Stroke II

Clinical features

A common feature of all strokes is the onset. The neurological deficit comes on over a short time, from seconds to a progression over hours. This contrasts with space-occupying lesions, which develop over weeks or months, and inflammatory lesions (such as plaques of demyelination in multiple sclerosis), which usually come on over days or weeks.

The clinical manifestations of stroke depend on the area of the brain affected, which in turn depends on which blood vessel is affected. The anatomy of the blood vessels supplying the brain can be subdivided according to vessel size (large or small) and vessel site (anterior or posterior) (Fig. 1):

Anterior circulation:

– large vessels: the internal carotid artery (ICA) and its main branches, the middle (MCA) and anterior (ACA) cerebral arteries

– small vessels: branches from the MCA and ACA.

Posterior circulation:

– large vessels: the vertebral arteries, which join to form the basilar artery and its main branches, the posterior cerebral arteries

– small vessels: branches from all these vessels.

Fig. 1 Anterior and posterior arterial circulation.

The anterior circulation supplies the anterior two-thirds of the cerebrum, while the posterior circulation provides the supply for the occipital lobes of the cerebrum and the brain stem and cerebellum (Fig. 1).

A simple syndromic classification divides strokes into the following categories, which have important differences in terms of pathogenesis, treatment and prognosis:

Total anterior circulation stroke.

Partial anterior circulation stroke.

Posterior circulation stroke.

Lacunar stroke.

Anterior circulation large vessel strokes

The MCA supplies most of the motor and sensory cortex, including that controlling the contralateral arm and face, both Wernicke’s and Broca’s areas in the dominant hemisphere, the internal capsule and optic radiation. The ACA supplies the motor cortex controlling the leg, the frontal lobe and the corpus callosum.

Total anterior circulation stroke

This can arise from a complete MCA infarct, from internal carotid disease or massive intracerebral haemorrhage.

Complete infarction of the area produces a devastating deficit. There is a dense flaccid hemiparesis, affecting the arm, face and leg and a homonymous hemianopia. The patient may be drowsy initially with eyes averted away from the hemiparetic side. There is a complete aphasia if the dominant hemisphere is affected and a marked inattention or neglect if the non-dominant side is involved. There may be a transient dysarthria and swallowing may be impaired. The patient may be incontinent. These strokes carry a high mortality and severe long-term morbidity.

Partial anterior circulation stroke

Infarction in the territory of one of the branches of the MCA produces different combinations of deficits depending on the affected hemisphere (Fig. 2). Some of the common ones are: inferior branch = hemianopia – Wernicke’s aphasia if dominant, or constructional apraxia if non-dominant; superior branch = hemiparesis – Broca’s aphasia if dominant or neglect if non-dominant. Distal branches lead to cortical infarcts with weakness only of one limb or isolated higher function deficits.

Fig. 2 Partial anterior circulation infarct.

An ACA infarct produces a hemiparesis, of the leg more than the arm, with apathy and incontinence, and mixed aphasia if dominant or dyspraxia if non-dominant.

Lobar haemorrhage can produce a similar clinical syndrome.

Posterior circulation strokes (Fig. 3)

Large vessel syndromes

Posterior cerebral artery infarcts result in contralateral homonymous hemianopia and contralateral hemisensory loss. There may be some disturbance of higher function, such as altered memory or speech or cortical blindness. Occlusion of the basilar artery produces lesions of both posterior cerebral arteries and high brain stem lesions that may lead to ‘a locked in’ state – where the upper brain stem lesion prevents the conscious brain having any control over bulbar function or the limbs, though some control of eye movements can remain. Vertebral artery occlusion may leave no deficit or may produce one of the syndromes described below.

Fig. 3 Posterior circulation infarct: left cerebellar.

Other posterior circulation strokes

A large number of clinical syndromes (often eponymous) have been described arising from posterior circulation strokes. Cerebellar signs are commonly seen, indicating damage to the cerebellum or its connections. Nystagmus, dysarthria and diplopia are features that point to a brain stem lesion. A feature in this, and other brain stem diseases, is the crossed cranial nerve and long tract sensory or motor deficit. For example, the lateral medullary syndrome (the site of the lesion is the lateral medulla) comprises: lesions to the brain stem nuclei and cerebellar connections which produce ipsilateral facial sensory loss; Horner’s syndrome; vocal cord paralysis and cerebellar ataxia; and damage to the spinothalamic tract which results in contralateral loss of pinprick and temperature sensation in the limbs.

In addition, brain stem events can result in lacunar syndromes.

Small vessel lacunar strokes

Lacunar strokes arise from occlusion of small branches of both the anterior and posterior circulation vessels. The lacunar syndromes are helpful in identifying the disease process but are often less helpful in identifying the exact site of the lesion. The lacunar syndromes are as follows:

Pure motor hemiparesis: face, arm and leg weakness with no other deficits. Usually an internal capsule lesion.

Ataxic hemiparesis: motor hemiparesis with cerebellar type ataxia on that side. Lesion site is variable: posterior internal capsule, midbrain or pons.

Dysarthria/clumsy hand syndrome: marked dysarthria with tongue and face weakness with hand clumsiness on the same side.

Pure sensory stroke: hemisensory loss of superficial sensation. Usually thalamic lesions.

Sensorimotor stroke is a combination of sensory and motor strokes.

Differential diagnosis

The diagnosis of stroke is usually straightforward (Box 1). Space-occupying lesions (SOLs) are usually more insidious in onset than stroke, though some tumours can present with a ‘vascular’ onset, particularly if there is bleeding into a tumour. Cerebral abscesses have a more rapid progression than most SOLs but the patient is usually unwell and septic. Chronic subdural haematoma is a very important diagnosis to consider because of the need for neurosurgical intervention. The onset is usually slower and very often the patient is mentally slower, as well as exhibiting focal deficits, and there may be signs of raised intracranial pressure.

Box 1 Differential diagnosis of stroke

Intracranial space-occupying lesion

– tumour

– bleed into tumour

– abscess

Subdural haematoma

Multiple sclerosis

Head injury

Hypoglycaemia

Seizures with Todd’s paralysis

In younger patients, the onset of multiple sclerosis can be mistaken for a stroke and vice versa. Head injury is usually easily diagnosed but sometimes it can be difficult to tell whether the stroke caused the fall or the head injury resulted in the neurological deficit, particularly in elderly patients. Hypoglycaemia can produce focal deficits and needs to be considered early in the assessment of diabetics with neurological deficits. A Todd’s paralysis, weakness in a limb after seizure, may mimic a stroke. In addition, patients with critical ischaemia, for example due to severe carotid stenosis, can present with focal seizures.

Special situations

Patients with multiple small deep infarcts may present with dementia (multi-infarct dementia). These patients often also have a gait disturbance, walking with small steps but a good arm swing. They may have focal neurological signs relevant to some of their strokes, such as hemianopias. There is considerable overlap with other dementing illnesses such as Alzheimer’s disease and both conditions may coexist and contribute to dementia.

Stroke II

The onset of the neurological deficit is important in the diagnosis of stroke.

Strokes can be classified clinically as total anterior circulation strokes, partial anterior circulation strokes, and posterior circulation and lacunar strokes.

Cerebral infarction cannot reliably be distinguished from haemorrhage on clinical grounds.