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Scleroderma (progressive systemic sclerosis) is a multisystem connective tissue disorder characterized by inflammation, fibrosis, and vasculopathy of affected tissues. CNS vasculitis, segmental vasospasm, and cerebrovascular calcifications may all play a role in causing strokes in patients with scleroderma. CNS vasculitis has been diagnosed in several patients with scleroderma and has been posited to cause strokes. Cerebral infarction in scleroderma patients in the absence of other plausible, causative factors should prompt an aggressive workup for vasculitis including angiography. Results of cerebral angiography in several patients thought to have vasculitis are consistent with the diagnosis of vasoconstriction. Arteriography revealed segmental, often smoothly contoured, narrowing of arteries of multiple sizes (small, medium, and large) in both the anterior and posterior circulations. Whether vascular calcium deposits were responsible for the patients' cerebrovascular symptoms is speculative. Scleroderma patients with cerebrovascular disease must take into consideration the potential causes of stroke.
Cogan's syndrome is characterized by nonsyphilitic interstitial keratitis, vestibulo-auditory Menière-like symptoms, and, occasionally, systemic manifestations of vasculitis. Although neurologic manifestations are rare, several patients with stroke in the setting of Cogan's syndrome have been reported. The most common and classic ocular manifestation of Cogan's syndrome is bilateral interstitial keratitis. The diagnosis is classically suggested by the association of interstitial keratitis with acute-onset sensorineuronal hearing loss in a patient who has a negative laboratory evaluation for syphilis. Computed tomography (CT) scans may occasionally show intralabyrinthine calcifications, whereas magnetic resonance imaging (MRIs) often show soft tissue obliteration of the membranous labyrinth and may also show multiple lesions of the white matter consistent with cerebral vasculitis. The treatment of Cogan's syndrome varies based on the severity of the clinical manifestations. Due to the presumed autoimmune mechanism with vasculitis, most treatments have included steroids and immunosuppressants.
This chapter reviews the role of calcium and magnesium in causing and ameliorating brain ischemia, respectively. Three different effects of hypercalcemia are posited to contribute to the development and severity of brain ischemia: (i) hypercalcemia stimulates vascular smooth muscle causing vasoconstriction; (ii) increased calcium concentrations enhance platelet aggregation and activate the body's intrinsic coagulation system; and (iii) calcium entry into cells, a process enhanced by an elevated extracellular-to-intracellular calcium ion gradient, causes cytotoxic effects that promote cell death and brain infarction. The rationale for the use of calcium antagonists in the prevention or treatment of secondary brain ischemia was based on the assumption that these drugs reduce the frequency of vasospasm by counteracting the influx of calcium into vascular smooth muscle cells. There is some benefit from the use of the dihydropyridine CCA nimodipine for improving outcome after aneurysmal subarachnoid hemorrhage.
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