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Infarcts with a cardiac source of embolism in the NINDS Stroke Data Bank

Neurologic examination

Departments of Neurology (Drs. Kittner, Sloan, and Price), Epidemiology and Preventive Medicine (Drs. Kittner and Price), University of Maryland, Baltimore, MD; Center for Devices and Radiological Health (Dr. Sharkness), Food and Drug Administration, Rockville, MD; Biometry and Field Studies Branch (Dr. Dambrosia), National Institute of Neurological Disorders and Stroke, Bethesda, MD; Department of Neurology (Dr. Tuhrim), Mount Sinai Medical Center, New York, NY; Department of Neurology (Dr. Wolf), Boston University School of Medicine, Boston, MA; Neurological Institute (Dr. Mohr), Columbia-Presbyterian Medical Center, New York, NY; Department of Neurology (Dr. Hier), University of Illinois Hospital, Chicago, IL; and Department of Neurology (Dr. Caplan), Tufts University School of Medicine, Boston. MA.

To gain insight into neurologic signs relevant to the diagnosis of cardiogenic embolism, we analyzed data from 1,290 patients with cerebral infarcts in the NINDS Stroke Data Bank. Based solely on the presence of potential cardiac sources of embolism, we divided patients into groups of high (N = 250), medium (N = 167), and low (N = 873) risk of a cardiogenic mechanism for their stroke. Diminished level of consciousness was highly associated with the presence of a cardiac source of embolism. Of the four primarily cortical deficits assessed, three (visual field abnormalities, neglect, and aphasia) showed a highly significant graded relationship to the cardiac risk groups. For the fourth cortical deficit (other nonlanguage cognitive functions), this relationship did not attain statistical significance. Conversely, hemiparesis without sensory or cortical deficits had a strong inverse association to the presence of a cardiac source of embolism. This inverse association was weaker for sensorimotor strokes and nonexistent for pure sensory strokes. Although some neurologic findings had highly significant associations with the presence of a cardiac source of embolism, their predictive value for an embolic source was low.

Address correspondence and reprint requests to Dr. Steven J. Kittner, Department of Neurology, University of Maryland Hospital, 22 South Greene Street, Baltimore, MD 21201.

Supported by the Stroke Data Bank (SDB) under Contracts NO1-NS-2-2302, NO1-NS-2-2384, NO1-NS-2-2399, and NO1-NS-6-2305 from the NINCDS. Dr. Kittner is the recipient of a Clinical Investigator Development Award (K08-NS01319) from NINDS and a Grant-in-Aid from the American Heart Association, with funds contributed in part by the AHA Maryland Affiliate. Dr. Tuhrim is the recipient of a CIDA (K08-NS0157) and also of a grant from the Hess Foundation.

The SDB Manual of Operations, which includes the SDB data forms, is available from the National Technical Information Service (NTIS), US Department of Commerce, 5285 Port Royal Road, Springfield, VA 22161 (NTIS Accession No. PB88 101852/AS).

Presented in part at the 114th annual meeting of the American Neurological Association, New Orleans, LA, September 24–27, 1989.

Received May 24, 1991. Accepted for publication in final form July 31, 1991.

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