Biomedical subjects
J C Brust
Publications and source records attributed to J C Brust.
Management of urban tetanus.
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Neurological complications of addiction to heroin.
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Pneumococcal meningitis at Harlem hospital.
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Quinine amblyopia related to heroin addiction.
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Glial tumor metastases through a ventriculo-pleural shunt. Resultant massive pleural effusion.
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Neurologic findings in neonates with intrauterine cocaine exposure.
To determine the effects of prenatal cocaine exposure on intrauterine growth and neurologic function, 30 term infants were evaluated prospectively: 14 cocaine-exposed and 16 unexposed. Cocaine-exposed infants had significantly lower mean birth weights, birth lengths, and head circumferences than urine-negative controls. Neurologic abnormalities among cocaine-exposed newborns included hypertonia of any type (86% vs 33%), axial hypertonia (79% vs 19%), plantar extension (46% vs 19%), and coarse tremor (57% vs 12%). The degree of hypertonia was sufficiently severe to warrant a diagnosis of "hypertonic tetraparesis" in 64% of cocaine-exposed and 12% of unexposed infants (P = .007). This diagnosis was highly correlated to small head size (r = 0.48; P = .01). Persistent tonic downward gaze was evident in two neurologically abnormal cocaine-exposed newborns. Gaze abnormalities improved slightly over the next 3 weeks of observation. One such infant re-evaluated at 6 months of age revealed resolution of tonic downward gaze and neurologic findings. We conclude that prenatal cocaine exposure is associated with tone and movement abnormalities in newborn infants.
Vascular dementia--still overdiagnosed.
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Selective proprioceptive loss from a thalamic lacunar stroke.
In an elderly woman a small thalamic infarct, documented by computed tomography and nuclear magnetic resonance imaging, caused proprioceptive loss contralaterally without impairment of other sensory modalities. This patient, the first so reported, demonstrates the anatomic separation of spinothalamic and dorsal column/medial lemniscus sensory modalities in the human thalamus.
Measurement of regional cerebral blood flow with 133xenon and a multiple-crystal scintillation camera.
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Aphasia in acute stroke.
Previous surveys of stroke populations have offered only cursory information on language disturbance, and, conversely, few surveys of aphasic populations have dealth exclusively with stroke or with acute phenomena. This paper describes aphasia in 850 acute stroke patients consecutively registered by the Harlem Regional Stroke Program, of whom 177 (21%) were aphasic; of these, nine were of Broca's type, 24 were of Wernicke's type, 14 were of anomic, ten were conduction, seven were of "isolation" type, and 107 were "mixed." An unexpected finding was a significant over-representation of men among the nonfluent aphasics. During the following four to 12 weeks, 12% of fluent aphasics died, and 12% remained moderately or severely impaired; among survivors, aphasia improved in 74%, and in 44% it cleared completely. During the same period, 32% of nonfluent aphasics died, and 34% remained moderately or severely impaired; among survivors, aphasia improved in 52%, and in only 13% did it clear completely. In both fluent and nonfluent groups, hemiparesis and/or visual field cut were associated with poor prognosis.
Frequency and course of pure motor hemiparesis: a clinical study.
A review of 850 acute unselected stroke cases at Harlem Hospital found only 25 (3%) who met a clinical definition of pure motor hemiparesis. Compared to other cerebral infarction survivors, the 23 pure motor syndrome survivors were slightly younger, not much more often hypertensive and did not make a faster recovery. The degree of motor deficit a year later was nearly the same in both groups. Brain scans were positive in one-third of the pure motor patients, which suggests that this clinical picture may be associated with larger brain lesions than had been suspected before, as well as with lacunar infarction.
Example of a community model for comprehensive stroke services: the Harlem Regionaal Stroke Program.
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Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. 1988.
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