The neuropsychiatry of head injury.
Head injury ‘imparts at a blow both physical and psychological trauma', (1) and the consequences are often devastating and enduring. (2) Not infrequently head injury leads to a psychiatric consultation, which will need to take into account the interplay between the brain and its injuries as well as the psychodynamic processes that follow from the injury. In the immediate aftermath of the head injury the management rests with the acute surgical and medical team. (3) The psychiatrist is usually not involved at this stage. Nevertheless, to understand the later neuropsychiatric effects of head injury it is first necessary to know what happens to the brain when it is injured.
Immediate and early effects
Open head injuries
In open head injuries there is penetration of the skull often with considerable destruction of brain tissue local to the trauma, but relatively less at a distance—particularly for lower-velocity injuries such as stabbing. Open head injuries may therefore be associated with little, if any, loss of consciousness, which is generally a marker of diffuse brain injury.
Closed head injuries
In closed head injuries acceleration/deceleration forces and shearing forces damage the brain. The soft brain moves within its hard bony box and is damaged. Contusion of the brain occurs, ranging from slight localized small vessel bleeding into surrounding tissue to almost complete local destruction of the brain. The medial orbital frontal cortex and the tips and undersurface of the temporal lobes are particularly vulnerable to contusions. The brain becomes traumatized on adjacent bone of the floor of the skull. Contrecoup localization of contusions is sometimes evident.
Contusions are often associated with localized haemorrhage into the brain. Scattered intracerebral haemorrhages are also often found at the interface between grey and white matter and are thought to be associated with diffuse axonal injury (see below). A large isolated haematoma suggests that a blood vessel has ruptured.
In very severe injury haemorrhages are also found round the aqueduct in the brainstem, perhaps caused by distortion of the brainstem as a result of cerebral herniation into the posterior fossa due to raised intracranial pressure. They are associated with the vegetative state or death.
Extradural and subdural haemorrhage
Haemorrhage into the extradural or subdural space will act as a space-occupying lesion and contribute to raised intracranial pressure. The extradural haemorrhage, being under high pressure, can rapidly cause coma and death. The patient may ‘talk and die', regaining consciousness after the head injury, only to lapse a few hours later into severe coma. Without acute neurosurgical intervention to drain the blood these patients will die. Subdural haematomas tend to run a subacute course and as such are of more interest to the psychiatrist. They may present with a failure to improve, or fluctuating drowsiness, weeks or months after the head injury. They may regress spontaneously or may require surgical drainage, but they do have a propensity to recur.
Diffuse axonal injury
Diffuse axonal injury occurs in the white matter tracts of the cerebral hemispheres, including the corpus callosum, and the brainstem, particularly the cerebellar peduncles. Axons break up over the course of the first 24 to 48 h following brain trauma with the formation of ‘retraction balls'—globular structures at the end of transected axons.(4)
Oedema and ischaemia
Oedema of damaged brain occurs over the first few hours following brain injury. The resulting raised intracranial pressure compromises the cerebral circulation and results in ischaemia, which may further contribute to brain injury. Cerebral oedema tends to resolve over the course of a few days or weeks.
Amyloid precursor protein may be an acute-phase reactant to traumatic brain injury (5) and results in b-amyloid deposition in 30 per cent of fatal brain injuries. Apolipoprotein E (APOE) genotype may influence the degree to which amyloid is deposited, being greater in those with the e4 allele. (6)
Hydrocephalus following head injury may be due to cerebral atrophy, which may develop over the weeks and months following injury. Diffuse ventricular enlargement is often associated with atrophy of the corpus callosum, and is usually attributed to diffuse axonal injury. More localized atrophy is observed when contusions resolve to leave a loss of brain tissue.
Of greater importance is hydrocephalus resulting from the residual effects of subarachnoid blood interfering with the normal cerebrospinal fluid flow and preventing it from escaping into the venous system. This may require insertion of a ventriculo-peritoneal shunt to prevent deterioration in cognitive function.
Fractures to the floor of the skull, particularly if they are associated with cerebrospinal fluid leaks, may allow infection into the subarachnoid space, causing meningitis sometimes years after injury. Cerebral abscesses may take months before they become clinically evident.
Loss of consciousness following head injury
The mechanism of loss of consciousness after mild blows to head is poorly understood. Some researchers suggest, based on animal work, that activation of cholinergic nuclei in the pons results in loss of consciousness. (7)
Loss of consciousness lasting for more than a few minutes is likely to be due to damage either to cortical areas necessary for consciousness, or the subcortical arousal systems. Raised intracranial pressure, partly as a result of compromising cerebral circulation, causes coma. Large or multiple haematomas are likely to be associated with a period of coma, particularly if they are associated with cerebral oedema.
Some patients, however, show prolonged coma with little to be found on brain scan apart from some evidence of generalized cerebral oedema. In these patients diffuse axonal injury may be the cause of their coma, possibly by damaging the white matter tracts that carry arousal signals from the brainstem to the cortex.
Remember that the head injury may have been caused by an accident triggered by a loss of consciousness, for example due to hypoglycaemia, alcohol intoxication, or an epileptic fit. Systemic effects (e.g. hypoxaemia or fat emboli) may exacerbate unconsciousness due to head trauma, as may drug intoxication.
Head injury severity
It is surprisingly difficult to predict the degree of brain injury from the size of the blow to the head. Some patients after a severe blow to the head sustain little injury to the brain. Others will suffer severe brain injury associated with prolonged unconsciousness, merely as a result of hitting their head on the ground by falling over from the standing position. There is anecdotal evidence that significant brain injury can result from a head injury with no, or momentary, loss of consciousness (see postconcussion syndrome below). The presence of a skull fracture says little about the severity of the brain injury incurred.
There are several clinical indicators of head injury severity ( Bullet list 1). Of these the duration of retrograde amnesia is probably the least valuable: it correlates very poorly with head injury severity. The duration of the retrograde amnesia tends to shrink as the patient recovers.
Bullet list 1: Clinical indicators of head-injury severity
- The duration of retrograde amnesia—the period leading up to the injury for which memories have been lost
- The depth of unconsciousness as assessed by the worst score on the Glasgow Coma Scale—a score of 3 indicates absent responses; 15 is normal consciousness
- The duration of coma—this may be difficult to ascertain because of routine sedation and ventilation following severe head injuries
- Neurological evidence of cerebral injury—abnormality on neuroimaging or EEG
- The duration of post-traumatic amnesia—the interval between injury and the return of normal day-to-day memories
The duration of post-traumatic amnesia is the best marker of outcome. (8) This is particularly useful because it can be measured retrospectively quite accurately. Most patients with a post-traumatic amnesia of less than 1 week will be left with little if any disability, while a duration of more than 1 month indicates that there is likely to be enduring and significant disability.
Predictors of a bad outcome after head injury are a previous head injury, older age, APOE e4 status, and alcohol dependence.
There is no universally accepted classification of head injury severity. However, the most widely used grading system is based on the lowest rating of the Glasgow Coma Scale (GCS) (9) following injury.
- Mild: GCS score 13 to 15. Likely to be associated with a loss of consciousness of less than 20 min and a post-traumatic amnesia of less than 24 h. There must be clinical evidence of concussion.
- Moderate: GCS score 9 to 12. Likely to be associated with a loss of consciousness of more than a few minutes but less than 24 h and a post-traumatic amnesia of more than 1 day but less than 1 week.
- Severe: GCS score 3 to 8. Likely to be associated with a loss of consciousness of more than 1 day or a post-traumatic amnesia of more than 1 week.
On average 200 to 300 per 100 000 population attend hospital with a head injury every year. (10) Socio-economic and cultural factors may have a two- to threefold effect on the rates of head injury, and even larger effects on the individual causes of head injury. About one-sixth of those people attending hospital will be admitted. This reflects the fact that, in most series, about 80 per cent of head injuries are mild, 10 per cent moderate, and 10 per cent severe.
At greatest risk are 15 to 25-year-olds. The sex ratio is about two to three males to one female. Risk factors included alcohol misuse as well as lower socio-economic class. Road traffic accidents are the largest single cause of head injury in most civilian cohorts, followed by assaults and falls. A significant proportion will sustain their head injury as a result of deliberate self-harm.
The prevalence rate for those experiencing considerable disability as a result of head injury is in the order of 100 per 100 000. (11)
Modern neuroimaging has transformed the investigation of head injury. Skull radiographs are now rarely performed if magnetic resonance imaging ( MRI) or CT brain scanning is available.
MRI scans cannot be performed if there is any magnetic material present either in the body (e.g. a pacemaker) or attached to the body. Therefore on the trauma unit CT brain scanning is the preferred investigation, with its faster acquisition time and good visualization of subdurals and extradurals.
However, in the postacute setting MRI is the better instrument. (12) Often cerebral contusions are found near the bone–brain interface (see above) where the image quality of CT is poor because of imaging artefacts from the adjacent bone. MRI has no such limitation. MRI is also able to detect, on T2-weighted images, changes in signal associated with a diffuse axonal injury when the white matter appears normal on CT brain imaging. The better image resolution of MRI is also in its favour.
Despite its greater sensitivity a normal MRI does not rule out significant brain injury. On the other hand, particularly in the elderly, MRI may detect abnormalities unrelated to the head injury.
The MRI scan can be normal and yet functional imaging of cerebral metabolism using single-photon emission computed tomography or positron-emission tomography will detect abnormalities. (13,14) In general, changes on functional imaging correlate better with neuropsychological test performance than do lesions found on structural imaging. (15) However, abnormalities on functional imaging are not necessarily due to brain injury. Hypometabolism may be seen in mental illness without brain injury, for example in depression. There is a recent report of marked hypometabolism on positron-emission tomography imaging in a man with cognitive impairment occurring immediately after a psychological trauma. (16) He had sustained no head injury.
If brain imaging is available the role of electroencephalography ( EEG) is largely confined to the investigation of a deteriorating conscious level and an unexpectedly prolonged unconsciousness, as well as the investigation of unusual behavioural disturbances that may be attributable to epilepsy. However, EEG is not a good predictor of post-traumatic epilepsy.
Non-specific changes are seen on EEG after head injury. An early sign is suppression of the alpha rhythm, while more severe injuries produce diffuse slowing. Haematomas produce localized reduction in amplitude and slowing. Improvements of the EEG correlate with clinical improvement, but the EEG is not a valuable prognostic marker.
A neuropsychological assessment is an invaluable accompaniment to the psychiatric history and examination, and good liaison with the neuropsychologist is essential. Areas of impaired performance can be documented and quantified. This is often useful as a baseline for future assessments and to guide rehabilitation.
The National Adult Reading Test, for people whose first language is English, gives a good estimate of preinjury IQ. (17) The present performance can then be compared with this preinjury estimate to see if there has been a drop in performance because of the head injury.
If subtle neuropsychological impairments are found, which are not obvious clinically, this suggests that the patient may have more problems when they return to work than would otherwise have been expected. On the other hand, if there is clinical evidence of underperformance, and standard neuropsychological test results are normal, then tests of executive function should be offered. (18)
Recovery of impairment, disability, and handicap
Psychological symptoms far outstrip neurophysical symptoms (e.g. hemiparesis or dysarthria) as determinants of chronic disability and suffering, both of the patient and their carer, following brain injury.
The ideas encapsulated in the International Classification of Impairments, Disabilities and Handicaps ( ICIDH) (19) are important for understanding recovery from brain injury.
- Impairments are abnormalities of structure, or physiological or psychological function. Thus poor performance on a test of memory or on a test of co-ordination is an impairment.
- Disability refers to the behaviour of the person and their ability to perform activities. Several impairments may contribute to a single disability.
- Handicap reflects the limitations on fulfilling the person's normal social role and participation in society. External factors (e.g. personal support systems or the availability of appropriate transport) play a large part in determining handicap. Handicap depends partly on the expectations of the individual patient.
The term ‘disability' will probably be replaced by ‘activity', and ‘handicap' by ‘participation', in the next version of ICIDH.
Recovery of impairment is usually complete by 1 year, with improvement in neurophysical impairments tending to stop before neuropsychological impairments.
However, the level of disability may continue to fall long after the recovery of the underlying impairment has stopped. This reduction in disability largely reflects improved coping strategies and these will be the focus of inpatient cognitive and behavioural rehabilitation. Once the person is back to living in the community then the rehabilitation team can focus on minimizing handicap, for example by improving access to local shops.
Psychiatric symptoms and quality-of-life measures do not fit easily into the ICIDH model. Psychiatric symptoms, with their multifactorial aetiology, show no simple pattern of recovery.
Psychological sequelae of head injury
To understand the mental symptoms that follow head injury it is necessary to know about the person who was injured, what brain injuries they sustained, and the consequences. However, the interaction between these three antecedents is complex and poorly understood.
People who take risks or get into fights are more likely to sustain a head injury; therefore these personality traits, present before injury, are over-represented in head injury survivors. Young men are at high risk, as are those who have already had a head injury or have cognitive dysfunction. (20)
The poor social adjustment of many patients before the head injury partly explains why so many run into behavioural problems afterwards. But premorbid characteristics do not strongly predict who will develop emotional and behavioural problems. Nevertheless, traumatic brain injury probably has the potential to turn preinjury personality traits into postinjury personality disorders.
The extent of brain injury probably explains less than 10 per cent of the variance in the amount of psychiatric morbidity that follows brain injury. (21) In general, early psychiatric symptoms, within weeks and months of the injury, correlate better with the extent and location of brain injury than do late psychiatric symptoms. Left hemisphere damage seems to be associated with greater psychiatric morbidity. Specific relationships between the location of brain injury and the psychiatric symptoms are discussed below.
But the head injury is also a psychological trauma. Amnesia for the event, as a result of the head injury, protects against post-traumatic stress disorder. However, it is a mistake to believe that amnesia for the event prevents a psychological stress reaction to the event itself.
- The meaning of the event may be distressing to the patient. (22) In the case of assaults, the head injury may act as a marker of the potential for further assaults. An accident may have been life threatening and a shocking reminder to the patient that they are mortal. They may feel aggrieved by an employer's negligent action that caused the accident.
- The patient may be amnesic for the event, lacking explicit memories of what happened, but retain implicit memory of what happened. The consequences of these implicit memories may be akin to those observed in one of Claperède's amnesic patients. (23) The doctor shook the patient's hand, pricking it while doing so with a concealed drawing pin. The next day the patient could not remember having met the doctor, but flinched from shaking his hand when it was offered.
- They may have islets of intact memories that may be extremely frightening. (24)
Post-traumatic factors deserve special attention because they are most likely to be amenable to intervention. The psychiatrist needs to consider the patient's reaction to any disability, as well as the consequences of the disability on the role of the patient in the family and society. There may be reinforcing cycles of maladaptive behaviour, and compensation claims may complicate the picture.
Cognitive impairment correlates with measures of head injury severity better than any of the other mental sequelae. For example, there is a strong correlation between the duration of post-traumatic amnesia and the severity of cognitive impairment.
Recovery of cognitive function, by and large, occurs within the first year. (25) After 2 years most improvement is a result of improved coping strategies, for example memory aids enabling return to work. Continuing improvements in participation in social life and work take place 5 to 10 years after head injury. (26) But sometimes early gains are made, for example as a result of being in a return-to-work rehabilitation programme, which are subsequently lost over the longer term.
Attention and concentration
Non-specific cognitive impairments include slowness and reduced concentration. With severe injury the patients are likely to be stimulus bound, i.e. responding to each and every stimulus they are exposed to in a rather concrete way. At the same time they may show perseveration, with previous responses inappropriately interfering with the answers to subsequent questions, or when the topic of a conversation has been changed.
More specific impairments, generally referred to as the dysexecutive syndrome, result from a disturbance of the executive system responsible for organizing, planning, scheduling, prioritizing, and monitoring cognitive activities. (27) In some patients with isolated medial orbitofrontal lesions the dysexecutive syndrome may stand alone. Disturbance of the executive system also results in difficulties in attending to two things at once, and distractibility.
Patients with the dysexecutive syndrome may be much more impaired in everyday life than is predicted by their performance on standard neuropsychological tests. They can manage with the clear instructions of the well-structured and constrained test situation. But in the real world these are absent; priorities have to be set, a strategy planned, decisions taken, and the unexpected dealt with, all without guidance. In the real world, impairment of the executive system may be catastrophic. Tests of the dysexecutive syndrome have been developed in order to be better predictors of these real-life problems. (18)
Memory impairment is perhaps the most common cognitive impairment that follows head injury, and can be very disabling. (28) People will have problems remembering where they put things, what to do next, how to get home from shops, what they did yesterday, or what their cousin is called. The term anterograde amnesia is used to refer to these enduring memory problems, and must be distinguished from retrograde and post-traumatic amnesia (see Bullet list 1 above).
No consistent pattern of brain injury is associated with anterograde amnesia and it seems likely that it is the combined damage to several areas which causes the amnesia. Frontal injury may be particularly implicated and this may be because frontal injury results in failure of the executive processes required for normal memory, for example in memory retrieval. As with most amnesic states the amnesia following brain injury is for explicit memories, namely those which are consciously remembered. Implicit memory, for example remembering and learning a motor skill, generally remains intact.
Anterograde amnesia is often characterized by distortions and inaccurate recall with poor monitoring and insight. Confabulations are often seen.
Dysphasia is quite common after head injury, and may be rather different from that seen after stroke. (29) The more diffuse and widespread injury of traumatic brain injury results in additional cognitive impairments which colour the picture. Monitoring language errors is often particularly poor and the patient may demonstrate a jargon aphasia in which they are apparently unaware that their speech is completely incomprehensible.
Dysprosody, in which the normal rhythms and intonations of speech are lost, is also seen, more so after right hemisphere damage. This interferes with social communication because the voice sounds flat and fails to convey emotion. Social communication is disrupted for other reasons, for example the patient fails in the turn-taking necessary for normal conversation. Word-finding difficulties are very common.
Visuospatial impairments are seen and may contribute to spatial disorientation. Visual agnosia is easy to miss in someone with quite widespread cognitive impairments.
Decline in cognitive function
Accelerated cognitive decline, but insufficient to result in dementia, has been found in head-injured soldiers 25 years later. (30) The reduced reserve of the injured brain probably makes it vulnerable to the effects of ageing. Follow-up and case–control studies have shown an association between head injury and subsequent Alzheimer's disease. Individuals with the APOE e4 allele may be at special risk. (31) However, the evidence for both an accelerated cognitive decline and an increased risk of Alzheimer's disease is inconsistent.
Personality change after head injury results in more suffering than any other single sequel. (32,33) In general, the personality change goes hand in hand with cognitive impairment. However, a severe personality change is occasionally found in somebody with almost no impairment of cognitive function. Normal test scores for memory and intellect do not rule out brain injury as a cause of personality change after head injury.
It is not easy to predict who will develop a change in personality after head injury. Sometimes a personality trait present before the injury becomes much more troublesome, but often there is no obvious predisposition. The site of the brain injury may play a role. Convexity lesions, on the lateral surface of the brain, can produce impairments of drive. Orbitofrontal lesions may cause a more troublesome personality change with impairments in social behaviour.
Post-traumatic factors also need to be considered. Some patients seem to learn maladaptive patterns of behaviour; for example the response of the carers may unwittingly reinforce unwanted behaviours. Chronic mental illness may be manifest as personality change, which may be aggravated by chronic psychosocial stressors. Dependence on drugs, particularly alcohol, frequently confounds the picture.
Characteristics of the personality change
Changes in personality (34) include apathy and impairment of motivation and ambition. Patients are often described as childish; this covers a range of traits including impulsivity, poor tolerance of frustration, being demanding and self-centred, and generally lacking the ability to take on the adult role in terms of independent decision-making. Patients may be fatuous and facetious. Antisocial behaviours (see below) and disinhibition are severe handicaps that make integration back into the community very difficult. Sexual disinhibition of any type is particularly worrisome. A spectrum of severity is seen, ranging from being inappropriately flirtatious through to indiscriminate sexual assaults. Head injury is a risk factor for borderline personality disorder. (35)
In acquired antisocial personality disorder (36) the person is often self-centred and relatively oblivious to the needs of others. They are likely to be tactless and, on occasion, offensively rude. Irritability and aggression and impulsive behaviour are seen. They may show a lack of remorse for the violent behaviour. These personality traits often are accompanied by the dysexecutive syndrome. Thus not only does the person show disturbed social decision-making, resulting in antisocial behaviours, but also disruption of the planning and organizational skills needed for cognitive tasks. For example, helpful and supportive friends may be alienated in favour of disreputable acquaintances, at the same time as money is impulsively spent, and lost, on risky projects without any attempt to weigh up the options.
Effects on family and carers
Families find personality change particularly difficult to cope with. (37) Children may be ignored and the partner's needs, particularly emotional needs, forgotten. The healthy balance of the relationship with the partner may be destroyed, with the head-injured person now unable to take an effective part in the household. The partner becomes a carer and the change in roles may have a serious impact on the sexual relationship. Divorce frequently follows. However, parents may find the childish personality of the brain-injured person easier to cope with; they revert to taking on the parental role.
Personality change may deteriorate. Supportive social networks are lost and social isolation and financial problems may contribute to depression or alcohol abuse, which then cause a deterioration in the behavioural problems associated with the personality change. Follow-up studies lend some support to this argument. Some behavioural problems are found to have deteriorated at 5 years after head injury (38), and family burden increases over this period.
Early mental symptoms following brain injury
On recovery of consciousness many patients after a severe head injury go through a period of delirium with clouding of consciousness. This may resolve, leaving a confusional state in clear consciousness with disorientation and thought disorder consisting of muddled thinking, rambling talk, and perseverations. The mental state is dominated by misperceptions and misrecollections as they flit from one false observation to another. (39) Fear is common.
Distortions of memory
Confabulations, brief-lived false memories, emerge at about this time. (24) Confabulations occur particularly in association with memory disturbance associated with frontal injury. The patient almost invariably shows poor insight into their memory problems, and is likely to be disorientated.
Occasionally after a severe head injury there are islets of memory in the dense amnesic period immediately around the time of the injury. These may be recollections of something that was consciously experienced at the time. On the other hand, the memories may have been fabricated from information subsequently given to the patient about what happened, or the memories may have no basis in reality and be properly described as a delusional memory.
Alterations of mood and perception
In the early recovery period oneroid states may be seen. The patient may be perplexed. He or she may feel that the trauma never occurred and that the whole event, including being in hospital, is a fabrication. Derealization/depersonalization may be associated with prominent anxiety, with the patient constantly asking for reassurance. Agitation is often observed in this early recovery period.
Hallucinations, particularly visual, are occasionally observed, whereas illusions of familiarity commonly occur after brain injury. The patient may have a sense of déja vu, or that he or she has met clinical staff or patients before. Distortions of the sense of familiarity also seem to be implicated in many of the delusions observed early after brain injury.
In many patients the recovery period lacks the positive features described above and is dominated by an apathetic withdrawn state.
Psychosis after brain injury
Delusions involving the misidentification of place, persons, objects, and events may be observed early in the course of recovery. These delusions are often associated with more generalized disturbances of insight, in particular denial of illness (anosognosia), impaired judgement, and disorientation. The best evidence for this comes from a study of delusions after right temporoparietal strokes. (40)
The vast majority of the delusions occurring during the recovery period will themselves remit spontaneously and not relapse. However, in some patients who have recovered from these early delusions amylobarbitone produced a return of symptoms. (41) This suggests that generalized disturbance of brain function plays an important part in the development of early delusions.
Perhaps the delusion that is most pathognomonic of brain injury, and which is also associated with postictal confusional states, is reduplicative paramnesia. The term reduplicative paramnesia covers a range of phenomena, which are often observed concurrently. Pick (42), who introduced the term, used it to describe a patient who believed she had visited a duplicate hospital. Other phenomena covered by the term include the following:
- any delusion involving duplication, for example that events have been duplicated or that the patient has a second left leg
- delusions involving misidentification of place, with or without duplication, including delusional disorientation for place.
Delusional disorientation for place may involve the belief that the current location is a duplicate of the true location or in some way displaced, for example that the hospital is in a different country. The patient may have two incompatible attitudes to orientation; this is sometimes referred to as a double orientation. For example, a patient who lives in Edinburgh acknowledges that he is in a hospital in London, but says that his home is just a few yards down the road.
Capgras syndrome and other delusional misidentifications of person
Whereas isolated delusional misidentifications of place are rare in the absence of manifest organic brain disease, most cases of delusional misidentification of person (e.g. Capgras syndrome) are to be found in schizophrenia. Delusional misidentifications of person may also be observed following brain injury, often alongside a reduplicative paramnesia.
Organic and psychological factors in delusional misidentification
Delusional misidentification syndromes can best be understood as the result of an interaction between organic brain disease and psychological disorder. (43) Lesions of the right hemisphere, often in combination with frontal injury or more diffuse evidence of brain disease, are particularly associated with delusional misidentification.
A psychotic illness may develop long after the acute confusional state has resolved, which is difficult to distinguish from psychotic illness occurring in the absence of manifest organic brain disease. The patient may develop a typical schizophrenia indistinguishable from idiopathic schizophrenia. Would he or she have developed schizophrenia regardless of having had a head injury?
The best estimate of the increased risk of developing a schizophrenia-like psychosis as a result of a head injury comes from Davison and Bagley's study of 30 years ago. (44) They estimated a two- to threefold increased risk compared with the general population. There were large variations in the different studies they examined, and most were cohorts of war veterans. It is not clear whether the same relative risk will be found in civilian cohorts with mainly closed head injuries. Those who develop schizophrenia after head injury may be at high risk anyway, for example due to a family history of schizophrenia or schizoid personality traits, but the findings are not consistent.
Conversely, case–control studies of patients with schizophrenia show increased rates of childhood head injuries. (45) The association between head injury and subsequent schizophrenia does not mean that head injury is causing the schizophrenia; they could both be linked to something else, such as behavioural problems. However, specific patterns of brain injury are associated with the development of schizophrenia-like states, and this suggests that brain injury plays a causal role. Late schizophrenic-like psychosis after brain injury is particularly associated with temporal lobe injury and to a lesser extent post-traumatic epilepsy. (44) However, these associations are weak.
Paranoid psychoses may emerge after brain injury. Not infrequently this occurs relatively early and in a patient with severe cognitive impairment and personality change. Memory impairment will facilitate the development of persecutory ideas; for example, the patient believes that belongings have been stolen. Persecutory ideas or delusions of reference are a fairly common cause of aggression and may be hidden by communication difficulties.
Effects of head injury on schizophrenia
The cognitive and behavioural problems of schizophrenia overlap considerably with those produced by traumatic brain injury. Antisocial behaviours, apathy and lack of spontaneity, and erratic mood swings are common to both. Both will show cognitive problems including disorders of communication, memory, and planning. Will a head injury therefore aggravate these more negative symptoms of schizophrenia? Given that a significant proportion of head trauma is found in people with schizophrenia who have jumped from a height, the question arises from time to time. As yet there are no studies of the outcome.
Mood disorders, including anxiety disorders
The study of depression after head injury raises two fundamental questions about the nosological status of depression. First, with a severe disability should the belief that life is not worth living be regarded as a symptom of depression or a ‘rational' reaction to an intolerable predicament? Second, what is one to make of symptoms of apathy or anhedonia when the brain pathways involved in generating spontaneous behaviour or the experience of pleasure have been damaged? Most of the biological symptoms of depression can be produced by brain injury.
The diagnosis of depression therefore relies heavily on identifying a depressive mood. Symptoms like self-deprecation or guilt are also particularly helpful in diagnosis. Estimates of the prevalence of depression after head injury vary, partly because of the lack of uniformity in defining depression. Perhaps 25 per cent of patients meet DSM-IIIR criteria for major depression 1 month after injury. (46) The majority have recovered from their depression by 6 months, while at 1 year 10 to 20 per cent of those previously not depressed have become depressed.
Aetiological factors include a personal history of depression, which is twice as common in those who become depressed, and lack of social support. Left frontal injury predicts the development of depression within 3 months of a closed head injury, but does not predict those who are depressed at 1 year. Two large follow-up studies have found that after penetrating injuries depression at 1 year is associated with right hemisphere damage, particularly of the frontal lobes.
Depression after head injury interferes with rehabilitation, and is associated with aggression. It may exacerbate cognitive impairment and in some cases produce a pseudodementia.
Emotional lability may occur, particularly after severe head injury, and is frequently associated with the presence of depression.
Manic illness after head injury is much less common than depression. It needs to be distinguished from the neurobehavioural symptoms of, for example, disinhibition and fatuous behaviour that may follow frontal injury. There is some evidence for a link with right hemisphere lesions and with post-traumatic epilepsy. Mania is particularly associated with aggressive and assaultive behaviour following brain injury.
Anxiety disorders are found in about 30 per cent of patients after head injury, and are at least as common in those who have suffered mild injury. (47)
Early symptoms may be observed in relation to derealization/depersonalization symptoms, or perplexity. Early on, the amnesic period surrounding the injury may cause great distress. In the catastrophic reaction, which is observed in patients with moderate to severe cognitive impairment, sudden distress occurs when they fail to perform a task, or because of their inability to communicate.
Anxiety symptoms, particularly those with a mild head injury, may develop over the weeks and months following a head injury. It is then more likely to be associated with depression, post-concussion syndrome, and with post-traumatic stress disorder. Phobic avoidance is seen, for example travel anxiety following a road traffic accident. Apprehension is a common complaint, perhaps reflecting problems caused by cognitive impairments, and the person may be indecisive. Therefore anxiety symptoms may emerge on return to work. Anxiety symptoms will be inflated in the presence of financial or family stress.
Obsessive–compulsive disorder is a recognized sequela of head injury. This may partly reflect the inflexibility and rigidity of the brain-injured person, or a response to doubt resulting from memory disorder.
The risk of suicide is increased following head injury. In a study of Finnish soldiers who suffered brain injuries during the Second World War and were followed up for 25 years, 1.6 per cent had killed themselves, about a threefold greater risk than the general male population. (48) A meta-analysis of six civilian cohorts followed up over 40 years found a threefold risk compared with standard mortality rates. (49) The increased risk attributable to head injury is probably slightly less than these estimates.
Agitation and aggression
The psychiatrist is more likely to be asked to advise about the management of agitation and aggression following head injury than any other psychological symptom.
Agitation in the early recovery period after severe brain injury will generally spontaneously improve over the course of days or weeks. (50) Usually no specific cause is found and it is a marker of a generalized disturbance of brain function. Epilepsy may be contributing, and partial complex seizures may not be immediately obvious clinically. The milder the head injury the more likely it is that psychological factors will be found. The patient's worries and fears need to be explored, and phobic anxiety disorder considered. Drugs may make agitation worse and paradoxical effects of sedative medication occur if the medication increases confusion or disinhibition, or results in akathisia. The patient may be in a withdrawal state having stopped a drug they were taking regularly before the head injury.
Early agitation may be followed by more intractable aggressive behaviour. (51) A major predictor of aggression is antisocial behaviour before the head injury. Other predictors of aggressive behaviour include confusion and disorientation, personality change with disinhibition or impulsivity, and epilepsy and anticonvulsant use. (52) Otherwise the predictors of aggressive behaviour are by and large no different from those found in the absence of head injury. Symptoms of mental illness, however, may not be immediately obvious because of communication difficulties. It is therefore necessary to search for evidence of persecutory delusions, mania, depression, and anxiety. Drug and alcohol dependence may be especially problematic.
If the aggressive behaviour emerges early, namely during the confusional state or shortly after it resolves, then this suggest that the aetiology is largely organic. A pattern of aggression that is highly stereotyped, or erupts over seconds with no or trivial triggers, or is bizarre, and is against a background of calm behaviour, suggests the possibility of epilepsy.
Alcohol and head injury
Alcohol dependence complicates the management of the head-injured person several-fold. The person may have suffered several previous head injuries, as well as the effects of alcoholic brain damage before the head injury. A blow to the head may result in much greater brain injury for reasons that are poorly understood. (53) Poor physical health is likely to prejudice immediate management after the head injury. Subdural haematomas may be problematic. Alcohol craving may interfere with medical care and rehabilitation. (54) Social networks are often poor, thus complicating discharge from hospital.
Very occasionally a head injury seems to cure the alcohol dependence. Unfortunately alcohol dependence often gets worse, indeed some patients develop alcohol dependence when they find that alcohol relieves their anxiety symptoms.
Sometimes called post-traumatic syndrome, the postconcussion syndrome is poorly defined. (55) The term is perhaps most usefully reserved to describe a constellation of symptoms that may result in surprisingly severe disability after mild head injury. These symptoms may be observed after moderate and severe head injuries, in which case they are likely to be in the company of other symptoms more readily understood as resulting from brain injury. There is no consistent relationship between the prevalence of postconcussion symptoms and injury severity.
Early symptoms tend to have a more neurological flavour and include headache, dizziness, and occasionally diplopia. Mild head injury fairly consistently results, in the immediate aftermath, in impairment of speed of information processing and concentration. Fatigue is also evident from early on, along with symptoms of noise sensitivity. Anxiety, depression, and irritability are common and may appear after a latent period. The symptoms of postconcussion syndrome overlap with those of post-traumatic stress disorder, and chronic fatigue. Other symptoms occasionally reported include tinnitus, unsteadiness, and muscle pain. In general, symptoms, particularly the more neurological symptoms, will have recovered by 2 to 6 months. But a few patients, often after a latent period, develop persistent symptoms that last for years. This suggests that psychological factors, as well as brain injury, are important.
Several observations support the contribution of brain injury. Microscopic lesions in the brain have been described at postmortem, following mild head injury. (56) Imaging, including functional imaging with single-photon emission CT or positron emission tomography, may show small abnormalities which are attributed to the mild head injury. Delayed brainstem auditory evoked potentials have been found and may predict chronicity of symptoms. (57)
Psychosocial factors have also been found to play a part in postconcussion syndrome, more so in those with symptoms lasting longer than 1 year. If the accident occurs at work, particularly if the person blames their employer, symptoms are more likely. A meta-analysis of the effects of compensation on symptoms, any symptom, after head injury concluded that, on average, being involved in compensation claims increases symptoms by about 25 per cent. (58)
Model of interaction
Lishman has proposed a model in which early disturbance of brain function after mild head injury results in the early symptoms of postconcussion syndrome. (1) In most patients these gradually resolve and a good recovery is made. However, the postconcussion syndrome may develop if psychological effects interfere with the normal process of recovery. Anxiety is thought to play a large part in impeding recovery; the patient worries about the symptoms and focuses on them. These may be aggravated if the patient is vulnerable to somatization, or there are compensation issues at stake. The symptoms may cause secondary disability provoking yet more anxiety, which will be made worse if there are additional psychosocial stressors.
The role of psychological factors is greatest in those with very mild head injuries and very chronic symptoms. For example, studies looking at the effects of compensation generally show more powerful effects in those with milder injuries.
Early fits, within the first week, are relatively benign, sensitive to prophylactic anticonvulsants, and are only weak predictors of later epilepsy.
Only about 5 per cent of closed head injuries go on to develop late seizures, compared with 30 per cent after an open head injury. The majority of these late seizures start in the first and second year following injury. By the time 5 years have elapsed without seizures any subsequent seizure development may be unrelated to the head injury. (59)
The likelihood of developing seizures in patients with a closed head injury is increased by the presence of a depressed skull fracture, intracranial haematoma, and early seizure, as well as by the severity of the injury. Mild head injuries result in only a small increased risk of epilepsy above population norms. Children are at increased risk of post-traumatic epilepsy. The EEG is generally not a good predictor of post-traumatic epilepsy (see above).
Post-traumatic epilepsy increases psychiatric morbidity, particularly mood disorders, behavioural problems, and psychotic illness, and may increase the risk of late dementia.
Prophylactic anticonvulsants have no effect on reducing the incidence of late post-traumatic epilepsy. (60) Carbamazepine, rather than phenytoin, is the drug of choice if an anticonvulsant is needed because it has less effect on cognition. (61) Half of all patients with post-traumatic epilepsy from open head injuries are found to be in remission by 5 to 10 years.
Head injury in children
It is possible that the greater potential for plasticity, which may be present in the younger child's brain, will result in a better outcome after head injury. There is some evidence for this for mild and moderate head injuries. However, children with severe head injuries are likely to be left with persistent cognitive deficits and behavioural problems. The quality of parenting has a powerful effect on outcome; those with poor parenting are much more likely to develop behavioural problems.
Children often sustain a bilateral prefrontal injury, which may explain the deficits in concentration, controlling impulsivity, and self-monitoring. The commonest psychiatric disorders that follow childhood head injuries are personality changes, attention-deficit hyperactivity disorder, and obsessive–compulsive disorder. (62) Children who develop attention-deficit hyperactivity disorder after head injury tend to demonstrate less hyperactivity than is seen in the idiopathic form of this disorder. In the long term the head-injured child may be at increased risk of developing schizophrenia. Children are more likely to develop post-traumatic epilepsy than adults.
Between 10 and 20 per cent of professional boxers go on to develop a chronic traumatic encephalopathy, (63) the punch-drunk syndrome, with damage to the extrapyramidal system as well as cerebellar and pyramidal pathways. They are slow and ataxic. Cognitive impairment, in particular memory impairment, is a frequent accompaniment and dementia is present in about half of the cases. Upper brainstem lesions may explain the neurological symptoms, while cerebral atrophy, white matter changes, and damage to diencephalic structures may account for cognitive changes. Perforation of the septum pellucidum, which separates the two lateral ventricles, is a characteristic finding in boxers' encephalopathy. APOE e4 status increases vulnerability to the punch-drunk syndrome, (64) and this is consistent with the finding that amyloid is present. Professional footballers may show evidence of subtle impairments of thinking, raising the possibility that repeated blows to the head from heading the ball may be sufficient to cause slight brain injury.
Management of early neurobehavioural problems
Behavioural problems, and mental symptoms, arising in the days and weeks following a brain injury should be regarded as a flag to indicate the need to check on the progress of recovery. The history needs to be reviewed, paying attention to the period leading up to injury. The patient will need to be examined physically, paying particular attention to the possibility of fever, and given a reasonably thorough neurological examination. It is essential to document the conscious level and orientation. Routine blood tests should be performed, and blood gases and a chest radiograph considered. The medication needs to be scrutinized. A neurological or neurosurgical opinion may be needed with a view to considering neuroimaging or an EEG. A lumbar puncture, for example looking for meningitis, should probably not be done without specialist advice.
Specific causes of deterioration after head injury are listed in Bullet list 2 below. Once these have been excluded then the principle of care should be to allow recovery to take place in a safe environment, paying attention to the general principles of the care of the delirious or demented patient as indicated. Explanation to the patient and his or her family of what is happening, is required.
Bullet list 2: Causes of deterioration in cognitive function after brain injury
- Subdural haematoma
- Epilepsy, particularly complex partial status
- Late intracranial infection, including cerebral abscess
- Systemic illness, including fat emboli and pain
- Drug intoxication
- Severe mental illness, in particular depression
- The patient ‘gives up' as he or she gains insight
- Independent dementing process
Management of late mental sequelae
General management principles
Good medical and surgical care, followed by transfer to appropriate rehabilitation services is required to optimize recovery from head injury. In addition, the individual and their family should have access to support as they try to adjust to the changes forced on them by the head injury. Education, and access to information, is an important part of the strategy. (65) Not infrequently psychological problems arise if any part of this process has not gone smoothly, or is perceived to have failed. The psychiatrist should explore any such concerns.
It is often necessary to find out what services are available in the area that might provide rehabilitation or support. Access to suitable programmes of rehabilitation, or vocational training, or appropriate support, may relieve mental symptoms. A social worker should be asked to undertake a community care assessment, which may identify the need for respite care or modifications to the home.
Specific neuropsychiatric interventions
It is important early on to ascertain the degree of brain injury that has been sustained. If there is any doubt then this may need to include a neuropsychological assessment. The severity of brain injury will suggest whether a particular symptom is mainly due to brain injury or to psychological processes. This will influence management. Cognitive-behavioural treatment will play a key part in the management of neurobehavioural symptoms. Behavioural strategies are particularly relevant to behavioural problems arising from brain injury. (66) The crucial task is to identify the responses of carers or family that seem to be reinforcing the behaviour.
Perhaps the majority of patients who suffer a traumatic brain injury, needing hospital treatment, are given psychotropic drugs, (67) despite the fact that animal studies suggest that some may interfere with recovery from brain injury. Patients should be given psychotropics only if absolutely necessary, using the principles described in Bullet list 3 and avoiding multiple drugs given concurrently.
Bullet list 3: Prescribing psychotropics in brain injury
- Small doses—start low, go slow
- Only continue treatment if definite evidence of effect
- Drug profile—choose drugs with less potential for:
- lowering seizure threshold—avoid chlorpromazine and clozapine
- anticholinergic activity—to minimize potential for increasing confusion
- extrapyramidal side-effects—especially akathisia, parkinsonism, and neuroleptic malignant syndrome
- Enzyme induction or other pharmacodynamic interaction with other drugs
- Regular medication with long-acting drugs, compared with short-acting drugs as required, is less likely to produce:
- withdrawal syndrome
- development of addiction
- reinforcement of unwanted behaviour
Agitation and aggression
Because of the lack of controlled trials, prescribing for agitation and aggression after brain injury is very much trial and error, requiring good monitoring and documentation of the behaviour. If there is no evidence of benefit then the drug should be withdrawn and another drug tried. Be wary of responding to every episode of aggression by increasing the dose or adding a new drug.
Of all the drugs used in the management of agitation and aggression only b-blockers, in very large doses, have been exposed to randomized controlled trials, (68) which showed a slight effect in favour of medication.
Nevertheless, for many psychiatrists carbamazepine is the drug of first choice for aggression after brain injury. It has the advantage of anticonvulsant properties, as well as mood-stabilizing effects. Perhaps a third of patients will respond. Some clinicians recommend sodium valproate.
Antipsychotics should be used in the presence of delusions or persecutory ideas of reference, and possibly when the patient demonstrates undue suspiciousness. Otherwise they should not be the first-line treatment, partly because of the danger that akathisia may perpetuate agitated behaviour which would otherwise have resolved spontaneously. Sulpiride and olanzapine can be recommended as first-line drugs, with risperidone and other new antipsychotic agents held in reserve.
Antidepressants may be helpful, and selective serotonin-reuptake inhibitors should be given in preference to tricyclics. Trazodone, which is sedative, may be particularly useful.
Benzodiazepines and chlormethiazole should be considered for agitation and aggression during the early recovery from severe head injury. But be wary of increasing the confusion, and paradoxical violence due to disinhibition. Because of the potential for addiction, benzodiazepines should not be given to a patient with a chronic aggressive disorder.
Mood disorders and psychosis
Clinically, one has the impression that depression after a head injury is more difficult to treat. This is consistent with the observation that depression, in those who have not suffered a head injury, is more difficult to treat if the patient is found to have evidence of brain damage. However, some studies in head-injured depressed patients have found good response rates. The selection of an antidepressant is no different from that used to treat depression in the absence of brain injury, provided that the principles given in Bullet list 3 are taken into account.
There has been no good trial of antipsychotic drugs in the treatment of psychotic patients after head injury. A case series has shown a good response in the majority of psychotic patients, and this fits with the clinical impression that some delusions and hallucinations do respond. The choice of drug is the same as that for the management of aggression (see above).
Bromocriptine and methylphenidate may be useful for treating apathetic states. An initial effect wears away in some patients, but in others a beneficial effect is maintained despite removal of the drug. Methylphenidate, with its risk of addiction and troublesome side-effects, should only be prescribed if bromocriptine has not been successful, under consultant supervision.
Insight, compliance, competence, and detention in hospital
Lack of awareness of deficits is a common problem for the head-injured person (69) and affects compliance with the treatment. As a result, the psychiatrist may be called when the patient demands to leave hospital, even though they would be at risk returning home. If there is evidence of mental disorder then it may be possible to justify detention under the Mental Health Act 1983 (England and Wales), but not if the purpose of doing so is merely to treat a physical condition.
Insight and capacity to consent to treatment should be assessed. Only the very exceptional patient who is demanding to leave hospital following a head injury, and who as a result would be putting his or her health severely at risk, will be found to be competent. In this situation, in England and Wales, it may be possible to detain patients in hospital under common law in their best interests for treatment of a physical condition.
The patient's capacity to give informed consent to any treatment that is being offered may need to be reviewed. They should also be assessed to see whether they are capable of managing their domestic and financial affairs. If they are not, appropriate legal arrangements should be made; in the United Kingdom a receiver may need to be appointed to protect their interests. The prospect of compensation should be considered and, if appropriate, they should be enabled to pursue a personal injury claim.
Service provision for the head-injured
Head-injury services tend to be very heterogeneous and poorly co-ordinated. (70) A head injury co-ordinator or team who identify patients at the outset, i.e. shortly after admission to hospital, is the best solution. They can identify the appropriate services for that individual and ensure continuity of service provision. It helps if there is a named local psychiatrist interested in neuropsychiatry for them to liaise with. The psychiatrist should also be part of the liaison service for the district general hospital, in particular to the trauma unit and neurosurgery. A regional neurobehavioural unit, managing challenging behaviour arising from head injury and other acquired brain injuries, should be available.
Generally brain-injury services are poorly funded. It is often difficult to find services to refer the patient to. In the United Kingdom a recent trial of case management failed to show a beneficial effect, probably because there were insufficient local resources to take on the patients' care.
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