There are 200-300 admissions annually for head injuryper 100000 population in most Western countries: 10 people per 100000 die annually and the prevalence of survivors with a major persisting handicap is of the order of a 100 per 100 000. Road traffic accidents and alcohol abuse are the principal aetiological factors in this major cause of morbidity and mortality.
Linear skull fracture of the vault or base is an indicationof the severity of injury, but is not necessarily associated with any neurological sequelae. Healing takes place and surgical intervention is usually unnecessary.
Depressed skull fracture of the vault is followed by a high incidence of post-traumatic epilepsy (see p.913). Surgical elevation and debridement are usually necessary. The principal local complications of skull fracture are:
RUPTURE OF A MENINGEAL ARTERY, causing an extradural haematoma (see p. 911).
TEARING OF DURAL VEINS, causing SDH (see p.911) or CSF rhinorrhoea and otorrhoea with its risk of meningitis.
Older classifications attempted to separate ‘concussion’,in which transient coma was followed by complete recovery, from brain contusion after which there were prolonged coma and focal signs. There is little pathological support for this. The mechanisms of brain damagefollowing trauma are complex and interrelated. They involve:
• Direct axonal and neuronal damage
• Raised intracranial pressure
• Brain oedema
• Brain ischaemia
• Brain hypoxia
In a mild injury a patient is first stunned or dazed for afew seconds or minutes. Loss of consciousness is transient and following this the patient is alert, and there is no amnesia. The period of loss of consciousness indicates severity; over several hours it is regarded as indicating severe brain injury. The Glasgow Coma Scale (see p. 901)can be used to assess the degree of coma and brain damage as well as indicating prognosis; a low score implies a severe injury and 50% of such patients die or remain in a vegetative state.
Recovery may take a long period of time, depending on the severity of the injury. During early recovery patients are often restless and lethargic and they may have mild focal neurological deficits. Gradually patients become more alert to their surroundings.
These are common causes of morbidity and haveimportant social and medicolegal consequences. They include the following:
PROLONGED AND INCOMPLETE RECOVERY occurs in many patients with severe head injuries. These patients are left with impairment of higher cerebral function, hemiparesis and other deficits.
POST-TRAUMATIC EPILEPSY may occur (see p.913). ‘CHRONIC TRAUMATIC ENCEPHALOPATHY’ follows repeated (and often minor) injuries. This ‘punch drunk’ syndrome is dementia and presents with extrapyramidal and pyramidal signs. It is seen mainly in professional boxers.
THE ‘POST-TRAUMATIC SYNDROME’ describes the vague complaints of headache, dizziness and malaise that follow even minor head injuries. Depression is prominent. Symptoms may be prolonged.
BENIGN POSITIONAL VERTIGO (see p. 891) is a transient sequel of head injury. CHRONIC SUBDURAL HAEMATOMA (see p. 911).
HYDROCEPHALUS (see p.934).
Patients with head injury require skilled, prolonged and energetic supportive therapy. Acute management of the unconscious patient.
Patients left with severe neurological deficits will requirerehabilitation in specialized units. Recovery requires not only intensive physiotherapy but also the overall care of their mental state. Many patients are depressed and have behavioural problems and they and their families need long-term support and counselling.