Rupture of microaneurysms (Charcot-Bouchard aneurysms, 0.8-1.0 mm in diameter) is the principal cause of primary intracerebral haemorrhage. This occurs typically in patients with hypertension and occurs at well-defined sites-basal ganglia, pons, cerebellum and subcortical white matter. Saccular (‘berry’) aneurysms and arteriovenous malformations also bleed into the brain.
Clinically, there is no entirely reliable way of distinguishing between haemorrhage and infarction, as both produce a focal deficit. Cerebral haemorrhage, however, tends to be accompanied by a severe headache and to cause a more severe general deficit (e.g. coma) than a thromboembolic stroke. On CT an intracerebral haemorrhage is almost always immediately visualized (cf. thrombosis, see p.908). It appears as a high-density lesion sometimes with blood in the ventricular or subarachnoid space.
MANAGEMENT The general management of cerebral haemorrhage is as for cerebral infarction, although the immediate prognosis is not as good. Only when an intracerebral haematoma behaves as an expanding mass lesion causing deepening coma and coning should urgent surgical removal be considered. Anticoagulant drugs are of course contraindicated. Cerebellar haemorrhage
It is important to recognize cerebellar haemorrhage because it causes an acute hydrocephalus. There is headache nd rapid reduction of consciousness with signs of brain stem origin (e.g. nystagmus, ocular palsies). The gaze deviates to the side of the lesion. Emergency surgery ay be necessary to remove a cerebellar haematoma.
The term subarachnoid haemorrhage (SAH) describes pontaneous rather than traumatic arterial bleeding into the subarachnoid space.
INCIDENCE SAH accounts for 10% of cerebrovascular disease and has an annual incidence of 15 per 100000.
The causes of SAH are shown in Table 18.30. It is unusual to find any contributing disease. Saccular (‘berry’) aneurysms (Fig. 18.18) Saccular aneurysms form on the circle of Willis and its adjacet branches. The common sites of aneurysms are: JUNCTION OF THE POSTERIOR COMMUNICATING ARTERY AND THE INTERNAL CAROTID ARTERYposterior communicating artery aneurysm
JUNCTION OF THE ANTERIOR COMMUNICATING ARTERY AND THE ANTERIOR CEREBRAL ARTERYanterior communicating artery aneurysm
BIFURCATION OF THE MIDDLE CEREBRAL ARTERYmiddle cerebral artery aneurysm Other sites are on the basilar artery, the PICA, the intracavernous internal carotid artery and the ophthalmic artery. Saccular aneurysms are an incidental finding in 1% of autopsies and may be multiple.Aneurysms cause symptoms either by spontaneous rupture (when there is usually no preceding history) or by pressure effects on surrounding structures, e.g. a posterior communicating aneurysm may cause a painful third
Arteriovenous malformation (A VM)
This is a lesion of developmental origin, usually withinthe hemisphere. An AVM may cause epilepsy, which is often focal. O nce an AVM has ruptured to cause an SAH there is a tendency to rebleed at a rate of 10% per year.
The onset is sudden with a devastating headache, often occipital. This is usually followed by vomiting and often by loss of consciousness. The patient remains comatose or drowsy for several hours to several days. Less-severe headaches may cause diagnostic difficulties. On examination, there is neck stiffness and a positive Kernig’s sign. Papilloedema is sometimes present and may be accompanied by retinal haemorrhages and subhyaloid haemorrhage (massive retinal haemorrhage tracking beneath the hyaloid membrane).
CT scanning shows subarachnoid or intraventricular blood. The CSF is yellow (xanthochromic) several hours after SAH. Lumbar puncture is not necessary if the diagnosis is made by CT.
Carotid and vertebral angiography is usually performed in all patients who are potentially fit for surgery (i.e. those who are young-below 55-60 years-and not in coma) to establish the site of the bleeding.
SAH must be differentiated from severe migraine. This is sometimes difficult. Acute meningitis may also cause a ery abrupt headache.
Blood clot in the subarachnoid space can lead to obstructionof CSF flow and hydrocephalus. This can asymptomatic but can be a cause of deteriorating conscious level a few days or weeks after the initial event. Diagnosis is by CT and a drainage procedure may berequired.
Nearly half the cases of SAH are either dead or moribund before they reach hospital. Of the remainder, a further 10-20% die in the early weeks in hospital from further bleeding.
Patients who are comatose or who have severe neurological deficits have a poor prognosis. In others, where angiography demonstrates aneurysm, a direct neurosurgical approach to clip the neck of the aneurysm is carried out. In selected cases the results of surgery are excellent. The immediate treatment of patients with SAH is bedrest and supportive measures. Hypertension should be controlled. Dexamethasone and antifibrinolytic agents are often prescribed, but their place in therapy is dubious. Nimodipine, a calcium-channel blocking agent, has been shown to reduce the mortality.
Severe spasm of the intraranial arteries sometimes complicates SAH and is a poor prognostic sign. It is usual to refer all cases of SAH to a specialist centre for a decision about angiography and possible surgery.
SUBDURAL AND EXTRADURAL HAEMORRHAGE AND
These conditions are of great neurosurgical importance as both may cause death unless treated promptly. Subdural haematoma (SDH) (see Fig. 18.20b, p. 931) SOH occurs when blood accumulates in the subdural space following rupture of a vein. It is almost always due to head injury, which may be minor, but the latent interval between injury and symptoms may be weeks or months. Chronic SOH is common in the elderly and in patients with alcohol abuse.
Headache, drowsiness and cofusion are common; the symptoms are indolent and often fluctuate. Focal deficits such as hemiparesis or sensory loss may develop and epilepsy may occur. Stupor and coma gradually ensue. Extradural haemorrhage (see Fig. 18.20a)
This follows a tear of a branch of a middle meningeal artery, usually underlying a linear skull fracture. Blood accumulates rapidly over minutes or hours in the extradural space. The most characteristic picture is of a head injury with a brief duration of unconsciousness followed by a ‘lucid interval’ of recovery. The patient then develops a progressive hemiparesis and stupor, and rapid transtentorial ‘coning’, with first an ipsilateral dilated pupil, followed by bilateral fixed dilated pupils, tetraplegia and death.
An acute subdural haemorrhage presents in a similar way
The diagnosis of extradural or subdural haemorrhage orhaematoma is confirmed by CT scan and/or arteriography. MRI scanning is also used. Surgical drainage is carried out. If it is performed early, the outlook is excellent. When far from specialist help (e.g. in wartime or at sea), drainage should be carried out when the diagnosis is suspected on clinical grounds alone; this procedure has been life-saving.
In the elderly, some SDHs resolve spontaneously and can be monitored with serial CT scans.
CORTICAL VENOUS AND DURAL VENOUS SINUS THROMBOSIS
These are unusual complications of skull and paranasal (air) sinus infection, dehydration or severe intercurrent illness. There is also an association with pregnancy and the contraceptive pill.
Cortical venous thrombosis The venous infarct caused by the thrombosis leads to focal signs (e.g. hemiparesis) and epilepsy. There is often a fever.
Dural venous sinus thromboses CAVERNOUS SINUS THROMBOSIS. This causes ocular pain, proptosis and chemosis. An external and internal ophthalmoplegia with papilloedema develop.
LATERAL AND SAGITTAL SINUS THROMBOSIS. This causes raised intracranial pressure with headache, papilloedema and often epilepsy.
Treatment and investigation is directed at the underlying cause of the thrombosis. Anticonvulsants are used in epilepsy and antibiotics in infection. Anticoagulants are sometimes used.