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Biomedical subjects

C Paschalis

Publications and source records attributed to C Paschalis.

35 records · Page 2Linked to original sources
PubMed1989

Prevalence rate of cerebrovascular disease in the rural population of northwest Peloponnese, Greece. A direct epidemiological study.

In a direct (door-to-door) epidemiological study, the prevalence rate of cerebrovascular disease in the rural population of northwest Peloponnese, Greece, was found to be 995 strokes per 100,000 inhabitants over 20 years of age. This number is considerably lower than the prevalence rate (1,417 strokes per 100,000 inhabitants over 20 years of age) found in the urban population of the same county (Patras, Greece).

Adult↗
PubMed1984

Myopathy due to juvenile acid maltase deficiency affecting exclusively the type I fibres.

The clinical and laboratory findings of a patient with juvenile acid maltase deficiency are presented. The patient died from respiratory muscle weakness at age 31 years. Muscle biopsy shortly prior to his death showed remarkable vacuolation affecting exclusively type I fibres and mild myopathic changes of both types of muscle fibres, while the muscle biopsy at age 26 years had shown no evidence of acid maltase deficiency.

Adult↗
PubMed1983

Electrolyte metabolism in patients with periodic affective disorders during treatment with rubidium.

Five patients suffering from periodic affective disorders with short mood-cycles were treated with rubidium chloride, producing peak erythrocyte concentrations between 9 and 13 mmol/l. Loading with rubidium was associated with decreased total body potassium, but red-cell potassium was unchanged. Regular mood-cycling was disturbed, together with the associated body-weight changes. There was a slight extracellular "metabolic" acidosis. Electrolyte concentrations fluctuate abnormally in these patients, and two muscle biopsy specimens had very low potassium contents.

Affective Disorders, Psychotic↗
PubMed1980

A stepped forty-eighty hour manic-depressive cycle.

This paper describes a patient with an almost 48-hour manic-depressive cycle but with a daily shift of the switching time, the latter having itself a cycle of five days. The mood change always occurred gradually and during the day, never at night. Between manic and depressive phases there was a difference in the frequency of the EEG alpha rhythm. The patient showed a good response to lithium treatment.

Aged↗
PubMed1979

Urinary dicarboxylic acids in patients receiving lithium or rubidium salts.

Lithium salts administered in therapeutic doses to four subjects who were kept on controlled diets increased up to fivefold the urinary output of some dicarboxylic acids. Some of the acids affected are intermediates in the tricarboxylic acid cycle, others are chemically similar but not directly related in metabolic terms. This is probably a direct effect on renal transport. Rubidium salts increased urinary 2-oxoglutarate output and blood 2-oxoglutarate levels, probably by some action on intermediary metabolism.

Bipolar Disorder↗
PubMed1978

Nerve fibre refractory period in patients treated with rubidium and lithium.

Nerve fibre refractory period distributions have been measured on the median nerves of six manic-depressive patients controlled with lithium carbonate, three chronic patients (two manic-depressives and one catatonic schizophrenic) controlled with rubidium chloride, and eight normal volunteers. Rubidium prolonged the refractory periods of all nerve fibres while lithium increased only the longer refractory periods.

Adult↗
PubMed1978

Effects of rubidium chloride on the course of manic-depressive illness.

Clinical studies of the effects of rubidium ions on the course of manic-depressive illness are reported. It seems that rubidium tends to increase the length of manic phases and possibly reduces the extremes of mood. Rubidium did not seem to produce any severe side effects in the dose administered, but it has a long biological half-life and caution is still required. Some details of the CSF, RBC, saliva and plasma and urine kinetics are also reported.

Adult↗
PubMed1976

Lithium and the antidiuretic hormone.

The effect of lithium on the urine concentrating response to antidiuretic hormone (ADH) and the excretion of ADH has been studied in rats and man. The maximum urine osmolarity following 18 h dehydration and Pitressin (5 u) was decreased in three out of four patients during lithium treatment compared to their response to the same test in the absence of lithium. In a fifth patient, tested only during lithium treatment, the urine remained hypotonic to plasma throughout this test. Lithium increased the excretion of ADH in non-polyuric patients from 9-22 mu/24 h in the absence of lithium to 36-202 mu/24 - during lithium treatment. In four patients with lithium-induced polyuria, a diuretic acting on the distal tubules, clorexolone, reduced the polyuria. Lithium increased urine volume and the excretion of ADH in four rats receiving lithium in their diet. The response to exogenous ADH was decreased during lithium administration.

Animals↗
PubMedDate not supplied

Effects of short-term oral acitretin therapy on peripheral nerve function: a prospective neurological and neurophysiological study.

The aim of the present prospective study was to substantiate possible side effects of short-term oral acitretin therapy (1 mg/kg/day) on peripheral nerve function of 13 patients with severe keratinization disorders. Clinical neurological examination before and 1 and 3 months after onset of treatment was unremarkable in all patients; however, a significant alteration of one or more neurophysiological, predominantly sensory, parameters was demonstrated in 3 out of 13 patients (23%) after 1 month and in 9 out of 13 (69%) after 3 months of oral acitretin therapy. These findings indicate that oral acitretin might be capable of causing a dysfunction of predominantly sensory nerve fibres in some individuals. Although in the investigated patients this dysfunction remained subclinical, it seems reasonable to suggest that neurological and neurophysiological evaluation of peripheral nerves should be added to the list of investigations that are routinely performed in patients receiving oral acitretin.

Acitretin↗
PubMedDate not supplied

Sensorimotor polyneuropathy after a three-month oral acitretin therapy.

We report a patient with chronic plaque psoriasis who developed clinical and electrophysiologic features of polyneuropathy affecting motor and sensory fibers in upper and lower extremities after three months of treatment with oral acitretin. Drug withdrawal resulted in a complete clinical recovery and normalization of all electrophysiologic abnormalities within two months.

Acitretin↗
PubMedDate not supplied

Peripheral sensory neuropathy associated with short-term oral acitretin therapy.

A 57-year-old female patient with widespread chronic plaque psoriasis and a 32-year-old male patient with severe oral lichen planus are reported, who developed sensory symptoms in the extremities 3 and 4 months after the onset of oral acitretin therapy, respectively. Both patients showed clinical and electrophysiological evidence of a sensory peripheral neuropathy, which completely resolved 2 and 2.5 years after discontinuation of oral acitretin administration, respectively.

Acitretin↗