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.

In the emergency room or on the trauma unit CT brain scanning is generally the preferred investigation, with its faster acquisition time and good visualization of subdural and extradural haematomas.

For later neuropsychiatric assessment magnetic resonance imaging (MRI) is preferred.⁽⁹⁾ Cerebral contusions are often found near the bone-brain interface (see above) where the image quality of CT is reduced because of imaging artefacts from the adjacent bone. MRI has no such limitation and generally has better sensitivity and anatomical definition. MRI is able to detect, on T2-weighted images, changes in signal associated with a diffuse axonal injury when the white matter would have appeared normal on CT brain imaging. Gradient echo MRI sequences should be performed to detect haemosiderin deposits from old small traumatic haemorrhages.

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. It may not be possible to perform an MRI scan if there is magnetic material present in the body (e.g. a pacemaker).

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. In general, changes on functional imaging correlate better with neuropsychological test performance than do lesions found on structural imaging.⁽¹⁰⁾ 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. Marked hypometabolism on positron-emission tomography imaging has been observed in a man with cognitive impairment occurring immediately after a psychological trauma.⁽¹¹⁾ He had sustained no head injury.

Electroencephalography (EEG) may be useful in the investigation of a deteriorating conscious level or unexpectedly prolonged unconsciousness, and in the investigation of unusual behavioural disturbances that may be attributable to epilepsy. However, EEG is not a good predictor of post-traumatic epilepsy and is generally not useful as a guide to prognosis.

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 pre-injury IQ.⁽¹²⁾ This can then be compared with the present performance on cognitive testing, to estimate the impairment produced by the head injury.

Subtle neuropsychological impairments, which are often not obvious clinically, suggest 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 yet standard neuropsychological test results are normal, then it is particularly important that executive function is tested.⁽¹³⁾

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.⁽¹⁹⁾

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 pre-injury personality traits into post-injury 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.⁽²⁰⁾ 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.

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.

Non-specific cognitive impairments include slowness and reduced concentration. The severely injured patient is 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.⁽²⁴⁾ In some patients with isolated medial orbito-frontal lesions or dorso-lateral prefrontal 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 reallife problems. ⁽¹³⁾

Memory impairment is perhaps the most common cognitive impairment that follows head injury, and can be very disabling.⁽²⁵⁾ People will have problems remembering where they put things, what to do next, how to get home from the shops, or what they did
yesterday. Anterograde amnesia refers to these enduring problems laying down new memories, and must be distinguished from retrograde and post-traumatic amnesia (see Box 4.1.10.1).

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 perhaps by interfering with 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, is relatively well preserved.

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. The more diffuse and widespread injury of traumatic brain injury results in additional cognitive impairments which colour the picture. Monitoring of language errors is often particularly poor and the patient may demonstrate a jargon aphasia such that they are apparently unaware that their speech is completely incomprehensible. Dysphasia often continues to improve even many years post-injury.⁽²⁶⁾

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 common.

Visuospatial impairments may contribute to spatial disorientation. Visual agnosia is easy to miss in someone with quite widespread cognitive impairments. Hemi-neglect can be troublesome.

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.⁽²⁹⁾ Lesions of the medial and lateral surfaces of the frontal lobe can produce impairments of drive. Whereas orbito-frontal lesions, on the undersurface of the frontal lobe, 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, aggravated by chronic psychosocial stressors, may be manifest as personality change. Dependence on drugs, particularly alcohol, frequently confounds the picture.

Changes in personality⁽²⁷⁾ 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 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 probably a risk factor for borderline personality disorder.⁽³⁰⁾