Recognition and management of lacunar strokes.

One in every five strokes results from injury to perforating arteries and arterioles in the deeper, non-cortical parts of the cerebrum and brain stem. ' The mechanism of these lesions remains controversial2 4: some are haemorrhagic but most present post mortem as small black dots5-lacunae-due to infarction and subsequent cavitation. Until the present decade virtually all lacunar strokes were associated with hypertension,3 but the proportion has now declined to around 700' with the other 30," due to thromboembolism or hypoperfusion from occlusive extracranial vascular disease. ' 6 A few lesions (35W') are asymptomatic but, because of their sensitive location, most (65°0)7 present as transient ischaemic attacks with stepwise deterioration or as a sudden, severe clinical deficit.8 The discrete nature of the lesion is often suggested by the absence of visual field defects, seizures, loss of consciousness, coma, combined motor and sensory deficits, apraxia, aphasia, or agnosia. Angiography does not disclose the affected vessel and the electroencephalographic pattern remains non-focal. In general the prognosis for recovery is excellent, and prolonged rehabilitation is rewarding.8 The recognition that small lesions (0.5 to 20 mm diameter) may produce lacunar syndromes has come from the careful correlation of clinical and anatomical data supported by relatively few necropsy studies. With successive improvements in computed tomography, the presence of a lacunar syndrome may be predicted where an acute neurological deficit, such as a pure motor hemiplegia, is accompanied by a normal CT scan.9 In some cases the scan can confirm the nature and location of a focal lesion. Nuclear magnetic resonance provides a similar degree of resolution but may prove more satisfactory for displaying infarction of the brain stem. "' With repeated computed tomography a positive scan is eventually obtained in more than two thirds of patients presenting with clinical syndromes. " In the first week most infarcts are recognisable without contrast, but as the hypodense lesion becomes isodense contrast is needed to prevent "fogging. "'I2 In practical terms, neurologists can now diagnose clinically most haemorrhagic lesions, many infarcts, and about one fifth of lacunae. If the lesion is haemorrhagic or the patient hypertensive no further investigative procedures are indicated. If the patient is normotensive angiography should be considered only when extracranial arterial surgery is a practical possibility. 13 In the future, however, the development of digital angiography and duplex scanning may be conducive to a more active approach.14 With increasing acceptance of the concept of lacunar syndromes a note of caution is inevitable. Many factors add to the hazards of diagnosis3 including the heterogeneity of presentation, incomplete syndromes in one third of those affected," variations in the nature of the lesions, and other manifestations of cerebrovascular disease such as superficial cortical infarction. A pure sensory stroke affecting the face, arm, and leg as a result of a lesion of the contralateral posteroventral thalamic nucleus may present with persistent numbness from the onset or with transient attacks leading to persisting numbness in only 10"" of patients. Some patients may complain of paraesthesia, others of anaesthesia, dysaesthesia, or, occasionally, spontaneous thalamic pain. In Fisher's series8 the CT scan was invariably negative. With pure motor hemiplegia, the lesion is usually in the posterior limb of the internal capsule, but similar manifestations may arise from infarction of the basis pontis. Although the CT scan is usually positive, cortical somatosensory evoked responses after stimulation of the median nerve may indicate a sensory, lemniscal lesion in some patients.15 The close proximity of structures within the brain stem provides the setting for several lacunar syndromes. In the upper basis pontis the corticospinal fibres are dispersed into bundles, and lesions placed a few millimetres apart may cause either homolateral ataxia with crural paresis16 or facial weakness, severe dysarthria, and a clumsy hand. '7 Lacunar strokes can produce Weber's syndrome of unilateral third nerve palsy with contralateral hemiplegia, Claude's syndrome of cerebellar ataxia and crossed third nerve palsy, hemiballismus from a lesion of the subthalamic nucleus of Luys,8 and bilateral lesions of the ventral pons in the locked in syndrome. '8 Perhaps the most interesting symptom complex is the mesencephalothalamic syndrome resulting from an embolus at the top of the basilar artery-producing unilateral or bilateral third nerve palsies, paralysis of downward gaze, and drowsiness as a result of infarction in the territory of a perforating arteriole arising from the posterior cerebral artery.8 The impression that multi-infarct dementia results from repeated infarction-some symptomatic, some not-is probably erroneous. The initial lesion is almost always a symptomatic stroke,8 and more than three lacunar infarcts in one patient are rare.3 " Dementia is usually associated with bilaterally distributed infarcts,21' but sudden impairment of memory may follow unilateral infarction of the fornix and corpus callosum, and dementia may result from an infarct in the central region of the thalamus or subthalamus.8 21 Other associated factors such as hypertension,22 non-occlusive arterial insufficiency,23 and normal pressure hydrocephalus8 24 25 frequently contribute to the clinical picture. The detection of lacunar infarcts by computed tomography has a practical value in the management of normal pressure hydrocephalus in that patients with this combination of diseases do not benefit from shunting.26