Middle cerebral artery territory stroke Total occlusion

The clinical features of occlusion of the main trunk of the middle cerebral artery with infarction of the whole territory of the artery (Figure 23.5) include conjugate eye deviation (frontal lobe damage), aphasia (in the dominant hemisphere), hemiplegia, hemisensory loss and hemianopia (from involvement of the visual radiation in temporal and parietal lobes). In middle cerebral artery occlusion (and

Figure 23.5 Complete middle cerebral artery territory infarction. CT at 48 hours shows infarction within the complete middle cerebral artery territory on the right with swelling of the hemisphere causing midline shift. The patient later began to develop signs of coning and decompressive surgery was carried out (see Figure 23.6).

Most lacunar syndromes) the hemiparesis affects the arm more than the leg, while in anterior cerebral artery occlusion the leg is characteristically much weaker than the arm because the leg area of the motor cortex is in the anterior cerebral artery territory. Neglect syndromes in which the patient is unaware of, or ignores, the hemiplegic side occur acutely with both non-dominant and dominant hemisphere cortical damage, but generally are more severe and persistent with non-dominant parietal lobe damage.

The middle cerebral artery most commonly occludes from embolism. Occasionally, atheromatous stenosis at the origin of the middle cerebral artery leads to occlusion, particularly in Asian and African races. Rarely, patients with complete middle cerebral artery territory infarction develop severe malignant oedema within 48 hours, leading to brainstem compression and death by coning. In appropriate cases, surgical decompression with hemicraniectomy is required (Figure 23.6).

Branch occlusion

Branch occlusion will produce partial syndromes with only some of the signs of complete territory infarction described above. Upper branch occlusion

Figure 23.6 Malignant hemisphere swelling relieved by surgical decompression after complete middle cerebral artery territory infarction. Magnetic resonance imaging shows herniation of the swollen brain following decompressive craniotomy. After two months, the defect was closed.

Outcome at six months was excellent (patient independently ambulant, no significant cognitive deficit), although the left arm remained plegic.

Affecting frontal structures produces hemiparesis, hemisensory loss, ocular deviation and a non-fluent expressive dysphasia in which the patient understands speech because of an intact temporal lobe but cannot produce speech. Lower branch occlusions involving the temporal lobe result in fluent receptive dysphasia, in which the patient has difficulty understanding language, but motor production of speech is either preserved or produces a non-stop flow of nonsensical speech (jargon dysphasia).

Distal embolism

Small cortical branches are usually occluded by emboli and the patient may present only with weakness or isolated cortical signs, for example, dysphasia.

Deep infarction (striatocapsular infarction)

Deep infarction occurs when the trunk of the middle cerebral artery has occluded but the cortex is protected by pial collateral circulation. Deeper structures (the striatum and internal capsule) are supplied by the perforating branches, which do not have collateral supply and therefore infarct rapidly (Figure 23.7). Usually, this results from an embolus obstructing the perforating lenticulostriate arteries, which then breaks up spontaneously or as a result of therapeutic thrombolysis before the cortex has infarcted. The patients have contralateral motor and sensory loss, but also exhibit cortical signs (unlike pure lacunar infarction). These cortical signs resolve more quickly than when the cortex itself is infarcted.

Figure 23.7 Striatocapsular infarction. This patient presented with acute right hemiplegia, neglect and dysphasia. The neglect and dysphasia resolved within a few days. The underlying aetiology was atrial fibrillation.

Anterior cerebral artery occlusion

The anterior cerebral artery is far less often affected than the middle cerebral artery, although the causes are similar. However, anterior cerebral territory infarction should raise the level of awareness for unusual aetiologies. It also occurs secondary to vasospasm after SAH. The clinical features of anterior cerebral artery occlusion are a contralateral hemiplegia in which the leg is more affected than the arm, because the cortical representation of the leg lies within its territory. Infarction of subfrontal cortex, especially if bilateral, may cause frontal neuropsychological deficits, particularly executive dysfunction, abulia, disinhibition and lack of insight, often without any other signs.

Carotid artery occlusion_

The internal carotid artery often occludes without any clinical evidence of stroke, because of the collateral supply provided by the circle of Willis. Strokes occur after carotid occlusion only if the collateral supply is inadequate or if thrombosis spreads (or embolises) to involve the middle cerebral artery or its branches. Internal carotid artery occlusion can also involve its first branch, the ophthalmic artery, resulting in transient or persistent monocular retinal ischaemia and blindness. The picture in carotid artery occlusion is therefore usually identical to that of middle cerebral artery occlusion. Infarction may be limited to a small portion of the territory or extend to involve the whole of the middle cerebral artery territory. If the carotid artery occludes from dissection, there may also be a Horner's syndrome on the side of the occlusion (i. e. contralateral to the limb signs). The anterior cerebral territory is often spared (via collateral flow) but may be affected in some cases. The bifurcation of the common carotid artery is the most common site of severe atheroma in the extracranial cerebral circulation and usually the internal carotid artery occludes at the origin from the common carotid. In dissection, the site of occlusion may be more distal. Rare obliterative arteriopathies, including moyamoya disease, may involve the terminal intracranial portion of the carotid artery and the origins of the middle cerebral artery.

Posterior cerebral artery occlusions_

Occlusion of the posterior cerebral artery is commonly embolic and more patients with posterior cerebral syndromes are in atrial fibrillation, than with other large vessel occlusions (Figure 23.8). Emboli usually reach the posterior cerebral arteries via the vertebrobasilar system, but it should be borne in mind that in about 5 per cent of individuals, one posterior cerebral artery is supplied by a dominant posterior communicating branch of the internal carotid artery. Thus, posterior cerebral artery occlusion is occasionally caused by embolization from carotid stenosis. The posterior cerebral artery prin-

Figure 23.8 Posterior cerebral artery occlusion. Coronal magnetic resonance imaging shows acute infarction of the left occipital pole.

Cipally supplies the occipital cortex, and occlusion usually causes an isolated hemianopia. This may spare the visual representation of the macular fibres when these may receive collateral supply from the middle cerebral artery. When infarction extends anteriorly to affect parieto-occipital areas, neglect syndromes may accompany the hemianopia. The posterior cerebral arteries also supply the thalami and the medial posterior temporal lobes. If these structures are involved, the patient may present with confusion, or memory impairment (thalamic or medial temporal amnesia). If both posterior cerebral artery territories are infarcted, as may happen when an embolus lodges at the top of the basilar artery, cortical blindness and confusion ensue. Sometimes, these patients may be left with tunnel vision and may recognize small but not large objects. Memory impairment following this may be severe, especially for the acquisition of new information.

Vertebral artery occlusion_

The most common consequence of occlusion of the distal vertebral artery is infarction of the dorsolateral medulla within the territory of the posterior inferior cerebellar artery (lateral medullary syndrome). This results in a Horner's syndrome, temperature and pain sensory loss on one side of the face and the other side of the body, nystagmus, ataxia of the ipsilateral limbs and palatal and vocal cord paralysis. Vertebral artery embolism or occlusion may also result in more extensive infarction of the brainstem and cerebellum and these syndromes are discussed next. The most common site for atheroma to affect the vertebral artery is at its origin from the aorta.

Basilar artery occlusion_

Whereas middle and posterior cerebral artery occlusions are more often the result of embolism, the opposite is true of the basilar artery. This is because the basilar is more commonly affected by severe atherosclerosis on which in-situ thrombus may form. Basilar artery occlusion also commonly occurs as a result of propagation of thrombus from an occluded vertebral artery. Basilar thrombus (Figure 23.9) may obstruct blood flow into perforating vessels supplying the central brainstem structures or the two upper cerebellar arteries. A number of clinical pictures may be encountered. In


Figure 23.9 Brainstem, cerebellar and occipital infarction secondary to basilar thrombosis.

The medulla, lower cranial nerves may be affected, giving rise to a lower motor neurone type bulbar palsy. Upper motor neurone impairment of the same structure may cause a pseudobulbar palsy, with brisk facial reflexes, jaw jerk and a spastic tongue. This is often accompanied by spontaneous laughter or crying (emotional lability). Above the medulla, pontine infarction may cause a sixth nerve palsy, gaze paresis, internuclear ophthalmoplegia and pinpoint pupils. Emboli may lodge at the top of the basilar causing midbrain infarction with loss of vertical eye movement, pupillary abnormalities and coma. All these syndromes will be accompanied by quadriplegia to some degree, which may be very asymmetric. Partial brainstem or midbrain syndromes may also be caused by localized occlusion of one of the perforating arteries from small vessel disease. The posterior cerebral arteries arise from the top of the basilar artery. Thus any of these basilar artery syndromes may be accompanied by contralateral or bilateral occipital infarction with hemianopia or cortical blindness.

Subclavian artery occlusion_

Subclavian artery occlusion is a rare cause of haemodynamic TIA and an even rarer cause of stroke. If the subclavian artery is occluded or severely stenosed before the origin of the vertebral artery, the arm may be supplied by blood flowing in a retrograde direction down the vertebral artery at the expense of the vertebrobasilar circulation. This is known as subclavian steal and may occasionally result in brainstem TIAs during exercise of the arm.

Border zone ischaemia and hypoxic ischaemic encephalopathy

The brain is particularly vulnerable to a global fall in perfusion pressure. Most often this is caused by cardiac disease (arrthymia or pump failure), especially when combined with hypoxia, although hypovolaemia alone may be sufficient to cause cerebral ischaemia. The usual circumstances in which perfusion failure leads to bilateral haemodynamic brain damage are following cardiac arrest, severe blood loss or cardiopulmonary bypass. Embolism is an alternative or additional cause of focal damage during cardiopulmonary bypass. In the nonanaesthetized, non-comatose patient, moderate or transient global perfusion failure results in acute reversible non-focal brain dysfunction (confusion, attention deficits, light headedess). Following a profound insult, a number of syndromes are recognized, resulting from border zone or ‘watershed' infarction in the areas of the brain at the distal ends of the arterial supply (Figure 23.10). Pathological studies suggest that many such cases result from a combination of diffuse embolism and haemodynamic failure of perfusion in the border zones. The parieto-occipital cortex, which lies at the border zone between the middle cerebral artery and posterior cerebral artery territories, is particularly vulnerable. Infarction of this region results in abnormalities of behaviour, memory and vision. The visual abnormalities are complex and include inability to see all the objects in a field of vision, incoordination of hand and eye movement, such that the patient cannot locate objects in the visual field, and apraxia of gaze in which the patient is unable to gaze where desired. Other areas of vulnerability are the superficial cortical and deep subcortical border zones between the anterior and middle cerebral artery, and the hippocampi, where infarction may result in an amnesic syndrome. In severe cases, necrosis occurs in the basal ganglia, cerebellum and brainstem. Unilateral border zone infarction, often in a patchy fashion involving the subcortical white matter in the centrum semi ovale,

Figure 23.10 Watershed infarction following cardiac surgery. CT scan of the brain shows bilateral ‘watershed’ infarction more obvious on the right. This has occurred in the border zone between the middle and anterior cerebral artery territories.

Intracerebral haemorrhage often has a sudden, devastating presentation. Patients who present in coma with vomiting and/or neck stiffness are more likely to have ICH than ischaemic stroke, but it is wrong to assume that patients with less severe stroke will have ischaemia. The symptoms of small cerebral haemorrhages are indistinguishable from cerebral infarction and the distinction can only be made in life by brain imaging.

May also occur in patients with ipsilateral carotid artery occlusion or severe stenosis.

Vascular dementia_

Vascular dementia is an umbrella term used to describe the development of cognitive deficits in multiple domains secondary to cerebrovascular disease. This is most commonly caused by multiple cortical or subcortical lacunar infarcts (Figure 23.11). Vascular dementia can also occur after multiple intracranial haemorrhages, for example, in cerebral amyloid angiopathy, after SAH, and as a result of cerebral venous thrombosis. Typically, patients have a stepwise deterioration associated with other features of stroke. In diffuse subcortical small vessel disease, (Binswanger's disease or subcortical arteriosclerotic encephalopathy) dementia may be accompanied by gait apraxia, which results in failure to initiate gait, postural instability (often falling over backwards) and a

Shuffling small-stepped, wide-based gait (marche a petit pas). This is often associated with diffuse periventricular demyelination secondary to ischaemia in the deep white matter, which causes patchy or diffuse changes, known as ‘leukoaraiosis’, and ventricular enlargement on CT and MRI. Urinary incontinence may occur. Characteristically, the dementia of small vessel disease has subcortical features including poor attention, slowing of men-

Figure 23.11 CT in vascular dementia. Atrophy, multiple lacunar infarcts and large vessel disease in a patient with vascular dementia.

Tal function (bradyphrenia) and impaired executive function in excess of discrete cortical patterns of dysfunction. Occasionally, these patients present with periods of encephalopathy associated with new infarction. Multiple cortical infarcts (from large vessel occlusions) are much rarer as causes of dementia. It is important to note that older patients with cerebrovascular disease are at increased risk of Alzheimer’s disease, and mixed dementia caused by a combination of the two disorders is common.

Asymptomatic leukoaraiosis without dementia may also be found on imaging, especially in patients over 50 years of age with appropriate risk factors. There is also an increased incidence of depression in these patients.

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