Vasculitis of the central nervous system

Abstract

Central nervous system (CNS) vasculitis occurs in a variety of clinical settings. Some exhibit a distinct age preference; others a tissue tropism. Most frequently encountered are giant cell arteritis (temporal arteritis) and vasculitis secondary to infections. The CNS may be involved in the systemic vasculitides, and neurologic abnormalities occasionally appear as a presenting manifestation of disease. Isolated angiitis of the CNS, a rare form of vasculitis restricted to the CNS, must be distinguished from other causes of CNS inflammation and from noninflammatory vascular disease. We are learning a great deal about the cellular mechanisms of vascular inflammation in the brain. Some manifestations of the clinical disease result from histologic features of the infiltrate and the size of affected vessel. However, the local consequences of inflammation such as increased coagulation and altered vasomotor tone, as well as the systemic consequences such as activation of the central noradrenergic systems, trigeminovascular system, and hypothalamic pituitary adrenal axis contribute to both pathogenesis of disease and recovery. Two central issues that confront us now are improving the accuracy of the diagnosis (including identifying any underlying infectious causes) and limiting the long-term damage both from disease and its therapies.

Diffuse cerebral vasoconstriction (Call–Fleming syndrome) and stroke associated with antidepressants

“…We did not perform a brain biopsy to exclude CNS vasculitis, but a "spontaneous" marked improvement in vascular stenoses would not be expected in this condition. 5 There was no evidence of a cardiac source of embolism. Urine toxicology screen was negative for drugs associated with vasoconstriction.…”

Ability of herpes simplex virus vectors to boost immune responses to DNA vectors and to protect against challenge by simian immunodeficiency virus

“…Glial nodules are nonspecific lesions that usually result from viral infection Prineas, MacDonald, and Franklin, 2002); in this case the nodules were negative by IHC for viruses, including SIV, and of unknown significance. Differential diagnoses for the occipital lobe lesion included a septic lesion of hematogenous origin (Kennedy, 2004;Moore, 2000), HSV encephalitis (Kennedy, 2004;Kennedy, 2005), and acute hemorrhagic leukoencephalitis (AHL). An extensive histopathologic workup failed to identify an infectious etiology, including HSV, as the cause of the vasculitis.…”

Systemic lupus erythematosus vasculitis: A current therapeutic overview

“…Nervous system Most SLE experts believe that the role of cerebral vessel vasculitis in the causation of central nervous system (CNS) lupus is overestimated, and that it is mostly caused by either a T cell-mediated or autoantibody-mediated damage to neuronal tissue [16][17][18]. In their original work, Johnson and Richardson [19] concluded that CNS involvement in SLE was due to vasculopathy (microinfarcts or fibrinoid degenerative changes).…”