Publications by authors named "David W"

A 39-year-old man developed sequential acute mononeuropathies involving both median, both ulnar, and the right radial and left peroneal nerves. Electrophysiology demonstrated an asymmetric sensorimotor axonal polyneuropathy; nerve biopsy confirmed a vasculitis. Laboratory evaluation revealed a mixed cryoglobulinemia and active hepatitis C infection.

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Tarsal Tunnel Syndrome (TTS) can be difficult to diagnose: electrophysiologic corroboration is important and has therapeutic implications. Conventional electrodiagnostic techniques are insensitive: motor latency abnormalities exist in only 52%; sensory responses are frequently absent (a nonlocalizing finding). Additionally, previously described near nerve techniques do not isolate conduction velocity (CV) measurement to the short segment across the flexor retinaculum (FR), which would theoretically improve sensitivity.

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Patients who undergo mechanical ventilation for severe asthma are at risk of developing diffuse muscle weakness because of acute myopathy. The relative importance of corticosteroids and neuromuscular paralysis in causing the myopathy is controversial, and it is uncertain whether the chemical structure of the drug used to induce paralysis influences the risk of myopathy. Using a retrospective cohort study design, we evaluated 107 consecutive episodes of mechanical ventilation for severe asthma to assess (1) the incidence of clinically significant weakness in patients treated with corticosteroids alone versus corticosteroids with neuromuscular paralysis, (2) the influence of the duration of paralysis on the incidence of muscle weakness, and (3) the relative risk of weakness in patients paralyzed with the nonsteroidal drug atracurium versus an aminosteroid paralytic agent (pancuronium, vecuronium).

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Eighty infants with nonarthrogrypotic floppy infant syndrome (FIS) were evaluated between 1979 and 1990. Electromyographic data were correlated with results of muscle and nerve biopsies in 41 of 80 who had concomitant biopsies (38) or other diagnostic analyses (3). A diagnosis was made of Werdnig-Hoffmann disease (WHD) in 15, a congenital infantile polyneuropathy (IPN) in 3, neuromuscular transmission defect (NMTD) in 2, myopathy in 12, and presumed "central" hypotonia in 9.

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The hemodynamic response 1 hour after 1.25 mg of intravenous (IV) enalaprilat was examined in 20 patients (mean age 75 years) with severe congestive heart failure (CHF) and mitral regurgitation (MR), secondary to ischemic heart disease (NYHA Class IV). Patients were classified into two groups based upon the magnitude of MR as derived from Doppler color flow imaging: Group I (n = 13) had severe MR and Group II (n = 7) had moderate MR.

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All computerized ECGs taken over a 17-week study period were reviewed for the detection of multifocal atrial arrhythmia (MAA)--tachycardia or rhythm--and correlated with the diagnostic statement of the ECG computer system. MAA was identified by the authors in 96 of 11,610 (0.8%) computerized ECGs.

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Of ten consecutive patients (eight men, two women; mean age, 59 years) seen over a ten-month period with acute inferoposterior infarction treated with thrombolytic therapy, seven patients demonstrated significant rhythm disturbances at a time interval consistent with clot lysis and in a setting of other clinical markers predictive of reperfusion. One patient had a ventricular arrhythmia treated with intravenous procainamide, but six patients had marked bradyarrhythmias (sinus bradycardia, four patients; and 2 degrees atrioventricular block, one patient) associated with hemodynamic compromise. Urgent treatment consisting of intravenous atropine sulfate (1 mg) briskly restored sinus rhythm and normal arterial pressure within 1 min.

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This study provides the first morphological evidence of significant structural damage following high doses of enflurane alone and confirms previous findings of transient renal functional abnormalities following high dosage enflurane. The study also indicates that enflurane may have a greater potential for renal toxicity in the presence of renal impairment. Treatment of Fischer 344 rats with a nephrotoxic dose of gentamicin prior to six hours of enflurane (GE) anaesthesia at 1 MAC resulted in increased serum concentration of the enflurance metabolite inorganic fluoride (GE, 43.

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