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Systemic Lupus Erythematosus Involvement of the nervous system is an important aspect of this disease In the pathologic and clinical series reported by Johnson and Richardson, the CNS was affected in 75 percent of cases, but our recent experience has suggested a far lower frequency of clinical manifestations Disturbances of mental function including alteration of consciousness, seizures, and signs referable to cranial nerves are the usual neurologic manifestations; most often they develop in the late stages of the disease, but they may occur early and may be mild and transient Hemiparesis, paraparesis, aphasia, homonymous hemianopia, movement disorders (chorea), and derangements of hypothalamic function occur but have been infrequent in our experience Larger infarcts are usually traceable to emboli from Libman-Sacks (nonbacterial thrombotic, marantic) endocarditis In some instances the CNS manifestations resemble multiple sclerosis, especially when there is an optic neuritis and myelopathy The presence of serum antinuclear antibodies is of help in the differentation of lupus erythematosus but in itself does not establish the diagnosis The CSF is entirely normal or shows only a mild lymphocytic pleocytosis and increase in protein content, although in some patients primarily those with peripheral neuropathy and myelopathy the protein content may be greatly increased Most of the neurologic manifestations can be accounted for by widespread microinfarcts in the cerebral cortex and brainstem; these, in turn, are related to destructive and proliferative changes in arterioles and capillaries The acute lesion is subtle; it is not a typical brinoid necrosis of the vessel wall, like that in hypertensive encephalopathy, and there is no cellular in ltration Attachment of immune complexes to the endothelium is the postulated mechanism of vascular injury Thus, the changes do not represent a vasculitis in the strict sense of the word Other neurologic manifestations are related to hypertension, which frequently accompanies the disease and may precipitate cerebral hemorrhage; to endocarditis, which may give rise to cerebral embolism; to thrombotic thrombocytopenic purpura, which commonly complicates the terminal phase of the disease (Devinsky et al); and to treatment with corticosteroids, which may precipitate or accentuate muscle weakness, seizures, and psychosis In other cases, steroids appear to improve these neurologic manifestations A similar set of neurologic problems arises in relation to the anti phospholipid antibody syndrome, which may be a feature of lupus or arise independently (see page 735) It is not been entirely clear to us what proportion of the cerebrovascular features of lupus might be explained on the basis of the coagulation disorder Arteritis Symptomatic of Underlying Systemic Disease and Sympathomimetic Drug Reactions Both AIDS and drug abuse (mainly cocaine) have been associated with a cerebral vasculitis that is similar to polyarteritis nodosa With respect to the former, if deep infarctions have occurred, a basal meningitis due to tuberculosis, cryptococcosis, or syphilis with occlusion of penetrating vessels must always be entertained Drug-induced vasculitis is dif cult to distinguish from a more common state of focal vasospasm that may also be induced by these same agents, as discussed earlier (page 730) Finally, a true cerebral or spinal cord vasculitis can rarely be found in association with systemic lymphoma, particularly with Hodgkin disease The nature of this process is indeterminate but may be related to the deposition of circulating immune complexes in the walls of cerebral vessels The cerebrovascular problems consequent to cocaine use are quite varied Seizures and death may occur as a result of a syn-.

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