Positional brain ischemia with MCA occlusion successfully treated with extra-intracranial bypass

408 Positional cerebral ischemia (PCI) is an extremely rare condition in which dramatic central nervous system deficits are triggered by standing in patients with severe stenosis or occlusion of the major brain-supplying blood vessels [1] . Because PCI is generally associated with orthostatic hypotension [2, 3] , a hemodynamic mechanism has been proposed [4] . However, PCI has been reported even in patients without orthostatic hypotension [1] . The treatment is medical, but surgery can be considered in refractory cases (endarterectomy for carotid artery stenosis or either highor low-flow extra-intracranial bypass – for carotid occlusion) [3] . We report a case of PCI associated with middle cerebral artery (MCA) occlusion and without orthostatic hypotension treated by lowflow extra-intracranial bypass. The patient, a 58-year-old male with a history of hypertension, suffered an ischemic stroke in the left hemisphere with sudden onset of speech disturbance and right hemiparesis in 1992. He experienced complete neurological recovery in approximately 1 month. Aspirin was the medical treatment. In December 2004, while the patient was still on aspirin, he presented with several stereotyped TIAs with acute onset of right-sided hemiparesis and paresthesias, and mild motor aphasia. Symptoms that were always triggered by standing presented nearly daily and rapidly improved (within few minutes) on returning to the supine position. Brain MRI showed multiple chronic ischemic lesions in the territory of the left MCA. Dual antiplatelet therapy with clopidogrel plus aspirin was started, followed by reduction in the frequency of the TIAs. In May 2005, recurrent episodes of right hemiparesis were associated with incomplete recovery when lying down, and he was hospitalized. General examination was normal and there were no hematological abnormalities. The supine blood pressure ranged between 130/80 and 150/90 mm Hg. There was no significant orthostatic hypotension and only occasionally was a slight reduction ( ! 10 mm Hg) in systolic blood pressure observed on standing. However, just a few blood pressure evaluations were performed on standing because of the worsening of neurological symptoms in this condition. MRI showed multiple ischemic areas in the territory of the left MCA ( fig. 1 A), whereas MR angiography demonstrated the occlusion of the left MCA ( fig. 1 B). A cerebral angiogram confirmed the occlusion of the left MCA at the M1 segment and a hypovascularized area in the left parietal region ( fig. 1 C). SPECT scans revealed a severe impairment of regional cerebral perfusion throughout the left hemisphere involving both deep and superficial territories; a marked reduction in 99m Tc ECD uptake was detected in the frontal and temporal cortices, while absence of radiotracer uptake was found in the parietal and occipital cortices ( fig. 1 E, F). Screening for vasculitis, Cerebrovasc Dis 2010;29:408–409 DOI: 10.1159/000288055