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Biomedical subjects

W W Wasiewski

Publications and source records attributed to W W Wasiewski.

6 recordsLinked to original sources

Chronic nonprogressive headaches in children and adolescents.

Chronic nonprogressive headaches (CNPHA) are common in children and increase in frequency in adolescents. Features are usually, but not always, distinct from those of migraine. CNPHA have also been called chronic daily headaches, tension-type headaches, muscle contraction headaches, and psychogenic headaches. These headaches represent a diagnostic and therapeutic challenge to family physicians, pediatricians, and pediatric neurologists. The evaluation is time-consuming and the treatment frustrating and often unsuccessful. They are a significant cause of school absences. This review addresses the epidemiology classification, pathogenesis, clinical characteristics, evaluation, and treatment of this disorder.

Absenteeism↗

Preventive therapy in pediatric migraine.

Preventive therapy for migraine headache includes identification of migraine precipitants, possible adjustments in lifestyle, appropriate management of acute headache, and, when necessary, the use of pharmacologic agents. There are no well-controlled clinical trials with sufficient patient numbers to support the use of any agent in the prevention of migraine headache in children. Data on the use of amitriptyline and divalproex sodium in open-label studies suggest that these agents may be efficacious. The mechanism of action for these agents is unknown but may be related to the 5-hydroxytyptamine-2 (5-HT2) receptor antagonism or regulation of ion channels. A review of the pertinent literature on migraine prophylaxis in children is presented. Dosing guidelines are presented based on the limited data available and clinical experience.

Adrenergic beta-Antagonists↗

Cerebral glycogenosis, alpha particle type: morphologic and biochemical observations in an infant.

A 3-month-old infant with congenital hypotonia suffering from an unusual form of glycogenosis is reported. The most striking neuropathologic findings were vacuolation of neuropile and glycogen accumulation, especially in the cerebral cortex and cerebellar molecular layer. Ultrastructurally, glycogen accumulation was present mainly in neurites and astrocytic processes, and mostly appeared as rosettes (alpha glycogen particles). Biochemical analysis of glycogen in various regions of the central nervous system showed an increase of up to 100-fold. The cerebral cortex, deep nuclei, and cerebellar cortex had the highest glycogen elevations, while the cerebral white matter glycogen level was normal. Among other tissues, the heart showed a several-fold increase in glycogen content. Muscle, liver, and kidney glycogen levels were not elevated. Findings in this case and in three other reported patients with cerebral glycogenosis of alpha particle type are discussed.

Brain↗

Equilibrium binding of thrombin to platelets.

Binding of human [125I]thrombin to washed human platelets was studied in order to analyze the nonenzymic aspects of the thrombin stimulation of platelets. Highly purified alpha-thrombin that was iodinated with lactoperoxidase retained full clotting and esterase activities and full activity toward platelets, was not distinguished from native thrombin by sodium dodecyl sulfate-polyacrylamide gel electrophoresis or gel chromatography, and bound to platelets the same as unlabeled thrombin. Bound and free [125I]thrombin were measured after rapid separation of platelets from the suspending medium by centrifugation through oil. Maximum binding was within 15 s, the shortest time measured. At concentrations of thrombin sufficient to cause less than maximal platelet stimulation, 90% of the total thrombin was free in the suspending solutions. Equilibrium binding was established, with both free thrombin and free platelets retaining activity, and with rapid reequilibration after dilution or addition of unlabeled thrombin. The equilibrium was complex, with the apparent number of binding sites and dissociation constants dependent on thrombin concentration. Analysis of bound thrombin as a function of thrombin concentration by double-reciprocal and Scatchard plots indicated 300-400 high affinity sites (Kdiss = 1.8-2 nM); these correlate with thrombin stimulation of Ca2+ secretion, which shows half maximal effect at 1.5 nM thrombin and maximal effect with 500-600 thrombins bound per platelet.

Binding Sites↗