributing to tissue damage. Zheng, H. and Savitz, J. (2024) ‘Herpesviruses and neuropsychiatric disorders: overlooked adversaries or innocent bystanders?’, Neuropsychopharmacology, 49(1), pp. 313–314. See our Infections page.

The Lancet Commission on dementia lists traumatic brain injury among its modifiable risk factors, alongside factors such as physical inactivity, depression, diabetes and obesity, and estimates that nearly half of dementia cases could be prevented or delayed by tackling these factors together. Livingston, G., Huntley, J., Liu, K.Y., Costafreda, S.G., Selbæk, G., Alladi, S. et al. (2024) ‘Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission’, The Lancet, 404(10452), pp. 572–628.. TBI is consistently linked to a higher risk of dementia in later life, Ogonah, M.G.T., Botchway, S., Yu, R., Schofield, P.W. and Fazel, S. (2025) ‘An umbrella review of health outcomes following traumatic brain injury’, Nature Mental Health, 3(1), pp. 83–91. which is one reason head injury prevention, such as wearing appropriate protective equipment and taking basic fall precautions, matters at every age.

Falls are the leading cause of TBI for most age groups in most regions, and are a particularly important cause in young children and older adults. Yan, J., Wang, C. and Sun, B. (2025) ‘Global, regional, and national burdens of traumatic brain injury from 1990 to 2021’, Frontiers in Public Health, 13, article 1556147.

Vehicle accidents and traffic collisions are a major cause of TBI. Cleveland Clinic (2025) Traumatic brain injury (TBI): what it is, symptoms & treatment. Cleveland, OH: Cleveland Clinic. Available at: https://my.clevelandclinic.org/health/diseases/8874-traumatic-brain-injury [Accessed 21 September 2026].

Interpersonal violence contributes to TBI globally, Yan, J., Wang, C. and Sun, B. (2025) ‘Global, regional, and national burdens of traumatic brain injury from 1990 to 2021’, Frontiers in Public Health, 13, article 1556147. and intimate partner violence is an important and under-recognised cause, with strangulation and blows to the head both involved. Toccalino, D., Moore, A.M., Cripps, E., Gutierrez, S.C., Colantonio, A., Wickens, C.M. et al. (2023) ‘Exploring the intersection of brain injury and mental health in survivors of intimate partner violence: a scoping review’, Frontiers in Public Health, 11, article 1100549.

Explosions, and penetrating injuries from sharp objects or bullets, can cause TBI.

Incidence is consistently higher in males than in females. Yan, J., Wang, C. and Sun, B. (2025) ‘Global, regional, and national burdens of traumatic brain injury from 1990 to 2021’, Frontiers in Public Health, 13, article 1556147.. Age also matters: childhood TBI has been linked with a higher risk of later psychosis and ADHD, while older adults face particular risks around falls and slower recovery. Ogonah, M.G.T., Botchway, S., Yu, R., Schofield, P.W. and Fazel, S. (2025) ‘An umbrella review of health outcomes following traumatic brain injury’, Nature Mental Health, 3(1), pp. 83–91.

If you or someone you know has had a head injury and is now experiencing changes in mood, thinking, sleep or behaviour, please speak to a doctor. Early assessment is important, and support is available even when symptoms appear well after the original injury.