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When Fisher examined a series of such lesions in serial sections, from a basal parent artery up to and through the lacuna, he found atheroma and thrombosis at the mouth of the branch vessels and less often embolic occlusion of small vessels to be the basic abnormality in some (usually the larger) lacunae, and a lipohyalin degeneration and occlusion in the initial course of small vessels in the smaller ones In some, lipohyalinotic changes had resulted in false aneurysm formation, resembling the Charcot-Bouchard aneurysms that underlie brain hemorrhage (see further on) In a series of 1042 consecutive adults whose brains were examined postmortem in past decades, Fisher observed one or more lacunae in 11 percent He found 4 to 6 and sometimes up to 10 to 15 lacunae in any given brain specimen.

FIGURE 7-3

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destruction of cortical neurons. Only if the cerebral lesions are bilateral and extensive is consciousness markedly impaired. It should be mentioned, however, that in many of the diseases in this category there is severe thalamic damage, as mentioned earlier, and it is the latter that is responsible for coma. Thus, the pathologic changes found in cases of coma are compatible with physiologic deductions namely that the state of prolonged coma correlates with lesions of all parts of the corticaldiencephalic system of neurons; but it is only in the upper brainstem that coma-producing lesions are small and discrete. Recent studies by Parvizi and Damasio suggesting that lesions in the pons may cause coma are, in our opinion, subject to alternative interpretation, but further study is justi ed. It should be noted again that in the largest group of cases of coma, no lesion is divulged by any technique of pathology; the lesion, caused by a metabolic or toxic abnormality or a generalized electrical discharge (seizure), is presumably subcellular or molecular, or the visible microscopic lesions are too diffuse for clinicoanatomic correlation.

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The differentiation of the childhood ataxias is dif cult The problem is twofold rst, to be certain that ataxia exists, and, second, to differentiate cerebellar ataxia from the sensory ataxia of peripheral nerve disease and from generalized tremor and polymyoclonus Since cerebellar ataxia is more a disorder of voluntary than of postural movements, its presence usually cannot be determined with certainty until intentional (projected) movements become part of the child s repertoire of motor activity As indicated in Chap 28, the earliest signs become manifest in the arms when the infant reaches for an object and brings it to his mouth or transfers it from hand to hand A jerky, wavering, tremulous movement then appears; in sitting, a titubation of the head and a tremor of the trunk may be apparent Once walking begins, apart from the usual clumsiness of the toddler, there is a similar incoordination of movement.

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In recent years, better treatment of hypertension appears to us to have reduced this number, at least as judged by MRI Lacunae are situated, in descending order of frequency, in the putamen and caudate nuclei, thalamus, basis pontis, internal capsule, and deep hemispheral white matter The cavities range from 3 to 15 mm in diameter, and whether they cause symptoms depends entirely on their location Fisher has delineated the more frequent symptomatic forms: 1 2 3 4 Pure motor hemiplegia Pure sensory stroke Clumsy hand dysarthria Ipsilateral hemiparesis ataxia.

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