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3.
Ann Neurol ; 44(2): 202-8, 1998 Aug.
Article in English | MEDLINE | ID: mdl-9708542

ABSTRACT

To investigate the pathophysiological role of anti-GM1 antibody in Guillain-Barré syndrome (GBS), we reviewed sequential nerve conduction studies of 345 nerves in 34 GBS patients. Statistically significant correlation between IgG anti-GM1 antibodies and electrodiagnoses was found. Sixteen IgG anti-GM1-positive patients were classified as having acute motor or acute motor sensory axonal neuropathy (AMAN or AMSAN) (12 patients), as having acute inflammatory demyelinating polyneuropathy (AIDP) (3 patients), or as undetermined (1 patient) by electrodiagnostic criteria. Besides axonal features, there was rapid resolution of conduction slowing and block. In 3 patients initially diagnosed as having AIDP, conduction slowing was resolved within days, and 1 of them and 3 AMAN patients showed markedly rapid increases in amplitudes of distal compound muscle action potentials that were not accompanied by prolonged duration and polyphasia. The time courses of conduction abnormalities were distinct from those in IgG anti-GM1-negative AIDP patients. Rapid resolution of conduction slowing and block, and the absence of remyelinating slow components, suggest that conduction failure may be caused by impaired physiological conduction at the nodes of Ranvier. Reversible conduction failure as well as axonal degeneration constitutes the pathophysiological mechanisms in IgG anti-GM1-positive GBS. In both cases, immune-mediated attack probably occurs on the axolemma of motor fibers.


Subject(s)
G(M1) Ganglioside/immunology , Immunoglobulin G/immunology , Nerve Degeneration/immunology , Neural Conduction/immunology , Polyradiculoneuropathy/immunology , Adult , Axons/immunology , Female , Humans , Male , Middle Aged
4.
Ann Intern Med ; 127(9): 848-53, 1997 Nov 01.
Article in English | MEDLINE | ID: mdl-9382413

ABSTRACT

Indiscriminate use of the terms dehydration and volume depletion, so carefully crafted by our predecessors, risks confusion and therapeutic errors. These two conditions should be distinguished at the bedside and in how we speak to one another. Dehydration largely refers to intracellular water deficits stemming from hypertonicity and a disturbance in water metabolism. The diagnosis of dehydration cannot be established without laboratory analysis of p[Na +] or calculation of serum tonicity. In contrast, volume depletion describes the net loss of total body sodium and a reduction in intravascular volume and is best termed extracellular fluid volume depletion. The diagnosis of this condition relies principally on history, careful physical examination, and adjunctive data from laboratory studies. The pathophysiology of both dehydration and extracellular fluid volume depletion must be understood if these conditions are to be recognized and appropriately treated when they occur separately or together. There is no inclusive therapy for all situations. For example, indiscriminate treatment with 0.45% saline cannot be recommended when these conditions coexist because extracellular fluid volume depletion is often treated rapidly with 0.9% saline and dehydration is often treated more slowly with 5% dextrose.


Subject(s)
Dehydration , Extracellular Space , Terminology as Topic , Dehydration/etiology , Dehydration/therapy , Humans , Water-Electrolyte Balance
6.
Respir Physiol ; 31(3): 309-25, 1977 Dec.
Article in English | MEDLINE | ID: mdl-609848

ABSTRACT

Weight specific VO2 of resting Pseudemys floridana at body temperatures (BT) between 12 to 38 C was studied in relationship to VE, VT, f, pulmonary and systemic blood flow, and blood PO2, PCO2, pH and O2 content. The slope of the curve for VO2 against body mass was similar to that for mammals and differed from that of lizards. VE increased with BT while VE/VO2 fell, resulting in an elevation of arterial PCO2 and a decline in arterial pH of 0.013 unit/degrees C [HCO-3] and total CO2 remained constant. Increments in VE were achieved by decreasing apneic time and increasing VT up to VT of 18 ml.kg-1 when further rise in VE was exclusively on account of breathing frequency. Mean pulmonary and arterial blood flows were incremented in direct proportion to VO2, and no net intracardiac shunts was demonstrable. Ventilation-perfusion ratio fell with BT while EO2 increased. Arterial hemoglobin saturation varied inversely with BT while the arteriovenous O2 difference remained constant. EO2 was found to be highly dependent on the constant blood convection requirement as VE/VO2 fell. At similar BT, VE/VO2 was similar to that for man while Qpul/VO2 was in inverse proportion to maximum O2 capacity of the blood for the two species.


Subject(s)
Acid-Base Equilibrium , Blood Circulation , Body Temperature , Oxygen/blood , Respiration , Turtles/physiology , Animals , Blood Pressure , Body Weight , Carbon Dioxide/blood , Pulmonary Circulation , Ventilation-Perfusion Ratio
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