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Original Article

Long-term psychiatric disorders after traumatic brain injury

Fleminger, S.*,†

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European Journal of Anaesthesiology: February 2008 - Volume 25 - Issue - p 123-130
doi: 10.1017/S0265021507003250



This review will consider the long-term psychiatric sequelae of head injury. Personality change, psychotic illness and mood disturbance, including the anxiety disorders, will be considered. Issues related to cognitive impairment will not be addressed except in so far as they impact on these psychiatric syndromes. Nor will this review address the complex and poorly defined post-concussion syndrome [1], despite its possible association with anxiety and depression. The role of psychiatric sequelae on the long-term functional outcome of head injury will be reviewed.

The selective vulnerability of certain parts of the brain to contusions following traumatic brain injury (TBI) partly explains why neuropsychiatric problems are often the most disabling sequelae of head injury. The orbital surface of the frontal lobes, particularly medially, and the temporal lobes, especially on the undersurface and anteriorally, are particularly vulnerable. These areas of the brain have a key role in social behaviour. As a consequence, TBI is a potent cause of disturbance of social behaviour. The personality change, often with disruptive or thoughtless behaviour, is likely to come to the attention of the psychiatrist or psychologist.

The contusions that are likely to affect social behaviour are to be found adjacent to where the brain meets the bone of the skull. Indeed it is probable that the damage occurs when the brain is injured as it hits the adjacent bone of the inner surface of the skull. As a result, the computed tomography (CT) brain scan is not the best neuroimaging modality to detect the contusions. CT brain scans are vulnerable to imaging artefacts at the brain-bone interface because of the very high signal of the bone compared to the brain. In addition, CT brain scans are generally less sensitive to subtle damage than is magnetic resonance imaging (MRI). Therefore, MRI scanning is the preferred modality for investigating neuropsychiatric sequelae in the longer term after TBI. The MRI imaging should include Gradient Echo T2 sequences, because these are the most sensitive way of detecting the haemosiderin that may be left behind after a haemorrhagic contusion [2].

One key role in the investigation and management of the neuropsychiatric sequelae of head injury is to ensure that there are no complications of the injury. Chronic subdural haemorrhage and hydrocephalus can present with failure to improve or a deterioration in the mental state, and may need active neurosurgical intervention. Epilepsy may complicate the picture in various ways. Sometimes brief-lived altered mental states are due to complex partial seizures. The development of major seizures, perhaps not till months after injury, can severely jeopardize recovery in part because of the psychological reaction to the diagnosis. And epilepsy may increase handicap, for example, because driving is forbidden. Some suggest that episodic outbursts of uncontrollable temper, episodic dyscontrol, an occasional symptom following TBI, is based on epileptic discharges in the temporal lobe, particularly involving the amygdala [3]. Cerebral infection is a rare complication, usually related to open head injury or where there has been a cerebrospinal fluid (CSF) leakage. Electrolytes may be disturbed due to pituitary damage.

Aetiology of psychiatric symptoms

Severity of brain injury

Neuropsychiatric assessment is likely to start with an assessment of the injury severity. The first task is to estimate the likely contribution of brain damage to the mental sequelae. Injury severity measures, taken at the time of the injury, will be determined (Table 1). This will be supplemented by consideration of the neurological sequelae, neuropsychometry and neuroimaging findings. By and large, the electroencephalogram (EEG) is not very valuable - indeed, studies have found that symptomatic patients after milder head injuries with abnormal EEGs are likely to do better than similar patients but whose EEG is normal [4].

Table 1
Table 1:
. Measures of injury severity.

Of the measures of injury severity, duration of loss of consciousness and duration of post-traumatic amnesia (PTA), the period from the time of injury to the return of continuous day-to-day memories, are probably the best for predicting outcome.

By and large the severity of brain injury will correlate reasonably well with the development of cognitive impairment and personality and behaviour changes. Aspects of cognition that are particularly vulnerable, even in the presence of diffuse brain injury, include speed of information processing, memory and executive function. On the other hand, in some patients the TBI may be relatively focal so that the patient, for example, shows a relatively severe aphasia in the absence of other impairments. In patients with the severest injuries, there is global and severe cognitive impairment. In such patients, changes in behaviour and personality are inevitable. The patient is likely to demonstrate reduced initiative, lack of awareness of the needs of others, an intolerance of changes in routine and stimulus-dependent behaviour such that they are distracted by, and respond to, sensory cues. They may be agitated or obtunded and be disinhibited, rude and violent. These problems are likely to be aggravated by the lack of insight and the lack of awareness of personal hygiene and safety.

Pre-injury constitution

Once the clinician has a reasonably confident grasp of the severity of the injury, it is necessary to turn to other factors that may lead to the development of psychiatric symptoms. It is therefore important to enquire about the patient's premorbid constitution. Have they already suffered mental health problems or is there a relevant family history? An underlying vulnerability to antisocial behaviour may only be revealed by a history of difficulties during adolescence. Pre-injury dependence on drugs and alcohol is a predictor of problems post injury, not just in the domain of continuing abuse of drugs and alcohol [5]. Is there evidence of previous brain injury, for example, because of an earlier head injury? It is known that some people seem to be injury prone, and having a head injury may make a person more likely to have further injuries. Is there a history of physical symptoms in the absence of physical illness, and therefore a vulnerability to somatization disorder? If so, this may be relevant in understanding why they now have severe persistent post-concussion symptoms after a very mild head injury.

Psychological effects of the trauma

The physical effects of the head injury, in terms of brain injury, have already been discussed. But what of the psychological consequences of the injury itself? When the patient is asked what they remember of the accident, in order to determine the duration of the retrograde (loss of memories leading up to the accident) and PTA, it is important to allow the patient to describe how those memories have affected them. For example, terrifying memories of being trapped in the car after impact, or of frightening hallucinations during the post-traumatic delirium, can lead to very troublesome post-traumatic stress disorder (PTSD). Although PTSD is less likely in those with prolonged unconsciousness [6], amnesia for the injury does not prevent PTSD [7]. Pilowsky [8] has coined the term ‘cryptotrauma' to describe the psychological stress that is occasionally found when the injury has some idiosyncratic and frightening meaning for the patient. If an injury, particularly a mild injury, occurs while the patient is having difficulties at home or work, then the patient is more likely to run into difficulties. Injuries that are the result of negligence or violence cause greater psychological effects than those that are perceived to be an ‘act of God' [9]. It is also necessary to consider the psychological effects of the other injuries sustained. For example, a recent study has highlighted the suffering some patients experience as a result of the facial scarring that many head-injured patients bear [10].

Post-traumatic life events

Finally the sequelae of the injury need to be explored to allow a full understanding of the causes of psychiatric symptoms. Psychological sequelae are more likely if as a result of the injury the patient is now facing social and financial problems. A not uncommon scenario occurs as the patient attempts to return to work. This is likely to expose subtle, yet potentially quite disabling, cognitive impairments that were previously not evident while the patients was convalescing in hospital and at home. Many react to the discovery that they are less efficient cognitively or that their memory is now letting them down, with increasing anxiety. This anxiety is likely to exacerbate any cognitive impairment and also intensify disabling symptoms like fatigue and headaches. There is therefore the potential for a vicious cycle with increasing anxiety causing greater symptoms and increasing anxiety further.

On the other hand, for some patients it is the social effects of the injury that are most damaging. Irritability and self-centred behaviour and changes in sexual behaviour may result in the break up of supportive relationships. Social networks tend to get smaller after TBI. It is not uncommon for a patient to find themselves isolated at a critical time when they are most in need of support, both emotionally and in terms of helping to restructure their life. In some patients drug and alcohol dependence are critical factors in determining a healthy recovery. In those who have suffered dependence before and at the time of the injury, it is not uncommon to observe a honeymoon period in the aftermath of the injury, such that during convalescence there is no evidence of craving or problems with drug-seeking behaviour. In the occasional patient this is maintained indefinitely and the injury seems to have acted to cure the dependence. But in the majority as recovery proceeds and as previous drug/alcohol taking cues return, e.g. walking past the local pub, so does the dependence. Indeed the brain injury may now undermine any previous control the patient had over their dependence. In addition, they are likely to be less tolerant to the alcohol or drug as a result of the brain injury. For example, many patients describe how they now get drunk on much smaller quantities of alcohol.

In some patients it may be an independent life event that is critical. For example, the chance death of a spouse may make all the difference between a healthy recovery and a collapse into severe depression; the bereavement is the last straw.


Other factors to consider include whether or not the patient is seeking compensation. Patients involved in a compensation claim have more symptoms on average than patients with injuries of equivalent severity but who are not seeking compensation; the effect of compensation is greater for milder injuries [11].

Psychiatric syndromes after head injury

Personality change

A change in personality refers to changes in the way the person generally behaves and how they react. It implies a long-standing change, though somebody who shows a variable pattern, for example, being pleasant and friendly for most of the time yet with periods of intense social withdrawal and anger lasting for hours, will often be described as showing personality change. As such, personality change overlaps with changes in mood and cognition. Somebody who is depressed or with a labile mood, or with severe global impairment of cognition will inevitably show changes in behaviour. Particularly for families and carers, personality change is one of the most distressing sequelae of head injury. It is a frequent cause of problems in returning to work.

The selective vulnerability of the orbitofrontal and anterior temporal lobes to contusions [12] partly explains why personality change is so troublesome. It is these areas of the brain that play a major role in social behaviour. For example, one model of ‘social cognition' is based on a hypothesis about the effects of orbitofrontal injury on interpreting unconscious cues that indicate that a decision that is about to be taken might be unwise in terms of its longer term social consequences [13].

After head injury, the most frequent changes in personality are not easily described by standard personality disorder classifications. Nevertheless, when such criteria are applied to cohorts of head-injured patients, the most common categories identified are in the domains of avoidant, borderline and paranoid personality disorder [14,15]. Lezak [16] proposes five domains of personality change:

  • reduced social perceptiveness;
  • reduced control and self-regulation;
  • problems initiating and planning behaviour, which is often stimulus bound;
  • emotional change especially apathy, silliness and lability;
  • difficulties learning from experience.

In those with very severe injuries, typical changes include disinhibition, apathy, irritability and labile mood, and self-centred and thoughtless behaviour. The severe cognitive impairment restricts the patient's understanding and appreciation of the environment and is often associated with poor insight. The patient may become child-like and spouses frequently describe how the role in the partnership has changed from being equal partners before the injury with both involved in decision making, to one that is more like parent and child.

On the other hand, in some patients personality change is to be found in the absence of cognitive impairment. In some this is caused by a psychological reaction to the injury, which has, for example, resulted in a chronic anxiety reaction perhaps associated with PTSD. But in others a discrete brain injury may cause an isolated change in social behaviour, with little or no effects on performance on neuropsychological testing. This is particularly the case with orbitofrontal lesions. But even in such patients more sophisticated testing may show impairments in tasks that require control of goal-directed behaviour or tests of social cognition. Tate [17] suggests that it is possible to predict changes in personality, viz. loss of emotional control, by scores on a test of executive function.

Studies of males suffering open head injuries in war have demonstrated that frontal lobe injury is particularly likely to produce personality change. For example, Feuchtwanger [18] compared 200 frontal wounds with 200 cases with injury to other parts of the skull. In those with frontal injuries, various changes were observed including defects of attention, euphoria and facetiousness, irritability or apathy. Many were described as tactless or lacking in moral behaviour. Lishman [19] found that a frontal lobe syndrome with euphoria, disinhibition, facile or childish behaviour and lack of judgment was most common after frontal injury, though 9 of the 32 veterans with such changes had little evidence of any frontal injury. It has been suggested [20] that frontal injury may produce a ‘pseudodepressed' syndrome with apathy and indifference, or a ‘pseudopsychopathic' change with antisocial and puerile behaviour, often accompanied by tactless, impulsive and irritable behaviour. The former is more common with convexity lesions, over the lateral surface, whereas the latter was associated with medial and orbital frontal lesions.

Irritability and aggression are particularly troublesome sequelae. A few patients require long-term secure accommodation because of their propensity for violence, although this is usually only in those with severe cognitive impairment. Some of the increased risk of aggression relates to pre-injury factors; many suffer their head injury because of risk taking or fights. On the other hand, those who suffer head injuries are at a greater risk of aggression than if the injury is to other parts of the body [21]. And the increased risk is particularly associated with frontal lobe damage [22].

It is said that uncontrolled rage attacks, with trivial provocation and with no obvious gain from the violent behaviour, are typical of the brain-injured patient, and that this is in contrast to the cold planned goal-directed aggression that is found in people with antisocial personality disorder. The organic aggression syndrome [23], or episodic dyscontrol syndrome, may be triggered by small quantities of alcohol. This observation perhaps supports the idea (see above) that epileptic-like discharges in the limbic system, including the amygdale, are responsible [3].


In the early stages of recovery after a severe head injury, a transient delusional misidentification is occasionally seen. This may accompany or post date the acute confusional state. For example, the patient may believe that the patient in the bed opposite is their mother, or that they are in a duplicate of the hospital at some distant location. A common delusion is that they are still at work. Brief-lived confabulations are common, for example, the belief that someone visited them the day before, whereas in fact there was no such visit. In a very few patients, usually those who are left with severe global cognitive impairment and lack of insight, such beliefs become chronic.

Large-scale epidemiological studies are needed to answer the question whether head injury is a risk factor for schizophrenia. There have been several studies, including small case-control studies, of patients who have been found to have post-traumatic psychoses that, for example, show that the majority of such psychoses are not due to post-traumatic epilepsy [24]. The finding from these studies is in line with clinical experience; a small proportion of cases, particularly those with severe head injury, develop a non-affective psychosis often involving non-systematized persecutory or grandiose delusions with or without hallucinations. But there are no good follow-up studies designed to test the hypothesis that head injury may produce schizophrenia. Some cohort studies have suggested that a surprisingly high rate of patients go on to suffer psychoses [14], but these studies are not adequately controlled. Head injuries are particularly common in males in their late teens and early 20s, and these males are at high risk of developing schizophrenia anyway. This effect is compounded by the observation that head injuries may be more common in families with a proband with schizophrenia [25]. If there is any association between head injury and schizophrenia, it may be a result of ‘reverse causality' [26].

Two large studies from Denmark [27] and Sweden [28], based on linkage of nation-wide hospital case registers, have shown that there appears to be no elevated risk of being admitted to hospital with a diagnosis of schizophrenia in those who have suffered a previous head injury. The Swedish study suggested that there might be a slight increased risk of non-affective psychoses, not diagnosed as schizophrenia. These studies do suggest that less-severe head injuries are not a risk for schizophrenia. But it seems unlikely that their design, resting as it does on the diagnosis given to patients on admission to hospital, can rule out the possibility that there is an increased risk of a chronic psychosis in those who are severely injured. Such patients are likely to be receiving care anyway, and hence are probably less likely to be admitted because they are psychotic, and if admitted would be given a diagnosis of organic psychosis, not schizophrenia.

Mood and anxiety disorder

In patients who have suffered a brain injury, it can be difficult to disentangle direct effects of the brain injury on behaviour, from those effects that are a manifestation of mood disturbance. For example, apathy with impairment of motivation is a common consequence of severe injury, perhaps as a result of damage to dopaminergic pathways involved in appetitive behaviour. Yet these symptoms may be evidence of a depressive illness. This would be particularly likely if increasing social withdrawal and disengagement from rehabilitation were of recent onset, months or years post injury. On the other hand, symptoms of mania may easily be confused with changes in personality associated with the frontal lobe syndrome, e.g. sexually disinhibited, thoughtless or fatuous behaviour. It is therefore important to have a high index of suspicion for mood disorder, and a willingness to explore this with a trial of psychotropic medication.

There is good evidence that head injury is a risk factor for bipolar disorder though the effect is not large; head injury survivors are about 1.5 times as likely to develop bipolar disorder as those without a head injury [29]. But bipolar disorder is uncommon, at most a small percentage of cases. Affective psychoses are therefore rare. There are occasional reports of patients suffering from nihilistic delusions when depressed [30].

On the other hand, major depression is a common sequelae. Estimates of the rates of depression after head injury vary widely [31]. Conservative studies find only about 14% meeting the criteria for major depression at 1 yr [32]. Several surveys describe 20-30% of patients become depressed during the first year (e.g. Jorge and colleagues [33]). The depression is quite mobile over the first year; many patients who are initially depressed recover, while some only develop depression at a later stage in recovery. On the other hand, some longer term outcome studies suggest that the prevalence of depression increases over time (e.g. 60% at 7 yr [34]), but others find much less worrying figures (life time prevalence = 18% [35]). It seems likely that psychosocial factors have a major impact on whether or not someone is depressed at longer post-injury intervals, and this explains the wide variation in reported prevalence. Some cohorts, for example, veterans from WWII, will be protected because of the esteem in which they are held and their financial security, whereas some civilian cohorts may be disadvantaged even before their head injury [36].

There is no good evidence that the symptoms of depression in the head-injured person differ from depression in patients without brain injury. Nevertheless, fatigue, concentration impairment and frustration are commonly seen [37]. Feelings of deprecation and hopelessness show good discrimination between head-injured patients who are depressed and those who are not [38]. On the other hand, biological symptoms of depression, like sleep disturbance, are less useful. Sleep disturbance is seen after head injury regardless of depression. Irritability is common and may be due to depression.

Anxiety after head injury is also common, as are mixed states of anxiety and depression. Sometimes anxiety is associated with good evidence of PTSD. PTSD may be manifest even when memories of the accident are limited by loss of consciousness, so that flashbacks are absent. Nightmares, hyperarousal and avoidance of situations that remind the patient of the accident, all suggest that PTSD may be active. Those who develop an acute stress reaction are more likely to develop PTSD [39]. PTSD may overlap with travel anxiety if the patient was injured, for example, in a road traffic accident [40].

Generalized anxiety disorder occurs in perhaps 10-15% of cases [41]. It is often associated with agoraphobia and/or panic disorder. As noted above, anxiety probably plays an important part in the problems that some patients experience when they return to work. It has been proposed that increasing anxiety over the weeks and months post injury, by jeopardizing a healthy recovery, may contribute to persistent post-concussion symptoms [42]. Headache, fatigue and concentration problems are all likely to be aggravated by increased anxiety.

Rates of suicide are increased after a head injury by the order of three- to fourfold [43]. But some of this excess risk may be personality factors, for example, risk-taking behaviour, which were present before the head injury, that are associated both with an increased risk of suicide and with an increased risk of head injury.

Long-term follow-up

Once about 2-5 yr have passed after a head injury, the majority of patients remain quite stable. They do not change much in the long term, though a small proportion continue to improve a little. However, several studies over the last few years suggest that some patients decline in function over time. In other words, compared with how there were a year or two post injury, the person is now, several years later, less independent. For example, in one study [44] when patients were followed up after 18 yr, twice as many had deteriorated (32%) as had improved (15%) compared with how there were on the Glasgow Outcome Scale at 6 months post injury. A study with similar findings, but at 5 yr follow-up [45], noted that those who deteriorated compared with those who improved were more depressed and anxious, had lower self-esteem and had more problems with alcohol.

It has been suggested that one cause of long-term decline is the development of Alzheimer's disease or other dementing illness; in other words, head injury is a risk factor for Alzheimer's disease. A meta-analysis of case-control studies that have looked at this suggests that there may be a small effect, particularly in males [46], and this finding is supported by one long-term follow-up of head-injured World War II veterans [47].


The management of psychiatric sequelae of head injury starts with investigations to rule out secondary complications, for example, hydrocephalus or subdural haemorrhage. In the early stages of recovery good general, surgical and nursing management is essential, for example, to minimize the period of acute confusion and facilitate rapid mobilization. The patient will then need timely access to rehabilitation. For the more severely injured patient, there is little doubt that prolonged care in the restricted environment of an acute hospital medical or surgical ward is likely to aggravate any behavioural problems. Such patients often show a degree of agitation, and there may be no choice but to sedate the patient. But this is likely to aggravate the confusion, increasing the behavioural problems, often requiring even higher doses of tranquillization. This vicious cycle might have been avoided had the patient been admitted to a rehabilitation unit with a locked door where sedative medication can be reduced [48]. In those with milder injuries, not requiring prolonged hospital admission, randomized controlled trials (RCTs) have demonstrated that brief treatment packages delivered early after injury can reduce the risk of persistent symptoms over the first year [49].

Behavioural and cognitive therapy should be considered for patients with persistent challenging behaviour. Behavioural therapy may be difficult to deliver outside of specialist inpatient rehabilitation units. Cognitive techniques are appropriate for those with milder injuries and without impaired insight. Cognitive rehabilitation can address cognitive impairments, for example, using memory strategies like errorless learning to help improve memory. On the other hand, cognitive therapy or cognitive behaviour therapy (CBT) uses strategies that are well established in mainstream psychiatry, to help depression and anxiety. A recent RCT suggests that cognitive behavioural techniques may be useful in the treatment of patients with persistent post-concussion syndrome [50].

There have been very few controlled trials to establish the value of drug treatment for psychiatric sequelae of head injury. The only RCTs looking at drug treatment for agitation or aggression have studied beta-blockers [51]. But the studies were weak and used very large doses of beta-blockers, and this probably explains why in fact these agents are rarely used to treat agitation or aggression. Instead, anti-psychotics and anti-convulsant mood stabilizers (carbamazepine and valproate) tend to be used. But these drugs have not been subject to an RCT.

Individual factors will guide which drug may be most appropriate for that patient. For example, when recommending which drug to use for a trial of treatment in a patient presenting with aggressive behaviour, if complex partial seizures are present, then an anti-convulsant mood stabilizer, carbamazepine or valproate will be chosen. On the other hand, if the patient shows evidence of fear and some evidence of persecutory delusions, rather than complex partial seizures, then an atypical anti-psychotic, for example, olanzapine, would be better.

Similar is the case when it comes to treatment of psychoses or anxiety or depression. No RCTs have been specifically undertaken in patients with head injury, and therefore decisions about what drug to use are based on treatment evaluations in mentally ill patients without organic brain disease.

Given the absence of a good evidence base for the selection of treatment in patients with brain injury, it is particularly important to adhere to some general principles of treatment:

  1. Principles of drug treatment
    1. no knee jerk reactions; if possible wait to see if the problem goes away spontaneously;
    2. start low, go slow, add drug one at a time;
    3. beware of cocktails and interactions;
    4. beware of chasing your tail, some drugs will increase confusion and agitation;
    5. beware of ‘as required' (pro re nata (PRN)) short-acting anxiolytics to control challenging behaviour. This can reinforce the behaviour that is being treated. The patient learns (unconsciously) that the best way of receiving the pleasant calming effect of the anxiolytic is by repeating the challenging behaviour;
    6. trial of treatment - if it does not work stop it - slowly.
  2. Choose drugs with less
    1. potential for lowering seizure threshold;
    2. extrapyramidal and anticholinergic side-effects;
    3. potential for drug interactions.


Work attributed to Lishman Unit, South London and Maudsley NHS Trust.


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