Major cerebral infarction from thromboembolism typically produces a stroke, but small infarcts may present as TIAs or may even be symptomless. The clinical picture is very variable and depends on the site and extent of the infarct. It is no longer usual to attempt to subdivide the site into the precise distribution of a single branch vessel. Nevertheless, the site of cerebral infarction may be inferred from the pattern of the physical signs (e.g. cortex, internal capsule, brain stem).
SYMPTOMS AND SIGNS
The commonest stroke is the hemiplegia caused by infarction of the internal capsule following thromboembolism of a branch of the middle cerebral artery. A similar picture is caused by internal carotid occlusion (Fig. 18.15).
The signs are those of an acute UMN lesion of one side, including the face. Aphasia is usual when the dominant hemisphere is affected. The limbs are at first flaccid and areflexic. Headache is unusual and consciousness is not lost. After a variable period the reflexes recover and becomeexaggerated and an extensor plantar response appears. Weakness is maximal at first, and recovers gradually over the course of days, weeks or months.
Brain stem infarction
Infarction in the brain stem causes complex patterns of dysfunction depending on the site of the lesion and its relationship to the cranial nerve nuclei, long tracts and brain stem connections (Table 18.27).
THE LATERAL MEDULLARY SYNDROME, formerly called posterior inferior cerebellar artery (PICA) thrombosis, or Wallenberg’s syndrome, is the most widely recognized syndrome of brain stem infarction. It is caused by PICA or vertebral artery thromboembolism (Fig. 18.16). There is sudden vertigo, vomiting and ipsilateral ataxia, with contralateral loss of pain and temperature sensation (Table 18.28).COMA may be caused by bilateral brain stem infarction that damages the reticular formation.
THE ‘LOCKED-IN SYNDROME’ is caused by upper brain
stem infarction; despite being conscious, the patient cannot speak, swallow or move the limbs. PSEUDOBULBAR PALSY (see p. 347) may be caused by brain stem infarction.
Other types of infarction
LACUNAR INFARCTION. Lacunes are small «1.5 ern”) areas of infarction seen at post mortem in patients with hypertension. Pure motor stroke, pure sensory stroke, sudden unilateral ataxia and sudden dysarthria with a clumsy hand are typically caused by single lacunar infarcts. Lacunar infarction may be symptomless.
MULTI-INFARCT DEMENTIA. Multiple lacunes or larger infarcts cause the picture of generalized intellectual loss that is sometimes seen in patients with cerebrovascular disease. The condition tends to occur with a stepwise progression with each subsequent infarct. The final picture is of dementia, pseudobulbar palsy and a shuffling
gait with small steps. There may be confusion clinically with Parkinson’s disease, and this syndrome has been called ‘atherosclerotic parkinsonism’ in the past.
HEMIANOPIC VISUAL LOSS OR CORTICAL BLINDNESS (Anton’s syndrome, see p. 883). This may follow infarction of the posterior cerebral arteries. WEBER’S SYNDROME. This consists of an ipsilateral third nerve paralysis with a contralateral hemiplegia due to a lesion in one half of the midbrain. Paralysis of upward gaze, due to a lesion localized in the region of the red nucleus, may also occur.
WATERSHED INFARCTION. This describes the multiple cortical infarcts that occur during prolonged episodes of very low cerebral perfusion (e.g. following massive myocardial infarction or hypotensive therapy). The border zones between the areas supplied by the anterior, middle and posterior cerebral arteries are damaged. A syndrome of cortical visual loss and memory and intellectual impairment is typical.
In addition to the neurological examination, particular care should be taken to find a possible source of embolus (e.g. carotid bruit, atrial fibrillation, valve lesion or evidence of endocarditis) and to determine whether hypertension or postural hypotension is or has been present. There may be evidence of other emboli or a history of
previous TIAs. The brachial blood pressure should be measured in each arm; a difference of more than 20 mmHg is suggestive of stenosis of a subclavian artery.
The usual preliminary investigations in thromboembolic stroke and their potential yields are listed in Table 18.29. Blood cultures should be taken if there is any possibility of endocarditis.
Autoantibody studies, e.g. antinuclear factor (AN F), double-stranded DNA (dsDNA), cardiolipin antibodies, should be performed in young patients to exclude diseases such as systemic lupus erythematosus (SLE) if clinically relevant.
Further investigation of thromboembolic stroke CT SCANNING. This is now widely available and is indicated in virtually all patients with a stroke or TIA. CT scanning will usually demonstrate the site of a lesion and distinguish between a haemorrhage (see p.910) and infarction. An infarct which appears as a low-density area without a mass effect is not usually visible in the first few hours. Detection increases over the succeeding few days and 90% of all infarcts are detected at 1 week. It will also rule out or show unexpected mass lesions, e.g. subdural haematoma, tumour or abscess. MRI SCANNING usually becomes abnormal within a few
hours. Haematomas are detected better than with CT. CAROTID DOPPLER AND DUPLEX SCANNING. These ultrasound studies are of value in screening for carotid artery disease: in skilled hands they are highly effective in demonstrating internal carotid artery stenosis, the principal surgical target in stroke patients.
ANGlOGRAPHY (conventional carotid arteriography or DSA) is valuable in anterior circulation TIAs to diagnose surgically accessible arterial stenoses (mainly internal carotid artery stenosis).
There is a high probability of finding a carotid stenosis when there is a loud localized carotid bruit in the neck. The majority of normotensive young patients (below 60 years) with TIA or stroke in the anterior circulation who recover well should be considered for angiography, though the yield in terms of internal carotid (and other
accessible) arterial stenoses is under 5%. In more elderly patients, the risks of the procedure and the relatively poor results of vascular surgery in preventing further stroke usually make further investigation unwise. Vertebral and arch angiography are rarely performed following posterior circulation TIAs and strokes unless there is a clinical suggestion of subclavian artery disease.
in stroke. It is indicated only in special circumstances (e.g. when blood syphilitic serology is positive).
The initial decision whether to admit a stroke patient to hospital depends upon the clinical state and facilities available at home. Often the practical difficulties of caring for the disabled for what may be a prolonged period determine these immediate decisions. In practice, many TIAs and mild strokes can be managed at home and specialist advic e sought when necessary. Patients admitted to stroke units fare better than those admitted to a general ward.
The management of the unconscious patient is described on p. 903. Immediate supportive measures and nasogastric fluids are given. Frequent turning to avoid bed sores is necessary.
AIl risk factors (see Table 18.25) should be identified and, if possible, treated. HYPERTENSIVE THERAPY. The control of high blood pressure is the single most important factor in the prevention of stroke. Hypertension is often seen in the acute stage of a stroke and hypotensive agents are not immediately necessary. Sustained or severe hypertension needs treatment (see p. 620), but the pressure must be lowered slowly to avoid a sudden fall in cerebral perfusion pressure. ANTICOAGULANTS are used when there is atrial fibrillation, other paroxysmal dysrhythmias or when there are certain cardiac valve lesions (uninfected) or cardiomyopathies. They can also be used in ‘stroke in evolution’.
Anticoagulants are potentially dangerous in the 2 weeks following cerebral infarction because of the risk of provoking cerebral haemorrhage. There are wide differences in clinical ractice regarding their use.
ANTI PLATELET THERAPY (see p. 347). Aspirin (300 mg daily) has been shown to reduce the incidence of stroke in patients who have had a TIA, although the exact dose is under review. Ticlopidine (250 mg twice daily), a platelet antiaggregant has also been shown to be effective but further studies are required.
OTHER MEASURES. Polycythaemia should be treated (see p. 328). Baclofen (a GABA agonist) is sometimes helpful in the management of severe spasticity following stroke.
INTERNAL CAROTID ENDARTERECTOMY. This is considered in symptomatic patients who are shown to have internal carotid artery stenosis (Fig. 18.17) that narrows the arterial lumen by more than 70%. In these patients, the risk of further TIA/stroke is reduce by approximately 75% following successful surgery. The procedure however has a mortality around 3%. It is not currently recommended for asymptomatic cases.
EXTRACRANIAL-INTRACRANIAL BYPASS. Anastomosis of the superficial temporal artery (external carotid) through a burr hole to a cortical branch of the middle cerebral artery (internal carotid) was widely advocated in the decade 1975-85 when there had been internal carotid occlusion. Trials suggest no overall benefit.
Physiotherapy and speech therapy
Skilled physiotherapy is of particular value in the first few months following the stroke. It is helpful in relieving spasticity, preventing contractures and teaching stroke patients to use walking aids. The effect of physiotherapy on the longer-term outcome is inadequately researched. Speech therapy is frequently recommended in aphasia.
It is possible that the spontaneous return of speech is hastened as much by normal conversation with a relative as by a therapist, though the trained therapist has a vita understanding of the problems and frustration of the aphasic patient.
Both physiotherapy and speech therapy have an undoubted psychological role. Stroke is frequently a devastating event and, particularly when it occurs during working life, radically alters the pattern of the patient’s remaining years. Many patients become unemployable and cannot lead independent lives. The financial consequences to the sufferer are usually considerable. The loss of self-esteem makes secondary depression common. Following recovery from stroke, various aids and modifications may be necessary at home, for example stair rails, portable lavatories, bath rails, hoists, sliding boards, wheelchairs, tripods, modification of doorways and sleep arrangements, stair lifts and kitchen modificatios.
A visit to the patient’s home with the occupational therapist and their primary care physician to discuss these problems is valuable.
Between one-third and one-half of patients will die in the first month following a stroke. This early mortality is lower for thromboembolic infarction (under one-quarter) than for intracerebral haemorrhage (around thre quarters). A poor outcome is likely when there is coma, a defect in conjugate gaze and a severe hemiplegia. Recurrent strokes are common (10% in the first year) and, in addition, many patients die subsequently of a myocardial infarction. Of initial survivors, 30-40% are alive after 3
years. Gradual improvement usually follows stroke, althoughthe patient may be left with a severe residual deficit. Of those who survive a stroke, about one-third return to independent mobility and one-third have severe disability requiring permanent institutional care. If, in general, there is sufficient language to be intelligible at 3 weeks, the outlook for recovery of fluent speech is good. Many stroke patients are, however, left with word-finding difficulties.