To investigate the epidemiology and clinical spectrum of neurosyphilis in a population with high rates of coexisting syphilis and human immunodeficiency virus (HIV) infection, a retrospective analysis of cases in all San Francisco hospitals from 1985 to 1992 was conducted. Neurosyphilis was defined by a newly reactive cerebrospinal fluid VDRL; 117 patients with neurosyphilis were identified. The median age was 39 years, 91% were male, 74 (63%) were white, and 75 (64%) were HIV-infected. Thirty-eight (33%) presented with an early symptomatic neurosyphilis syndrome. Six (5%) had late neurosyphilis. Thirty-eight (32%) patients were asymptomatic, and 35 (30%) had findings attributable to coexisting neurologic diseases. Patients demonstrated high serum nontreponemal (VDRL) titers (median, 1:128) at neurosyphilis presentation. In contrast to the findings from the preantibiotic era, neurosyphilis was identified in young patients most often with HIV coinfection, and early symptomatic syndromes were identified more frequently than late neurosyphilis syndromes.
Our results demonstrate that POLG mutations account for a substantial proportion of patients (13%) with PEO and multiple mitochondrial DNA deletions and cause both clinically and genetically heterogeneous disorders.
The systemic vascular response to seizures is known but information on the hemodynamics of the pulmonary circulation is lacking, clouding an understanding of the pathophysiology of postical pulmonary edema. We investigated this problem using electrically induced single seizures and bicuculline-induced status epilecticus in halothane-anesthetized sheep. Aortic, pulmonary arterial, and left atrial pressures were recorded throughout the seizure activity, and the responses of the systemic and pulmonary pressures were compared. All monitored pressures rose precipitously with the onset of seizures. In all types of seizure the pulmonary pressure elevation was brief, lasting only one-third as long as did the systemic. Pulmonary microvascular pressures rose well above the level of plasma oncotic pressure. Pulmonary vascular pressures were elevated in proportion to the duration of the seizure stimulus, while the systemic response did not so vary. Cervical spinal cord transection abolished all systemic and pulmonary vascular response to seizures, demonstrating ultimate neural mediation.
Magnetic resonance imaging and water-suppressed proton magnetic resonance spectroscopic imaging were used to study N-acetylaspartate and other metabolites in a patient with severe hypoxic-ischemic encephalopathy. The N-acetylaspartate signal, a putative marker of neuronal density, was markedly reduced in the forebrain. The relative signal intensity of choline-containing metabolites, which are more abundant in astrocytes than neurons, was increased. These results support the hypothesis that water-suppressed proton magnetic resonance spectroscopic imaging measurements of N-acetylaspartate may be useful for noninvasive detection of selective neuronal loss in a variety of disease states in the human brain.
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