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R. Michael Scott, MD
From the Department of Pediatric Neurosurgery, The Children's Hospital, and Harvard Medical School, Boston, Mass.

Corresponding author: R. Michael Scott, MD, Department of Pediatric Neurosurgery, The Children's Hospital, 300 Longwood Ave, Bader 319, Boston, MA 02115 (e-mail: scottr@a1.tch.harvard.edu).

Arch Neurol. 2001;58:128-130.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

THE CLINICAL presentation of most patients with moyamoya syndrome is cerebral ischemia. In my own series of 100 patients younger than 21 years [unpublished data, 1985-1999], 66 presented with stroke and 18 with transient ischemic attacks (TIAs). Cerebral hypoperfusion in these patients can be documented by a variety of imaging studies including diffusion-weighted magnetic resonance imaging (MRI), xenon flow studies using computed tomography (CT) or positron emission tomography (PET), and single photon emission computed tomography (SPECT) studies with acetazolamide challenge. One of the most striking observations in these patients is that TIAs can be precipitated by hyperventilation, an indication of how marginal the cerebral blood flow can become owing to the basal arterial stenoses seen in this syndrome. As the moyamoya inevitably progresses to complete occlusion of the internal carotid artery,¹ the clinical syndrome also progresses unless the spontaneous leptomeningeal or transdural collateral blood supply is . . . [Full Text of this Article]

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