GCS and Mayo classification

The GCS relies on evaluating clinical findings related to three aspects of responsiveness: eye-opening, verbal and motor responses (total scores range from 3, completely unresponsive, to 15, fully responsive). Severity of TBI is classified as mild (GCS score 13–15), moderate (score 9–12) or severe (score less than 9).

The Mayo classification (Malec Reference Malec, Brown and Leibson2007) is an alternative system, often used by specialists in neurology and neurosurgery. It relies on evaluating clinical factors and CT scan results, classifying TBI severity in three categories: Moderate-Severe (Definite); Mild (Probable); and Symptomatic (Possible). The criteria for this system are outlined in Box 3.

Although the GCS and Mayo criteria are both widely used, they are not without problems. These include the stigma and expectations associated with being assigned a categorical marker of injury severity: for example, a patient with ‘mild’ TBI on the GCS may feel frustrated if they experience long-term symptoms, and classifying someone as having ‘severe’ TBI may lead to hopelessness. Furthermore, both systems lack details of the traumatic incident, the GCS lacks neuroimaging and Mayo criteria do not include blood results – these are all factors required to inform decision-making regarding treatment and suitability for clinical trials (Manley Reference Manley, Dams-O’Connor and Alosco2025).

NIH-NINDS classification and nomenclature

In 2022, the US National Academies of Science, Engineering and Medicine (2022) made recommendations for a new classification for TBI. In the same year, the US National Institutes of Health (NIH) and NINDS launched an international initiative to characterise TBI more accurately. This resulted in the NIH-NINDS TBI Classification and Nomenclature. In the NIH-NINDS framework, the diagnosis of TBI rests on four pillars: a clinical pillar, which consists of the GCS and pupil responses; a biomarker pillar; an imaging pillar; and a modifier pillar, outlining features that affect the patient’s clinical presentation and outcome (Manley Reference Manley, Dams-O’Connor and Alosco2025). The NIH-NINDS classification enables a clinically informed descriptive brain injury picture that meaningfully informs decision-making regarding treatment interventions, helps identify suitability for clinical trials and engenders hope for recovery (Manley Reference Manley, Dams-O’Connor and Alosco2025).

Post-traumatic amnesia

Post-traumatic amnesia (PTA) is a state of altered consciousness following TBI and occurs in over 70% of individuals admitted to hospital with TBI. The condition is characterised by anterograde amnesia but also includes wider cognitive impairments, confusion, behavioural disturbances and agitation (Marshman Reference Marshman, Jakabek and Hennessy2013). A number of scales are available to measure the severity of post-traumatic amnesia. Examples include the Westmead Post-Traumatic Amnesia Scale (WPTAS) for moderate to severe TBI, the Abbreviated WPTAS (A-WPTAS) for mild TBI and the Galveston Orientation and Amnesia Test (GOAT).

The presence and duration of post-traumatic amnesia is used in neurosurgical wards to predict prognosis and inform management. This includes determining whether patients have capacity for decision-making about treatment options, deciding the level of supervision a patient requires, whether referral for in-patient rehabilitation is necessary and suitability for hospital leave, and discharge planning. The duration of post-traumatic amnesia can also help predict length of in-patient treatment as well as cognitive and functional recovery (Marshman Reference Marshman, Jakabek and Hennessy2013).

Spasticity

Spasticity following TBI occurs in 55% of patients admitted to in-patient rehabilitation units and includes muscle hypertonicity, spasms, heightened reflexes and the presence of clonus, which is the involuntary repetitive contraction of muscles, often in a rhythmic nature (Dragojlovic Reference Dragojlovic, Romanoski and Verduzco-Gutierrez2022). Spasticity following TBI requires multidisciplinary treatment, which can include medication such as baclofen or diazepam, physical therapy such as stretching exercises or use of splints or casts, and, in severe or refractory cases, surgical intervention (Zafonte Reference Zafonte, Elovic and Lombard2004).

Post-TBI fatigue

Post-TBI fatigue (PTBIF) is reported to occur in 21–70% of individuals and can have pervasive adverse effects on day-to-day activities, including capacity for physical rehabilitation, work or social activities, and can also impair concentration (Cantor Reference Cantor, Ashman and Bushnik2014). The effects can be chronic and impair overall recovery. Methylphenidate and melatonin have been found to help reduce symptoms in post-TBI fatigue. Exercise in the form of walking or water aerobics has also been found to be effective (Ali Reference Ali, Morfin and Mills2022).

Post-traumatic epilepsy

An increased risk of epilepsy has also been found following TBI. Concussive seizures occur immediately after the trauma, early seizures within 7 days and late seizures after 7 days. The risk of post-traumatic epilepsy (PTE) increases with severity of TBI.

A population-based retrospective cohort study (Yeh Reference Yeh, Chen and Hu2013) reported the risk of seizures in the general population to be 0.29%, with the risk of late seizures increasing only modestly (1.1%) following mild TBI. The risk increased to 1.6% for patients with contusions, 2.2% when positive brain injury findings on imaging were present, 4.8% with skull fracture, 4.8% with subarachnoid haemorrhage, 6.3% with extradural haemorrhage, 7.8% with subdural haemorrhage, 10.2% with intracerebral haemorrhage and 13.9% when multiple haemorrhages were present. The risk of epilepsy following TBI persisted for several years following the initial trauma and then gradually reduced. Risk factors for post-traumatic epilepsy, in addition to trauma, included alcohol misuse, signs of ageing in the brain and a family history of epilepsy.

Persisting symptoms after concussion

Concussive symptoms often heighten within hours or days after head injury and then gradually ameliorate. It has been reported that in 80–90% of cases of concussion, symptoms will resolve within 2 weeks of the head injury (Makdissi Reference Makdissi, Darby and Maruff2010), with resolution in most cases typically expected within 30 days (Patricios Reference Patricios, Schneider and Dvorak2023). However, the course of recovery is variable and influenced by modifying factors. Longer-lasting concussive symptoms are associated with more severe initial symptoms, history of previous concussions, the development of headaches or depression, history of mental health problems and being a female teenager of high school age (Iverson Reference Iverson, Gardner and Terry2017).

The diagnosis of post-concussion syndrome is now considered outdated, given that concussive symptoms may not be specific to the head injury and the diagnosis gives no indication of the prospects for recovery or potential to benefit from treatment (Broshek Reference Broshek, Pardini and Herring2022). Following a working group at the International Congress of the Athlete Brain Health Foundation in 2019, calls were made for new terminology to be used when describing concussive symptoms that persist beyond the typical timescale for recovery (Broshek Reference Broshek, Pardini and Herring2022). It is generally accepted that, rather than a specific time period for recovery, the overall recovery trajectory should be considered to evaluate whether concussive symptoms are worsening in the days or weeks after the head injury and whether new symptoms are starting to occur. The working group called for a paradigm shift in the management and treatment of all individuals who do not recover within the typical time frame after concussion, suggesting that if symptoms are not improving or new symptoms are appearing approximately 1 month after the head injury, a diagnosis of persisting symptoms after concussion (PSaC) should be made.

The term persisting symptoms after concussion (or, similarly, persisting post-concussion symptoms) is preferred to post-concussion syndrome, persistent post-concussion symptoms or persistent symptoms after concussion, as it highlights that symptoms occurring after the head injury may have contributory, secondary or alternative causes, such as changes in a person’s physiology, mental health, level of functioning or social circumstances and are time limited and amenable to treatment (Broshek Reference Broshek, Pardini and Herring2022; Fordal Reference Fordal, Iverson and Maietta2025).

Both ICD-10 and DSM-IV included post-concussion syndrome as diagnostic terms, but the diagnosis is no longer contained in ICD-11 or DSM-5. DSM-5 instead uses the term ‘neurocognitive disorder due to TBI’ and subclassifies this as being mild or major depending on symptom severity (American Psychiatric Association 2022). In ICD-11, post-concussion syndrome now falls under the diagnosis ‘mild neurocognitive disorder’ (World Health Organization 2022). However, mild neurocognitive disorder has a range of aetiologies, so when using ICD-11 for diagnostic purposes, the condition should be recorded as mild neurocognitive disorder due to TBI.

Factors associated with prolonged duration of PSaC include acute cognitive symptoms, pre-existing anxiety and/or depression, sleep disorders, loss of consciousness at the time of injury and post-traumatic amnesia (McIntosh Reference McIntosh, Vergeer and Galarneau2025). Symptoms may be long term: persisting problems with concentration following head injury have been reported up to 10 years after the initial concussion (Faulkner Reference Faulkner, Theadom and Snell2023).

Targeted interventions for PSaC should focus on improvement of specific symptoms and increased functioning. Psychiatrists should take the lead in treating any mental health conditions that are present, such as depression, given its significant role in perpetuating symptoms. Cognitive–behavioural therapy incorporating psychological principles specific to the patient’s needs is recommended to promote rehabilitation and recovery (Silverberg Reference Silverberg and Iverson2023). Medical treatment of treatable persisting symptoms, such as fatigue, headaches, sleep problems, and vestibular and oculomotor disturbance should be considered (Herring Reference Herring, Kibler and Putukian2021). Addressing physiological factors, problems with behaviour, cognition and emotions, and social factors such as the ability to take part in work are important treatment goals (Fordal Reference Fordal, Iverson and Maietta2025).

Functional neurological disorder

Functional neurological disorder (FND) is a neurological condition involving changes in how brain networks work, leading to genuine, non-intentionally produced physical symptoms that cannot be explained by changes in the structure of the brain. Symptoms can affect any part of the body, last from days to years and typically increase with attention and reduce with distraction. Although neurological tests and braining imaging may prove negative, functional neuroimaging and neurophysiological tests increasingly demonstrate abnormalities related to connectivity between different brain regions, suggestive of brain signalling failures leading to physical symptoms.

FND has been divided into functional/dissociative seizures and functional movement disorder. The latter typically involves limb weakness or paralysis, abnormalities of gait, tremors, myoclonus, dystonia, muscle stiffness, spasms and tics (NINDS 2024). Functional movement disorder following TBI is diagnosed when symptoms such as limb weakness, paralysis, stuttering, swallowing problems or visual disturbances occur that are inconsistent with PSaC but fit the criteria for FND. FND may be an isolated finding or may occur comorbidly with other neurological disorders and/or PSaC. The careful evaluation and identification of FND therefore enables tailored treatment. This includes adapting rehabilitation to take into account FND, such as using distraction techniques during gait therapy (Nielsen Reference Nielsen, Stone and Matthews2015). Psychological therapies such as cognitive–behavioural therapy and psychodynamic therapy have also been found to improve symptoms (LaFrance Reference LaFrance, Tedesco and Baird2023).

Functional/dissociative seizures

In 2017, the International League Against Epilepsy (ILAE) Psychiatry Commission mandated a task force to review terminology used for what was previously termed psychogenic non-epileptic seizures (PNES) (Hingray Reference Hingray, Popkirov and Kozlowska2025). Following a consultation process from 2021 to 2025, which included two workshops, the task force proposed the term functional/dissociative seizures (FDS). This terminology enables clinicians to choose between functional, dissociative or a combination of both terms to describe seizures depending on the circumstances and characteristics of each case.

A review article reported that 81–89% of cases of FDS occurred within the first year following TBI and that 20% of patients referred to epilepsy clinics with a diagnosis of post-traumatic epilepsy were found to actually have FDS (Fordington Reference Fordington and Manford2020). FDS do not generally respond to anti-epileptic medication and psychological therapy is therefore recommended (Reuber Reference Reuber, Pukrop and Bauer2003).

Diminished motivation, apathy and abulia

TBI associated with damage to the prefrontal cortex and ventral pallidum can cause disorders of diminished motivation associated with a reduction in goal-directed behaviour, thoughts and emotions and a loss of spontaneity, and can lead to significant functional impairment, with impaired quality of life (Smith Reference Smith, Tindell and Aldridge2009; Palmisano Reference Palmisano, Fasotti and Bertens2020). These changes occur in the absence of cognitive or motor deficits that would otherwise explain the observed findings (Marin Reference Marin and Wilkosz2005; Palmisano Reference Palmisano, Fasotti and Bertens2020). Apathy involves a milder loss of motivation, whereas abulia is a severe loss of motivation resulting in significantly reduced drive, reduced speech and lack of concern for safety.

Therapeutic interventions for diminished motivation following TBI include therapies involving graduated tasks such as goal-setting therapy (Lane-Brown Reference Lane-Brown and Tate2009). Pharmacological treatment for abulia includes use of dopamine agonists such as methylphenidate (Zhang Reference Zhang and Wang2017).

Emotion dysregulation, irritability and anger

Emotion dysregulation is a common feature following TBI and can occur in isolation or as part of other mental health problems, such as depression or PTSD. Symptoms of emotion dysregulation include mood swings, irritability, agitation and anger.

Emotion regulation is a complex process utilising the ventromedial prefrontal cortex as well as subcortical structures such as the amygdala, hippocampus and periaqueductal grey matter (Rice Reference Rice2016). It has been postulated that molecular changes following TBI adversely affect the neural pathways involved in emotion regulation, leading to symptom presentation (Weiss Reference Weis, Webb and DeRoon-Cassini2022).

Where underlying mental health conditions such as depression or PTSD are present, psychiatrists should lead on their treatment. In cases where emotion dysregulation occurs in isolation, specific treatment interventions may be attempted based on the presenting symptoms. Isolated problems with irritability and aggression have been shown to improve following treatment with amantadine or beta-blockers such as propranolol (Hammond Reference Hammond, Malec and Zafonte2017). Medications with mood-stabilising properties, such as valproate and carbamazepine, have been found to improve behavioural dyscontrol following TBI (Azouvi Reference Azouvi, Jokic and Attal1999; Lindenmayer Reference Lindenmayer and Kotsaftis2000). Lamotrigine and lithium have been shown to improve agitation (Pachet Reference Pachet, Friesen and Winkelaar2003), and antidepressant medication has been shown to help improve aggression (Mysiw Reference Mysiw, Jackson and Corrigan1988).

Depression

Depression is reported to occur in 9–30% of individuals in the first 12 months post-TBI (Ouellet Reference Ouellet, Beaulieu-Bonneau and Sirois2018). The risk of developing depression following TBI has been found to be higher among females, those with a history of depression or psychiatric problems, those who are unemployed, have severe physical injury and/or injuries due to traffic accidents or violence, and those with a smaller brain volume (Mikolić Reference Mikolić, Van-Klaveren and Jost2025).

Selective serotonin reuptake inhibitor (SSRI) medication remains a safe and well-tolerated treatment for depression following TBI. Tricyclic antidepressants have also been found to be effective, with desipramine and nortriptyline being the most tolerated. Tricyclics have the additional benefit of assisting with problems related to neuropathic pain, headaches and insomnia, which are often found to be persisting symptoms. Medications such as the alpha-blocker prazosin, and moclobemide, which is a reversible monoamine oxidase A inhibitor, have been found to be effective. Repetitive transcranial magnetic stimulation (rTMS) has also shown beneficial effects. A range of studies have demonstrated the effectiveness of psychological therapies in treating depression following TBI, including use of cognitive–behavioural therapy (Fann Reference Fann, Quinn and Hart2022).

Suicidality

Suicidal thoughts and the risk of engaging in suicide attempts are significantly increased following TBI (De Luca Reference De Luca, Calderone and Maggio2025). The factors most frequently associated with an increased risk of suicide are comorbid depression, feelings of hopelessness and substance misuse (Lu Reference Lu, Wu and Zhang2020).

Psychiatrists should manage the risk of suicide in patients with TBI, communicating the risk appropriately to the brain injury team and engaging interventions appropriate to the risk presented, such as formulating a safety plan, referral for psychological support, involvement of crisis resolution and home treatment teams or in-patient admission where required.

Pseudobulbar affect

Pseudobulbar affect is characterised by the occurrence of frequent episodes of short-lived intense emotions, often laughing followed by crying. These episodes can occur without a specific trigger or may be an exaggerated or incongruous response, causing significant social distress. Pseudobulbar affect can occur in isolation or comorbidly with other conditions, such as depression (Zeilig Reference Zeilig, Drubach and Katz-Zeilig1996).

When depression occurs secondary to the debilitating effects of pseudobulbar affect, specific treatment for both conditions should be given. Pharmacological treatment for pseudobulbar affect caused by TBI includes use of dextromethorphan, quinidine, SSRIs and tricyclic antidepressants (Fann Reference Fann, Quinn and Hart2022).

Anxiety, adjustment disorder and PTSD

Anxiety may be subclinical, occur in isolation or as part of other psychiatric disorders. Anxiety immediately following a TBI may subside and resolve over time. Distress, anxiety or depressive symptoms occurring within the first month after a TBI that become persisting can lead to a diagnosis of adjustment disorder due to the distress of adapting to potentially life-changing circumstances following TBI. Anxiety may occur as part of PTSD. The prevalence of PTSD following TBI has been reported to be around 16% (Van Praag Reference Van Praag, Cnossen and Polinder2019).

Treatments for anxiety following TBI should be based on the presenting symptoms and underlying diagnosis. Severe anxiety may benefit from short-term use of benzodiazepines. Antidepressant medication for anxiety has been shown to be effective. SSRIs such as sertraline and the serotonin–noradrenaline reuptake inhibitor (SNRI) venlafaxine have been found to be effective for PTSD following TBI. Psychological therapy post-TBI remains an important treatment (Fann Reference Fann, Quinn and Hart2022).

Psychosis, schizophrenia and bipolar disorder

In rare cases, TBI has been found to increase the risk of mania and psychosis. This includes an increased risk of schizophrenia and bipolar disorder, with moderate and severe TBI being associated with higher risks, especially among older adults and females. Pathological explanations for the increased risk include a reduction in the effectiveness of the blood–brain barrier in blocking inflammatory molecules and the effects of axonal degeneration (Zhao Reference Zhao, Topolski and Tusconi2022).

Psychiatrists should consider the possibility that the TBI may have contributed to the development of psychosis. Where this is suspected, treatment with antipsychotics is recommended, with initial reviews suggesting atypical antipsychotics are to be preferred. Mood stabilisers can be used where indicated, with valproate being shown to have fewer neurocognitive side-effects compared with lithium and carbamazepine (Fann Reference Fann, Quinn and Hart2022).

Chronic traumatic encephalopathy and traumatic encephalopathy syndrome

TBI should be differentiated from chronic traumatic encephalopathy, which is recognised both in the literature and in clinical practice as a distinct clinical condition. Chronic traumatic encephalopathy is a progressive neurodegenerative condition caused by repeated head injury leading to cellular changes in the brain, followed by a highly specific pattern of hyperphosphorylated tau (p-tau) protein deposition (Munakomi Reference Munakomi and Puckett2024). The greatest risk factor for developing chronic traumatic encephalopathy is repeated head injury from contact sports such as boxing, with greater length of exposure increasing the risk of developing the condition (Munakomi Reference Munakomi and Puckett2024). Although the condition is associated with a history of repeated head injury, a clear pattern of neurocognitive changes and cerebral atrophy with ventricle enlargement (McKee Reference McKee, Mex and Abdolmohammadi2023; Munakomi Reference Munakomi and Puckett2024), a definitive diagnosis can only be made neuropathologically by way of post-mortem identification of perivascular p-tau protein aggregates involving neurons extending deeper than the subpial layer (McKee Reference McKee, Mex and Abdolmohammadi2023).

Previous descriptive terms for the clinical manifestation of chronic traumatic encephalopathy have included punch drunk syndrome, following the pathologist Harrison Martland’s findings in 1928 of perivascular microhaemorrhages in the brains of deceased boxers, and dementia pugilistica, reported by J.A. Millspaugh in 1937. Montenigro and colleagues coined the term traumatic encephalopathy syndrome in 2014, in a paper attempting to define diagnostic research criteria. They highlighted cognitive, behavioural and mood symptoms as the three core features of the condition, with an additional nine supportive features (delayed onset, documented decline, headache, anxiety, apathy, impulsivity, paranoia, motor signs and suicidality) (Montenigro Reference Montenigro, Baugh and Daneshvar2014). However, this diagnostic rubric is considered to be problematic and non-specific. To address these difficulties, NINDS led on the development of up-to-date consensus research diagnostic criteria for traumatic encephalopathy syndrome (Katz Reference Katz, Bernick and Dodick2021), as summarised in Box 4.