It is unlikely that high intracranial pressure alone directly damages neuronal tissue, but brain damage occurs as a result of tonsillar or tentorial herniation (see page 81). A progressive increase in intracranial pressure due to a supratentorial haematoma initially produces midline shift. Herniation of the medial temporal lobe through the tentorial hiatus follows (lateral tentorial herniation), causing midbrain compression and damage. Uncontrolled lateral tentorial herniation or diffuse bilateral hemispheric swelling will result in central tentorial herniation. Herniation of the cerebellar tonsils through the foramen magnum (tonsillar herniation) and consequent lower brain stem compression may follow central tentorial herniation or may result from the infrequently occurring traumatic posterior fossa haematoma.

Infection

The presence of a dural tear provides a potential route for infection. This seldom occurs within 48 hours of injury. Meningitis may develop after several months or years.

DIFFUSE DAMAGE

Diffuse axonal injury

Shearing forces cause immediate mechanical damage to axons. Over the subsequent 48 hours, further damage results from release of excitotoxic neurotransmitters which cause Ca²⁺ influx into cells and triggers the phospholipid cascade (page 246). Genetic susceptibility conferred by the presence of the APOE ͛4 gene may also play a part. Depending on the severity of the injury, effects may range from mild coma to death.

The macrosopic appearance may appear entirely normal but in some patients pathological sections reveal small haemorrhagic tears, particularly in the corpus callosum or in the superior cerebellar peduncle.

Microscopic evidence of neuronal damage depends on the duration of survival and on the severity of the injury. After a few days, retraction balls and microglial clusters are seen in the white matter.

If the patient survives 5 weeks or more after injury then appropriate staining demonstrates Wallerian degeneration of the long tracts and white matter of the cerebral hemispheres. Even a minor injury causing a transient loss of consciousness produces some neuronal damage. Since neuronal regeneration is limited, the effects of repeated minor injury are cumulative.

Cerebral swelling

This may occur with or without focal damage. It results from either vascular engorgement or an increase in extra- or intracellular fluid. The exact causative mechanism remains unknown

Cerebral ischaemia

Cerebral ischaemia commonly occurs after severe head injury and is caused by either hypoxia or impaired cerebral perfusion. In the normal subject, a fall in blood pressure does not produce a drop in cerebral perfusion since ‘auto-regulation’ results in cerebral vasodilatation. After head injury, however, autoregulation is often defective and hypotension may have more drastic effects. Glutamate excess and free radical accumulation may also contribute to neuronal damage (see page 246).

MULTIPLE INJURY – PRIORITIES OF ASSESSMENT

Patients admitted in coma with multiple injuries require urgent care and the clinician must be aware of the priorities of assessment and management.

When intracranial haematoma is suspected, a CT scan is essential, especially before clinical signs are masked by a general anaesthetic required for the management of limb or abdominal injuries. However, if difficulty occurs in maintaining blood pressure, then urgent laparotomy or thoracotomy would take precedence over investigation of a possible intracranial haematoma.

HEAD INJURY – ASSESSMENT

Some patients may describe the events leading to and following head injury, but often the doctor depends on descriptions from witnesses.

Points to determine:

Period of loss of consciousness: relates to severity of diffuse brain damage and may range from a few seconds to several weeks.

Period of post-traumatic amnesia: the period of permanent amnesia occurring after head injury. This reflects the severity of damage and in severe injuries may last several weeks.

Period of retrograde amnesia: amnesia for events before the injury.

Cause and circumstances of the injury: the patient may collapse, or crash his vehicle as a result of some preceding intracranial event, e.g. subarachnoid haemorrhage or epileptic seizure. The more “violent” the injury, the greater the risk of associated extracranial injuries.

Presence of headache and vomiting: these are common symptoms after head injury. If they persist, the possibility of intracranial haematoma must be considered.

HEAD INJURY – CLINICAL ASSESSMENT

PETROUS FRACTURE

Bleeding from the external auditory meatus or CSF otorrhoea:

3. Conscious level – Glasgow Coma Score (GCS)

Assess patient’s conscious level in terms of eye opening, verbal and motor response on admission (see page 5) and record at regular intervals thereafter. An observation chart incorporating these features is essential and clearly shows the trend in the patient’s condition. Deterioration in conscious level indicates the need for immediate investigation and action where appropriate.

Note: This chart shows a ‘14 point scale’ with a maximum score of ‘14’ in a fully conscious patient. Many centres use a 15 point coma scale where ‘Flexion to pain’ is divided into ‘normal’ or ‘spastic’ flexion (see page 29).

4. Pupil response

The light reflex (page 142) tests optic (II) and oculomotor (III) nerve function. Although II nerve damage is important to record and may result in permanent visual impairment, it is the III nerve function which is the most useful indicator of an expanding intracranial lesion. Herniation of the medial temporal lobe through the tentorial hiatus may damage the III nerve directly or cause midbrain ischaemia, resulting in pupil dilatation with impaired or absent reaction to light. The pupil dilates on the side of the expanding lesion and is an important localising sign. With a further increase in intracranial pressure, bilateral pupillary dilatation may occur.

5. Limb weakness

Determine limb weakness by comparing the response in each limb to painful stimuli (page 30). Hemiparesis or hemiplegia usually occurs in the limbs contralateral to the side of the lesion. Indentation of the contralateral cerebral peduncle by the edge of the tentorium cerebelli (Kernohan’s notch) may produce an ipsilateral deficit, a false localising sign more often seen with chronic subdural haematomas. Limb deficits are therefore of limited value in lesion localisation.

6. Eye movements

Evaluation of eye movements does not help in immediate management, but provides a useful prognostic guide.

Eye movements may occur spontaneously, or can be elicited reflexly (page 30) by head rotation (oculocephalic reflex) or by caloric stimulation (oculovestibular reflex).

Abnormal eye movements may result from: brain stem dysfunction, damage to the nerves supplying the extraocular muscles or damage to the vestibular apparatus. Absent eye movements relate to low levels of responsiveness and indicate a gloomy prognosis.

Vital signs

At the beginning of the century, the eminent neurosurgeon Harvey Cushing noted that a rise in intracranial pressure led to a rise in blood pressure and a fall in pulse rate and produced abnormal respiratory patterns. In the past, much emphasis has been placed on close observation of these vital signs in patients with head injury, but these changes may not occur and when present are usually preceded by deterioration in conscious level. Close observation of consciousness is therefore more relevant.

Cranial nerve lesions

Basal skull fracture or extracranial injury can result in damage to the cranial nerves. Evidence of this damage must be recorded but, with the exception of a III nerve lesion, does not usually help immediate management. Full cranial nerve examination is difficult in the comatose patient and this can await patient co-operation.

Clinical assessment cannot reliably distinguish the type or even the site of intracranial haematoma, but is invaluable in indicating the need for further investigation and in providing a baseline against which any change can be compared.

HEAD INJURY – INVESTIGATION AND REFERRAL CRITERIA

IN THE ACCIDENT AND EMERGENCY DEPARTMENT (A&E)

Various guidelines now exist. The following are based on those from the National Institute for Health and Clinical Excellence (NICE). (Further details available at http://www.nice.org.uk).

Admit to Hospital	Discharge from A&E
• New abnormalities on imaging • Glasgow coma score < 15 (even if imaging normal) • Persistent vomiting or severe headache • Fits criteria for a CT scan within 8 hours • Other concerns, e.g. drugs, alcohol intoxication, other injuries, shock, meningism, CSF leak, suspected non-accidental injury

• If Glasgow coma score = 15

AND

• Appropriate supervision at home

• CT not indicated or

• Normal imaging head and spine

• All symptoms and signs resolved

Referral to Neurosurgical Unit

Transfer to the neurosurgical unit

Prior to the transfer, ensure that resuscitation is complete, and that more immediate problems have been dealt with (see page 221). Insert an oropharyngeal airway. Intubate and ventilate if the patient is in coma or if the blood gases are inadequate (PO₂ <8 kPa on air, 13 kPa on O₂ or CO₂ > 6 kPa). If the patient’s conscious level is deteriorating, an intravenous bolus infusion of 100 ml of 20% mannitol should ‘buy time’ by temporarily reducing the intracranial pressure.

NOTE: for comatose patients with an unstable systemic state from multiple injuries, a negative CT scan in the local hospital may avoid a dangerous transfer to the neurosurgical unit.

Cervical spine injury may accompany head injury. Guidelines also exist with criteria for investigation. (For full details see http://www.nice.org.uk/guidance/index.jsp?action=download&o=36259).

For ADULTS and CHILDREN 10 years and over

AP, Lateral and Odontoid Peg X-rays if	CT cervical spine if
• Impaired neck rotation to right or left • No indication for CT scanning • Not safe to assess clinically • Neck pain/midline tenderness + ≥ 65 years or dangerous mechanism of injury • To exclude injury urgently e.g. prior to surgery

• Patient intubated

• Continued suspicion despite X-rays

• Inadequate X-rays

• Undergoing CT scanning for another reason e.g. Glasgow coma score < 13 or multi-region trauma

HEAD INJURY – INVESTIGATION

CT scan: the investigation of choice for head injury (and cervical spine injury incertain circumstances – see page 227).

Scans must extend from the posterior fossa to the vertex, otherwise haematomas in these sites will be missed.

With diffuse axonal shearing injuries, small haematomas may be seen on CT scan scattered throughout the white matter, particularly in the corpus callosum, the subcortical white matter and in the brain stem adjacent to the cerebellar peduncles.

If hydrocephalus is present on the upper scan cuts, look carefully for a haematoma (extradural, subdural or intracerebral) in the posterior fossa, compressing and obstructing the 4th ventricle.

Further investigation may be required to exclude other coincidental or contributory causes of the head injury, e.g. drugs, alcohol, postictal state, encephalitis (Cause of coma, see page 86).

If a CT scan is not available, a skull fracture on X-ray identifies those at high risk of intracranial haematoma. In those patients, referral to a neurosurgical unit for a CT scan is essential (see page 227).

HEAD INJURY – MANAGEMENT

Management aims at preventing the development of secondary brain damage from intracranial haematoma, ischaemia, raised intracranial pressure with tentorial or tonsillar herniation and infection.

– Ensure the airway is patent and that blood oxygenation is adequate. Intubation is advisable in patients ‘flexing to pain’ or worse. Ventilation may be required if respiratory movements are depressed or lung function is impaired, e.g. ‘flail’ segment, aspiration pneumonia, pulmonary contusion or fat emboli. Hypoxia can cause direct cerebral damage, but in addition causes vasodilatation resulting in an increase in cerebral blood volume with subsequent rise in ICP.

– A space-occupying haematoma requires urgent evacuation (see over). If the patient’s conscious level is deteriorating, give an initial or repeat i.v. bolus of mannitol (100 ml of 20%). Coagulation should be checked and any deficits corrected.

– Scalp lacerations require cleaning, inspection to exclude an underlying depressed fracture and suturing.

– Correct hypovolaemia following blood loss – but avoid fluid overload as this may aggravate cerebral oedema. In adults, 2 litres/day of fluid is sufficient. Commence nasogastric fluids or oral fluids when feasible.

– Anticonvulsants (e.g. phenytoin) must be given intravenously if seizures occur; further seizures and in particular status epilepticus significantly increase the risk of cerebral anoxia.

– Monitor intracranial pressure (ICP), blood pressure and cerebral perfusion pressure (CPP) in selected patients with diffuse swelling or after evacuation of an intracranial haematoma. Maintain CPP either by raising blood pressure if low or by treating raised intracranial pressure.

– Brain protective agents include corticosteroids, free radical scavengers, calcium channel blockers, and glutamate antagonists. The evolution of axonal damage after a diffuse shearing injury provides a potential window of opportunity for treatment. Despite experimental animal studies revealing encouraging results, trials of these agents in head-injured patients have failed to show efficacy, perhaps due to insufficient patient numbers or a failure to target treatment at appropriate patients. A recent study of corticosteroids involving 10 000 patients has shown a worse outcome in the treatment group (the CRASH study).

– Operative repair of a dural defect is required if CSF leak persists for more than 7 days. (Many still use prophylactic antibiotics in patients with a CSF leak, but there is no conclusive evidence of their efficacy and they may do more harm than good by encouraging the growth of resistant organisms.) The development of meningitis requires prompt treatment with an empirical antibiotic.

INTRACRANIAL HAEMATOMA

Most intracranial haematomas require urgent evacuation – evident from the patient’s clinical state combined with the CT scan appearance of a space-occupying mass.

Extradural haematoma

Using the CT scan the position of the extradural haematoma is accurately delineated and a ‘horse shoe’ craniotomy flap is turned over this area, allowing complete evacuation of the haematoma. For low temporal extradural haematomas, a ‘question mark’ flap may be more suitable. If patient deterioration is rapid, a burr hole and craniectomy positioned centrally over the haematoma may provide temporary relief, but this seldom provides adequate decompression.

Subdural/intracerebral haematoma (‘burst lobe’)

Subdural and intracerebral haematomas usually arise from lacerations on the under-surface of the frontal and/or temporal lobes. Again the CT scan is useful in demonstrating the exact site. A ‘question mark’ flap permits good access to both frontal and temporal ‘burst’ lobes. The subdural collection is evacuated and any underlying intracerebral haematoma is removed along with necrotic brain.

N.B. Burr holes are insufficient to evacuate an acute subdural haematoma or to deal with any underlying cortical damage.

Conservative management of traumatic intracranial haematomas

Not all patients with traumatic intracranial haematomas deteriorate. In some, the haematomas are small and clearly do not require evacuation. In others, however, the decision to operate proves difficult, e.g. the CT scan may reveal a moderate-sized haematoma with minimal or no mass effect in a conscious but confused patient.

If conservative management is adopted, careful observation in a neurosurgical unit is essential. Any deterioration indicates the need for immediate operation. In this group of patients, intracranial pressure monitoring may serve as a useful guide. An intracranial pressure of 25 mmHg or more suggests that haematoma evacuation is required as the likelihood of subsequent deterioration with continued conservative management would be high.

TREATMENT OF RAISED INTRACRANIAL PRESSURE (ICP)

Raised ICP in the absence of any easily treatable condition (e.g. intracranial haematoma or raised pCO₂) requires careful management. The various techniques used to lower ICP have already been described (pages 83–84) but these must not be applied indiscriminately.

Recent studies show that even in a modern ITU head injured patient are still at risk of sustaining potentially harmful “insults” to the brain in the first few days after head injury from high ICP, low BP, low cerebral perfusion pressure (CPP), hypoxaemia, hypoglycaemia or raised temperature.

Most believe that both raised ICP and reduced cerebral perfusion pressure (CPP) can exacerbate brain damage. What is less clear is whether treatment should focus on lowering ICP or increasing CPP. When autoregulation is impaired, raising CPP beyond 70 mmHg could cause harm. The blind use of hyperventilation in the past to lower ICP by causing vasoconstriction and reduced intracranial blood volume has now been recognised to produce worse outcomes by aggravating cerebral ischaemia.

Patient selection for ICP monitoring: Monitoring ICP and CPP is most relevant in patients with a flexion response to painful stimuli or worse (a response of ‘localising to pain’ signifies a milder degree of injury and spontaneous recovery is likely). Such patients may have already undergone removal of an intracranial haematoma or may have had no mass lesion on CT scan (i.e.: diffuse injury or contusional damage). Each neurosurgical unit is likely to have its own policy for ICP monitoring but the following outline may serve as a guide for patients with no intracranial mass lesion –

DIFFUSE BRAIN DAMAGE/NEGATIVE CT SCAN

A proportion of patients have no intracranial haematoma on CT scan or have only a small haematoma or contusion without mass effect.

In these patients, coma or impairment of conscious level may be due to:

Several of these factors may coexist and contribute to brain damage in patients with intracranial haematoma.

The management principles outlined above apply; in particular it is essential to ensure that respiratory function is adequate and that cerebral perfusion pressure is maintained.

Fat emboli usually occur a few days after injury and may be related to fracture manipulation; deterioration of respiratory function usually accompanies cerebral damage and most patients require ventilation.

Meningitis may occur several days after injury in the presence of basal fractures.

Cerebral swelling may occur at any time after injury and cause a rise in intracranial pressure.

REPEAT CT SCANNING

Occasionally, small areas of ‘insignificant’ contusion on an initial CT scan may develop into a space-occupying haematoma requiring evacuation. Following haematoma evacuation, recollection may occur in 5–10% of cases.

DEPRESSED SKULL FRACTURE

This injury is caused by a blow from a sharp object. Since diffuse ‘deceleration’ damage is minimal, patients seldom lose consciousness.

SIMPLE DEPRESSED FRACTURE (closed injury)

There is no overlying laceration and no risk of infection. Operation is not required except for cosmetic reasons. Removal of any bone spicules imbedded in brain tissue does not reverse neuronal damage.

COMPOUND DEPRESSED FRACTURE (open injury)

A scalp laceration is related to (but does not necessarily overlie) the depressed bone segments. A compound depressed fracture with an associated dural tear may result in meningitis or cerebral abscess.

Investigation

Double density appearance on skull X-ray suggests depression but tangential views may be required to establish the diagnosis. Impairment of conscious level or the presence of focal signs indicate the need for a CT scan to exclude underlying extradural haematoma or severe cortical contusion. Selecting bone window levels on CT scan will clearly demonstrate any depressed fragments.

Management

Treatment aims to minimise the risk of infection. The wound is debrided and the fragments elevated within 24 hours from injury. Bone fragments are either removed or replaced after washing with antiseptic. Antibiotics are not essential unless the wound is excessively dirty.

If the venous sinuses are involved in the depressed fracture, then operative risks from excessive bleeding may outweigh the risk of infection and antibiotic treatment alone is given.

Complications

Most patients make a rapid and full recovery, but a few develop complications:

Infection: May lead to meningitis or abscess formation. Some believe that operation does not reduce the infection risk and advocate a conservative approach unless contamination is severe.

Epilepsy: Early epilepsy (in the first week) occurs in 10% of patients with depressed fracture. Late epilepsy develops in 15% overall, but is especially common when the dura is torn, when focal signs are present, when post-traumatic amnesia exceeds 24 hours or when early epilepsy has occurred (the risk ranges from 3 to 60%, depending on the number of the above factors involved). Elevation of the bone fragments does not alter the incidence of epilepsy.

DELAYED EFFECTS OF HEAD INJURY

POST-TRAUMATIC EPILEPSY

Early epilepsy (occurring within the first week from injury)

Early epilepsy occurs in 5% of patients admitted to hospital with non-missile (i.e. deceleration) injuries. It is particularly frequent in the first 24 hours after injury. Focal seizures are as common as generalised seizures. Status epilepticus occurs in 10%.

The risk of early epilepsy is high in

– children under 5 years.

– patients with prolonged post-traumatic amnesia

– patients with an intracranial haematoma

– patients with a compound depressed fracture.

Late epilepsy (occurring after the first week from injury)

Late epilepsy also occurs in about 5% of all patients admitted to hospital after head injury. It usually presents in the first year, but in some the first attack occurs as long as 10 years from the injury. Late epilepsy is prevalent in patients with

– early epilepsy (25%)

– intracranial haematoma (35%)

– compound depressed fracture (17%).

Prophylactic anticonvulsants appear to be of little benefit in preventing the development of an epileptogenic focus. Management is discussed on page 102.

CEREBROSPINAL FLUID (CSF) LEAK

After head injury a basal fracture may cause a fistulous communication between the CSF space and the paranasal sinuses or the middle ear. Profuse CSF leaks (rhinorrhoea or otorrhoea) are readily detectable, but brain may partially plug the defect and the leak may be minimal or absent. Patients risk developing meningitis particularly in the first week, but in some this occurs after several years. When this is associated with anterior fossa fractures, it is usually pneumococcal; when associated with fractures through the petrous bone, a variety of organisms may be involved.

Clinical signs of a basal fracture have previously been described (page 222). The patient may comment on a ‘salty taste’ in the mouth. Anosmia suggests avulsion of the olfactory bulb from the cribriform plate.

Management

*A Cochrane Review has concluded that evidence does not support the use of prophylactic antibiotics. Prophylactic antibiotics only encourage resistance and late attacks of meningitis may still occur despite their use.

(Lancet (1994) 344:1547–1551)

Preoperative investigations

Coronal high definition CT scanning should identify the fracture site.

CT cisternography – CT scanning after running contrast injected into the lumbar theca, up to the basal cisterns may identify the exact site of the leak.

CSF isotope infusion studies combined with pledget insertion into the nasal recesses may also be of value, but results can be misleading.

Operation

As fractures of the anterior fossa often extend across the midline, a bifrontal exploration is required. The dural tear is repaired with fascia lata, pericranium or synthetic dural substitute. A CSF leak through the middle ear requires a subtemporal approach.

Failure to repair a CSF fistula may result from impaired CSF absorption with an intermittent or persistent elevation of ICP. In these patients a CSF shunt may be required.

POSTCONCUSSIONAL SYMPTOMS

Even after relatively minor head injury, patients may have persistent symptoms of:

– headache, dizziness and increased irritability

– difficulty in concentration and in coping with work

– fatigue and depression.

This condition was once thought to have a purely psychological basis, but it is now recognised that in an injury of sufficient severity to cause loss of consciousness, or a period of post-traumatic amnesia, some neuronal damage occurs; studies show a distinct delay in information processing in these patients, requiring several weeks to resolve. Vestibular ‘concussion’ (end-organ damage) may contribute to the symptomatology (‘dizziness’ and vertigo).

CUMULATIVE BRAIN DAMAGE

The effects of repeated neuronal damage are cumulative; when this exceeds the capacity for compensation, permanent evidence of brain damage ensues. The ‘punch-drunk’ state is well recognised in boxers; dementia may also occur from repeated head injury in jockeys.

CRANIAL NERVE DAMAGE

Cranial nerve damage occurs in about one-third of patients with severe head injury, but treatment is seldom of benefit. These lesions may contribute towards the patient’s residual disability.

OUTCOME AFTER SEVERE HEAD INJURY

Head injury remains a major cause of disability and death, especially in the young. Of those patients who survive the initial impact and remain in coma for at least 6 hours, approximately 40% die within 6 months. The extent of recovery in the remainder depends on the severity of the injury. Residual disabilities include both mental (impaired intellect, memory and behavioural problems) and physical defects (hemiparesis and dysphasia). Most recovery occurs within the first 6 months after injury, but improvement may continue for years. Physiotherapy and occupational therapy play an important role not only in minimising contractures and improving limb power and function but also in stimulating patient motivation.

Outcome is best categorised with the Glasgow Outcome Scale (GOS – see page 214) which uses dependence to differentiate between intermediate grades. After severe injury, about 40% regain an independent existence and may return to premorbid social and occupational activities. Inevitably some remain severely disabled requiring long term care, but few (< 2%) are left in a vegetative state with no awareness or ability to communicate with their environment (see page 214). Prognosis in this group is marginally better than for non-traumatic coma – with about one-third of those vegetative at one month regaining consciousness within one year; of those who regain consciousness, over two-thirds either subsequently die or remain severely disabled. Of those vegetative at 3 months after the injury, none regain an independent existence.

Prognostic features following traumatic coma

The duration of coma relates closely to the severity of injury and to the final outcome, but in the early stages after injury the clinician must rely on other features – age, eye opening, verbal and motor responses, pupil response and eye movements.

	Poor outcome (GOS 1–3)	Favourable outcome (GOS 4–5)
Patients in coma for > 6 hours	61%	39%
Best Glasgow Coma Score > 11	18%	82%
Best Glasgow Coma Score 8–10	32%	68%
Best Glasgow Coma Score < 8	73%	27%
Pupillary response – reacting	50%	50%
Pupillary response – non-reacting	96%	4%
Age < 20 years	41%	59%
Age > 60 years	94%	6%

CHRONIC SUBDURAL HAEMATOMA

Subdivision of subdural haematomas into acute and subacute forms serves no practical purpose. Chronic subdural haematoma however is best considered as a separate entity, differing both in presentation and management.

Predisposing factors

Breakdown of protein within the haematoma and a subsequent rise in osmotic pressure was originally believed to account for the gradual enlargement of the untreated subdural haematoma. Studies showing equality of osmotic pressures in blood and haematoma fluid cast doubt on this theory and recurrent bleeding into the cavity is now known to play an important role.

Clinical features tend to be non-specific.

– Dementia.

– Deterioration in conscious level, occasionally with fluctuating course.

– Symptoms and signs of raised ICP.

– Focal signs occasionally occur, especially limb weakness. This may be ipsilateral to the side of the lesion, i.e. a false localising sign (see page 224).

Diagnosis

CT Scan appearances depend on the time between the injury and the scan.

With injuries 1–3 weeks old, the subdural haematoma may be isodense with brain tissue. In this instance, i.v. contrast enhancement may delineate the cortical margin.

Beyond 3 weeks subdural haematomas appear as a low density lesion.

If CT scan shows midline shift without any obvious extra- or intracerebral lesion, look at the shape of the ventricles.

Management

CEREBROVASCULAR DISEASES

Vascular diseases of the nervous system are amongst the most frequent causes of admission to hospital. The annual incidence in the UK varies regionally between 150–200/100 000, with a prevalence of 600/100 000 of which one-third are severely disabled.

Better control of hypertension, reduced incidence of heart disease and a greater awareness of all risk factors have combined to reduce mortality from stroke. Despite this, stroke still ranks third behind heart disease and cancer as a cause of death in affluent societies.

RISK FACTORS

Prevention of cerebrovascular disease is more likely to reduce death and disability than any medical or surgical advance in management. Prevention depends upon the identification of risk factors and their correction. Increasing age is the strongest risk factor (but is not amenable to correction).

Hypertension

Hypertension is a major factor in the development of thrombotic cerebral infarction and intracranial haemorrhage.

There is no critical blood pressure level; the risk is related to the height of blood pressure and increases throughout the whole range from normal to hypertensive. A 6 mmHg fall in diastolic blood pressure is associated in relative terms with a 40% fall in the fatal and non-fatal stroke rate.

Systolic hypertension (frequent in the elderly) is also a significant factor and not as harmless as previously thought.

CEREBROVASCULAR DISEASE – MECHANISMS

‘Stroke’ is a generic term, lacking pathological meaning. Cerebrovascular diseases can be defined as those in which brain disease occurs secondary to a pathological disorder of blood vessels (usually arteries) or blood supply.

CEREBROVASCULAR DISEASE – NATURAL HISTORY

Approximately one-third of all ‘strokes’ are fatal. The age of the patient, the anatomical size of the lesion, the degree of deficit and the underlying cause all influence the outcome.

Immediate outcome

In cerebral haemorrhage, mortality approaches 50%.

Cerebral infarction fares better, with an immediate mortality of less than 20%, fatal lesions being large with associated oedema and brain shift.

Embolic infarction carries a better outcome than thrombotic infarction.

Fatal cases of infarction die either at onset, within a few days because of cytotoxic cerebral oedema or later from cardiovascular or respiratory complications.

The level of consciousness on admission to hospital gives a good indication to immediate outcome. The deeper the conscious level the graver the prognosis.

Long-term outcome

The prognosis following infarction due to thrombosis or embolisation from diseased neck vessels or heart is dependent on the progression of the underlying atherosclerotic disease. Recurrent cerebral infarction rates vary between 5% and 15% per year. Symptoms of coronary artery disease and/or peripheral vascular disease may also ensue. Five year mortality is 44% for males and 36% for females.

The long-term prognosis following survival from haemorrhage depends upon the cause and the treatment.

CEREBROVASCULAR DISEASE – CAUSES

EMBOLISATION (25%) from:

DISEASES OF BLOOD

e.g. Coagulopathies or Haemoglobinopathies

CEREBRAL VENOUS THROMBOSIS

Thrombosis of cerebral veins may occur with infection, dehydration or in association with oestrogen excess, either post-partum or combined oral contraceptive use.

DECREASED CEREBRAL PERFUSION

Hypotension, from cardiac arrhythmia or GI bleed, can lead to infarction in the watershed between arterial territories.

HAEMORRHAGE (20%)

Into the brain substance – parenchymal (15%) and/or subarachnoid space (5%)	Neoplasm
	Coagulation disorder e.g. haemophilia
Hypertension	Anticoagulant therapy
Amyloid vasculopathy	Vasculitis
Aneurysm	Drug abuse e.g. cocaine
Arteriovenous malformation	Trauma