![]() (2) The proximal arterial disease group included patients with 1 or more significant lesions in the aortic arch, subclavian artery, vertebral artery, or basilar artery previously described criteria were used. (1) The intrinsic PCA disease group included patients with PCA-occlusive disease involving the main trunk or cortical branches that correlated with infarct topography in the absence of any significant proximal arterial or cardiac disease. The patients were divided by cause into the following etiologic groups. Seventy-nine patients remained for analysis. Thirty-one patients did not meet our criteria 4 because they had only transient ischemic attacks (TIAs), 21 because either the clinical information was inadequate or neuroimages had been destroyed, 5 because they did not fulfill the neuroimaging criteria, and 1 because the patient had a subarachnoid hemorrhage complicated by an infarct. Among the 415 patients in the registry, 110 had symptoms and signs indicating PCA territory ischemia. Isolated infarcts that involved only the thalamus or midbrain were excluded, as these might be caused by penetrating artery disease. For our review, we included all patients in whom brain imaging scans showed infarcts that involved 1 or more cortical territories of the PCA (ie, occipital, parieto-occipital, and medial-inferior temporal lobes). This registry is a prospective collection of all patients with posterior circulation strokes seen at one medical center. We reviewed the New England Medical Center Posterior Circulation Stroke Registry during the 10-year period from January 1986 through December 1995 for all patients with PCA territory infarcts. Intrinsic PCA disease, vasoconstriction, and coagulopathy are less common causes of infarction. Motor weakness, cognitive and behavioral abnormalities, and ataxia were found in 20 patients (25%) only 12 (15%) had sensory signs.Ĭonclusions The great majority of pure PCA and PCA+ territory infarcts are caused by cardiac or intra-arterial embolism. ![]() Visual abnormalities were present in 66 patients (84%). Patients with cardiogenic embolism and intrinsic PCA disease often had pure PCA territory infarcts, while patients with proximal arterial disease more often had PCA+ infarcts. Stroke mechanisms were embolism of cardiac origin (32 ), proximal arterial disease (25 ), cryptogenic embolism (8 ), intrinsic PCA disease (7 ), vasoconstriction (4 ), and coagulopathy (3 ). Infarcts that were cortical and deep were more common in PCA+ lesions. Infarcts were in the cortical territory of the PCA in 47 patients (59%) and were cortical and deep in 32 (41%). Results Forty-eight patients (61%) had infarcts limited to the PCA territory (pure PCA), while 31 (39%) also had infarcts in other territories (PCA+). Patients and Methods We studied stroke mechanisms, infarct distribution, and clinical findings among 79 patients in the New England Medical Center Posterior Circulation Registry in whom brain imaging scans showed infarcts that involved 1 or more cortical territories of the PCA. Published reports have selected only special subgroups of patients. Although associated clinical symptoms and signs are known, the mechanisms of stroke and the anatomical distribution of PCA territory lesions caused by the various stroke mechanisms are less well defined. Shared Decision Making and Communicationīackground Infarcts in the territory of the posterior cerebral arteries (PCAs) are common.Scientific Discovery and the Future of Medicine.Health Care Economics, Insurance, Payment.Clinical Implications of Basic Neuroscience.Challenges in Clinical Electrocardiography.
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