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A faulty production line

Unexpected aspects of head injury

Head injuries may cause subtle, long-term behavioural problems that often go unrecognised in primary care

­ Dr Jonathan Bird explains

Head injury has been called the silent epidemic. It accounts for one in 10 of all visits to A&E and severe disability in 0.1 per cent of the population. Cognitive and personality problems, rather than physical disability, are the main issues resulting from traumatic brain injury (TBI). These characteristic disabilities arise from the mechanics of head injury as it affects the functional anatomy of the brain.

Primary damage to the brain occurs as a result of either rotational forces or horizontal acceleration/deceleration. The brain is tethered at the brain stem; rotational forces cause it to oscillate around the central axis, resulting in shearing of long central fibres and micro haemorrhages in the central 'connecting' areas of the brain. Such microscopic but widespread injuries are termed 'diffuse axonal injury' and in severe TBI result in degeneration of sub-cortical white matter and enlargement of the cerebral ventricles.

Rotational forces also cause centrifugal pressure waves, so the poles of the brain undergo repeated buffeting against the skull and tentorium. This particularly affects the frontal poles, the orbital frontal regions, the temporal poles and the medial temporal structures. Contusion of the brain stem and mid brain may also occur.

A horizontal acceleration/deceleration injury is likely to cause contusion both at the site of the injury and on the opposite side (contre-coup).

Secondary injury can result from other factors, including haemorrhage (subdural, extradural or intracerebral) and reactive brain swelling leading to coning of the brain stem. Peripheral injuries may give rise to hypotensive shock, anoxia and fat emboli.

Thus a common accumulation of injuries to the frontal and temporal poles, the orbital frontal region, central regions and the brain stem lead to the characteristic sequelae of diffuse TBI. In contrast, localised brain injury (such as gunshot and other penetrating wounds) may cause very focal damage alone.

Predictors of outcome

The three main measures of severity are the Glasgow Coma Scale score (GCS) on admission to hospital, the period of post-traumatic amnesia (PTA) and the results of brain imaging. The GCS is an early but rather crude indicator of likely severity; the PTA, however, is one of the best later indicators, except where severe localised damage has occurred.

PTA is the time from injury to restoration of normal continuous memory (it does not include brief 'islands' of memory). A PTA of less than an hour is taken to indicate mild injury, between one and 24 hours is moderate and more than 24 hours suggests a severe injury likely to be associated with some permanent cognitive and personality deficit. The results of CT and MRI imaging, both at early and late stages, will indicate the presence of localised or diffuse (and probably permanent) injury.

Neuropsychiatric sequelae

Frontal polar damage leads to poor judgment and insight, apathy and impaired problem-solving. The injured person often has little understanding of the impact of their behaviour on others; they may deny that anything is wrong.

Orbito-frontal damage to the brain results particularly in impaired social judgment with a tendency towards impulsivity, excitability, lack of tact and childishness. Damage to the frontal regions is probably the most common and disruptive effect of severe TBI and gives rise to what is rather loosely termed 'dysexecutive syndrome'. In addition, many frontal injuries result in poor or variable motivation, lack of concentration and fatigue.

Many of these symptoms, however, are also the result of damage to the subcortical regions; this is very common and is usually due to the diffuse axonal injury described above. It results in slowed thinking, impaired arousal and drive, poor attention and concentration and poor cognitive endurance.

Attentional problems are the most common single complaint in head injury rehabilitation.

Temporal lobe damage typically results in memory impairment and speech difficulties. Damage to the dominant temporal lobe can lead to impaired verbal abilities, difficulty with word finding (even if obvious dysphasia is not present) and reduced verbal memory; damage to either temporal lobe frequently results in irritability, aggressive dyscontrol and labile mood. Occasionally there is major disruption of affect and behaviour, due to temporal lobe damage without formal neurological impairment or apparently significant cognitive deficit on neuropsychological testing.

Psychological reactions to the effects of brain injury (on both the patient and their family) are likely. Depression, anxiety, general loss of confidence and irritability are frequent responses to the changes wrought by the injury to the person's lifestyle, employment and family. In about 5 per cent of patients psychotic disorder will emerge after severe injury. Schizophreniform disorders arise in about 2.5 per cent and purely paranoid psychoses in a further 1-2 per cent; psychotic depression occurs in about 1 per cent. There is a clearly increased risk of suicide.

Specific neurological sequelae after head injuries include anosmia (as a result of damage to the olfactory bulbs and their connections), various cranial nerve deficits and, occasionally, complex movement disorders.

Post traumatic epilepsy (PTE) tends to fall into two groups. Early seizures are those that occur in the first week ­ they are seen in 2 to 5 per cent of cases. These are usually focal and reflect acute brain injury; about 25 per cent develop late PTE.

The risk of developing epilepsy is greater (up to 35 per cent) in those with very severe injuries (PTA of more than one week), depressed fracture, intracranial haematoma and identified focal injury on brain scanning. Some 50 per cent will have their first seizure in the first year after injury, with a peak at six months.

About 80 per cent will have their seizure in the first four years, but after a severe injury the risk of developing epilepsy does not drop to the population norm for about 15-20 years. The development of late PTE is associated with a worse psychological and social prognosis.

Age at injury significantly affects prognosis, older people having a relatively poor outcome. However, there is increasing acknowledgement of the potentially damaging long-term effects of TBI in childhood, although this remains under-recognised.


Rehabilitation after head injury must start early and continue long. It is best carried out by a comprehensive head injury team who can be involved in the initial triage of all TBI patients followed by early and continuing assessment and then, if relevant, by long-term rehabilitation.

In the absence of such facilities in many parts of the UK, however, the GP is often left trying to understand the effects of the injury on the patient and their family and doing their best to provide support, understanding and appropriate referral. Medication is often indicated, usually in the form of antidepressants or mood stabilisers (such as the SSRIs and carbamazepine), both for depression and anger control.

Occupational and cognitive rehabilitation will include re-education of the individual, their family and sometimes their employer; it should involve neuropsychological as well as occupational therapy. Careful family support is likely to be necessary and it may be that a work assessment with the help of the disability employment adviser will be worthwhile.

In most major cities the self-help organisation Headway (The National Head Injuries Association) can offer support and sometimes respite day care as well as, occasionally, more specific rehabilitation.

The GP is therefore often left to seek help for their patient from a motley collection of local resources. Sometimes there will be a well-developed brain injury rehabilitation service, but more often help will be available from a local Headway centre.

Quite often referral to a local psychiatric team may be necessary, although they may not have the right facilities or understanding of the problem to carry the process forward. Until a nationally co-ordinated brain injury rehabilitation service is developed this unsatisfactory situation will continue.

Which patients are vulnerable

While traumatic brain injury (TBI) can dramatically alter the personality, the person's pre-morbid personality must be taken into account. The population of people who suffer brain injuries is more likely to have shown previous behavioural and personality problems, which may result in their brain injury (due to driving too fast, not wearing a seat belt, getting into fights and so on).

This is also likely to have a bearing on their family and social support network, which come under considerable strain; their psychological reaction to the injury is important. Previous work record will be relevant ­ work may provide continuing support, or the person may find they are particularly vulnerable to loss of employment after what seems a minor injury. In many cases of TBI, compensation issues will seriously complicate the picture (this particularly applies to very minor injuries resulting in so-called 'post-concussional syndrome').

A head injury is an injury to the whole family. TBI results in a huge burden of care, largely borne by the immediate relatives.

Stress within the family is usually due to behavioural and personality changes and not to physical handicap. After a severe TBI, only 50 per cent of patients can be left in charge of the home for any time; there are likely to be major role changes for spouses as well as severe financial strain.

Social isolation often affects the whole family. Disinhibition of anger as well as disruptive and childish behaviour are usually the most damaging changes, and the children of a parent with TBI are especially at risk of developing emotional and behavioural problems.


The National Head

Injuries Association:

Jonathan Bird

is consultant neuropsychiatrist at the Burden Centre for Neuropsychiatry, Frenchay Hospital, Bristol

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Readers' comments (1)

  • As Dr Bird says, the risk of suicide after head injury is 'clearly increased.' Indeed, according to this study it is tripled or quadrupled. . When he comments that "Depression, anxiety, general loss of confidence and irritability are frequent responses to the changes wrought by the injury to the person's lifestyle" he may be missing a more direct physiological cause. After TBI, whether severe or mild, the incidence of hypopituitarism is generally reckoned to be 20-30% and depression has been linked to deficiencies in the anterior pituitary hormones GH, FSH/LH, TSH and ACTH. It has also been linked with excess prolactin, another frequent consequence of a damaged pituitary. If one adds these direct hormonal effects to the 'changes in lifestyle' - the impact of a broken relationship or loss of employment (hypopituitarism can cause impotence and fatigue) - it is easy to see why the patient might consider suicide. Hypopituitarism is treatable. Dr Mark Porter wrote recently that there are 500k undiagnosed patients in the UK It is a scandal that GPs are not alerted to this treatable complication of head injury and are encouraged instead to prescribe antidepressants, CBT and exercise therapy.

    (For the evidence linking anterior hormone deficiencies with depression see )

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