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Biomedical subjects

S Calzetti

Publications and source records attributed to S Calzetti.

At least 55 records · Page 3Linked to original sources
PubMed1981

Progressive supranuclear palsy in the course of subclavian steal syndrome.

A 70-year-old man manifested during four years a progressive clinical picture consisting in palsy of gaze, axial rigidity, disorders of standing and gait, dysarthria, dysphagia. Neuroradiological investigations demonstrated proximal thrombosis of the left subclavian artery with subclavian steal. At necropsy, degenerative changes in several areas of the basal ganglia and brain stem, with presence of globose neurofibrillary tangles, were found, consistently with the pathologic pattern of the Progressive Supranuclear Palsy (PSP). The association of PSP and subclavian steal syndrome has not been previously reported, to our knowledge. We hypothesize that chronic ischemia, due to subclavian steal syndrome, in the vertebral basilar system and its watershed versus carotid system may have favoured the appearance, in these same areas, of the changes of the PSP.

Aged↗
PubMed1981

Facial myokymia in the course of a pontine tumor.

A patient with facial myokymia, suffering from an infiltrating grade II astrocytoma originating within the pons with vegetations invading the cerebellopontine angle, was studied clinically and electromyographically from 1973 to 1979. The myokymias started in the muscles of the right side of the face and later spread to the left side. The latter point is worth noting because the myokymias of the left side were detectable by EMG but not by inspection. They preceded clinical and instrumental evidence of a contralateral spread of tumoral damage to the brainstem. From the physiopathogenetic angle they point up the importance of a mechanism of hyperexcitability and release of the facial motoneuronal pool. The results of the EMG study suggest that the persistence of myokymia, its association with an ingravescent neurogenic impairment of the facial musculature and its polymorphism in the course of pontine tumors are more reliable features than their discontinuity and rhythmicity.

Adult↗
PubMed1981

Phenylethylmalonamide in essential tremor. A double-blind controlled study.

A randomised double-blind placebo-controlled trial of phenylethylmalonamide, the major metabolite of primidone was performed in eight patients with essential tremor. Phenylethylmalonamide was given in a daily dose of 400 mg for one week and 800 mg for a second week. The compound had no statistically significant effect on the amplitude of tremor assessed by an accelerometric method, tests of performance, clinical evaluation and patient self assessment. No side effects occurred. Serum levels of phenylethylmalonamide on a daily dose of 400 mg were 11-27 micrograms/ml and on 800 mg daily were 16-48.5 micrograms/ml.

Adult↗
PubMed1981

Metoprolol and propranolol in essential tremor: a double-blind, controlled study.

Single oral doses of propranolol (120 mg), metoprolol (150 mg) and placebo were given in a randomised, double-blind fashion to 23 patients with essential tremor. Both beta blockers were significantly more effective than placebo in reducing the magnitude of tremor. The decrease in tremor produced by metoprolol (47, sem 9%, n = 23) was not significantly different from that observed propranolol (55, sem 5%, n = 23). Tachycardia on standing was antagonised by both drugs to a similar extent. These findings suggest that metoprolol may represent a valuable alternative to propranolol in the treatment of essential tremor. The data is consistent with the hypothesis that the tremorolytic effect of beta blockers in these patients may be unrelated to peripheral beta-2 adreno-receptor blockade, being possibly mediated by other central or peripheral modes of action of these drugs. However, it cannot be excluded that at the dose used, metoprolol had lost its relative cardio-selectivity and that the reduction in tremor was mediated by competitive antagonism at beta-2 receptor sites in skeletal muscle.

Adult↗
PubMed1981

[Late myopathy with mitochondrial changes in the muscle].

The ultrastructural finding of abnormal muscle mitochondria has been reported in various conditions, but mostly in association with the clinical picture of ophthalmoplegia, and in cases of "floppy infant" syndrome. In the case herein reported, the mitochondrial abnormalities were found in the muscle biopsy of a 49-year-old man suffering from a late onset proximal myopathy; he was affected also by polyneuropathy, subclinical thyroid dysfunction, disturbances of heart conduction, and unilateral gynaecomastia. The association of abnormal muscle mitochondria and late onset myopathy without involvement of the extraocular muscles has been reported in a very few cases. It is not possible, at present, to state that these cases represent a nosological entity; the existence of an underlying biochemical defect, accounting for the mitochondrial abnormalities, could be suspected, but it seems more probable that these changes are non-specific features of muscular damage, possibly related to the stage and the degree of the process. In this view, the coexistence of neurogenic damage, gastrointestinal malabsorption, and thyroid dysfunction, could play an additional role in the case herein described. Finally, the coexisting findings of cardiac, endocrine, and neuropathic damage are discussed with regard to the Kearns-Sayre syndrome, which also associates mitochondrial myopathy and multisystemic involvement.

Humans↗
PubMed1980

Transient hemiballismus and subclavian steal syndrome. Case report.

Transient hemiballismus was observed in a 74-year-old man, displaying subclavian steal syndrome. Such a correlation has not been previously reported in the literature. In this case, transient hemiballismus seemed to depend on hemodynamic factors, but other mechanisms possibly explaining early recovery of the hyperkinesias are discussed. In particular, stress is laid upon the role of preexisting pathological changes of the central nervous system (diffuse cerebral atrophy) associated to the "releasing" lesion.

Aged↗
PubMed1978

Disposition of sodium valproate in epileptic patients.

1 Serum levels of valproic acid have been determined at fixed intervals after the administration of single oral and intravenous doses (800 mg) to six epileptic patients receiving chronic treatment with other antiepileptic drugs. 2 Serum levels declined monoexponentially shortly after the intravenous administration. Biological half-lives averaged 9.0 +/- 1.4 h (s.d.). Volumes of distribution were 0.175 +/- 0.025 l/kg. There was a statistically significant negative correlation between volumes of distribution and serum half-lives (P less than 0.005). 3 After oral doses serum levels rose rapidly to peak values within 0.5--2 h. Biological availability was 96 +/- 9%. 4 Comparison with a previous study performed according to the same protocol in healthy volunteers showed significantly increased volumes of distribution and rates of elimination in the patients. Total serum clearance was 85% higher in the patients as compared to the healthy subjects (P less than 0.001). Possible explanations for these findings are discussed.

Adult↗
PubMedDate not supplied

[The not choreic neurological complications of rheumatic disease (author's transl)].

The authors discuss the importance of neurological complications of rheumatic disease, which differ from those of Sydenham's chorea: encephalitis; acute cerebral circulatory insufficiency of cardiovascular basis; thrombosis and cerebral haemorrhage; cerebral emboli; and vasculitis. The case of a 13 year old boy who presented with an acute cerebral episode during an active phase of rheumatic fever is described. The E.E.G. showed a right hemisphere disturbance with a slight involvement of the controlateral hemisphere. The cardiac evidence was indicative of a rheumatic carditis. The clinical progress and EEG were rapidly favourable. The possible pathogenetic hypotheses of this case are taken into consideration, and the authors suggest that one must suspect a rheumatic etiology when an acute cerebral syndrome is established in a child or a young adult with current or previous rheumatic fever.

Acute Disease↗
PubMedDate not supplied

[Epidemiological observations on plasma levels of diphenylhydantoin in 130 patients on prolonged treatment (author's tranls)].

Plasma levels of diphenylhydantoin have been measured in 130 epileptic patients undergoing long-term anticonvulsant therapy. Only in a small percentage of the patients (15,38%) plasma levels were found to lie within the therapeutic range. Most patients (75,38%) exhibited subtherapeutic values, while in a few cases (9,24%) the upper limit of therapeutic range was exceeded. Although plasma concentrations significantly correlate with the administered dose, predictability of plasma levels in the individual patients given fixed dosage schedules is strongly limited by large interindividual variability. Sex, age and simultaneous administration of other drugs seem not to affect significantly DPH plasma levels. Our observations carried out in a meaningful sample of epileptic patients suggest that at present the practice of monitoring diphenylhydantoin plasma levels is still an essential tool for the management of epilepsy when a safe and effective therapeutic regimen is required.

Epilepsy↗
PubMedDate not supplied

Palatal "myoclonus" and inferior olive hypertrophy with one-sided cerebellar lesion. Clinico-pathological report of one patient.

A case of palatal myoclonus and inferior olive hypertrophy is reported. Lesions located other than in the medulla were cerebellar infarction, lymphomatous infiltrates and, supratentorially, progressive multifocal leukoencephalopathy. It is suggested that double innervation of the olives from either side dentate nucleus may be why in the case reported here and in several cases in the literature, one-sided supra-olivary lesions can produce bilateral hypertrophy. As with palatal "myoclonus" and olivary hypertrophy, it is proposed that if the characteristic rhythmical movements occur, lesions besides those along the dentate-olivary pathway and the olivary hypertrophy itself have to be present.

Cerebellum↗