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Biomedical subjects

A Quattrone

Publications and source records attributed to A Quattrone.

At least 163 records · Page 9Linked to original sources
PubMed1987

Subacute spongiform encephalopathy with periodic paroxysmal activities: clinical evolution and serial EEG findings in 20 cases.

Evolution of both clinical and EEG abnormalities was analyzed in 20 (16 pathologically confirmed) patients suffering from subacute spongiform encephalopathy with periodic paroxysmal activities (PPA) on the EEG. Illness duration was less than 4 and greater than 17 months in 65% and 10% of cases, respectively. All data but EEG were utilized to assess 3 conventional clinical stages in 20 patients. The early clinical stage was characterized by gradual presentation of gait disturbances, mental deterioration, sensory or autonomic disorders. In contrast with other reports, no PPA were observed in 10 EEG recordings from 7 patients examined at the early clinical stage. Both clinical and EEG findings were not in contrast with a hypothetic subcortical onset of disease. Similar to recent data in the literature, early PPA appeared within 12 weeks of disease evolution in 88% of patients who underwent EEG recordings in the first 3 months of disease. Nonetheless, these early PPA always occurred at an intermediary stage, when our patients showed a marked worsening of the clinical picture. Focal, segmental and/or generalized myoclonic jerks were observed in 15%, 53% and 100% of cases at prodromal, intermediary and terminal stages respectively. Different kinds of PPA were observed: bi-tri-phasic periodic complexes (PC), periodic complexes with multiphasic configuration (PPC) and periodic polyspiking discharges (PPD). Abnormal "pacing" of PC by slowly repeated flashes was found in 4 patients presenting visual hallucinations or cortical blindness. Burst-suppression activity was frequently found at the terminal stage in decorticate patients.

Aged↗
PubMed1986

Saccadic eye movements analysis as a measure of drug effect on central nervous system function.

Peak velocity (PSV) and duration (SD) of horizontal saccadic eye movements are demonstrably under the control of specific brain stem structures. Experimental and clinical evidence suggest the existence of an immediate premotor system for saccade generation located in the paramedian pontine reticular formation (PPRF). Effects on saccadic eye movements have been studied in normal volunteers with barbiturates, benzodiazepines, amphetamine and ethanol. On two occasions computer analysis of PSV, SD, saccade reaction time (SRT) and saccade accuracy (SA) was carried out in comparison with more traditional methods of assessment of human psychomotor performance like choice reaction time (CRT) and critical flicker fusion threshold (CFFT). The computer system proved to be a highly sensitive and objective method for measuring drug effect on central nervous system (CNS) function. It allows almost continuous sampling of data and appears to be particularly suitable for studying rapidly changing drug effects on the CNS.

Amobarbital↗
PubMed1985

Brainstem auditory evoked responses in Lafora disease.

Brainstem auditory-evoked responses (BAERs) have been studied in five patients suffering from Lafora-type of progressive myoclonus epilepsy proven by skin biopsy and in ten healthy volunteers. At the time of examination the patients were not taking benzodiazepines and showed myoclonic jerks. In all patients the central conduction time (interpeak latencies I-V, I-III, III-V) and the amplitude (amplitude ratio I/V) of BAERs were within the +/- 2 S.D. limits of the normal values. Since Lafora disease is a neuropathologically prevalent grey-matter illness (typical inclusion bodies are stored intraneuronally) these data indicate that diseases primarily affecting the brainstem grey-matter are usually associated with normal BAERs.

Adolescent↗
PubMed1984

Release of endogenous dopamine from tuberoinfundibular neurons.

Release of endogenous dopamine(DA) from arcuate-periventricular nucleus-median eminence fragments has been analyzed in an in vitro static incubation system. Exposure of these hypothalamic fragments to increasing concentrations of K+ ions produced a dose-dependent release of endogenous DA. The highest rate of K+-stimulated DA efflux occurred in the first 10 minutes, thereafter it progressively declined reaching prestimulated levels at 30 minutes. If two consecutive depolarizing stimuli of 40 mM KCl were applied to the same hypothalamic fragment, after a 40 minutes rest period, an equivalent release of endogenous DA occurred. Removal of Ca++ ions from the incubation medium containing the Ca++ chelator EGTA caused a decrease of basal DA efflux and completely prevented the K+-induced release of DA. Furthermore when verapamil, a blocker of Ca++ entrance, was added to the incubation medium in a concentration of 50 microM, the K+-induced DA efflux was completely counteracted, whereas spontaneous release was unmodified. Finally nomifensine, a potent blocker of DA uptake, added in vitro in a final concentration of 10 microM, significantly reinforced K+-induced release of endogenous DA. Since nomifensine did not modify basal DA release, this study confirmed its prevalent uptake blocking property rather than its releasing action on DA.

Animals↗
PubMed1984

Electroencephalographic and anatomo-clinical evidences of posterior cerebral damage in hypertensive encephalopathy.

The authors describe two patients suffering from hypertensive encephalopathy associated with epileptic seizures and anatomo-clinical evidences of posterior cerebral damage. The concordant electroencephalographic features with clinical signs and anatomic lesions of these two patients are discussed, in order to make some considerations about the role played by the blood-brain-barrier damage on the physiopathology of the hypertensive encephalopathy.

Adult↗
PubMed1983

Increased GH responsiveness to dopamine receptor stimulation in alcohol addicts during the late withdrawal syndrome.

In humans the release of growth hormone (GH) elicited by dopamine (DA) and DA agonists may represent a reliable model to assess change in sensitivity of DA receptors. We now report that in chronic alcoholics, 4-7 days after the suspension of alcohol consumption, the increase of GH response to DA infusion was higher than that seen in non alcoholic volunteers. The specificity of this GH response to DA administration was demonstrated by the use of domperidone, a novel peripheral antagonist of DA receptors. These results suggest the development of hyper-responsiveness of DA receptors involved in the control of GH secretion in chronic alcoholics during the later phases of the "withdrawal syndrome".

Adult↗
PubMed1983

Effect of the orally absorbed dopamine analogue N-methyldopamine diisobutyric ester on plasma prolactin levels.

The effect of the diisobutyric ester of N-methyldopamine (Ibopamine) on plasma prolactin levels was investigated in normoprolactinaemic subjects and in hyperprolactinaemic patients with prolactin-secreting tumours or idiopathic hyperprolactinaemia. In hyperprolactinaemic states oral Ibopamine 50 mg induced a significant decrease in elevated plasma prolactin (PRL) levels, 30, 60 and 90 min after administration. The peak effect occurred at 90 min when the mean PRL level was 61% of its basal values.

Adult↗
PubMed1983

Stroke in two young siblings with congenital dysfibrinogenemia.

Two young siblings (a male of 21 and his sister of 26 years) suffered from arterial thrombosis episodes of the carotid and abdominal aorta documented by angiographic studies. In the absence of any known predisposing factor in the family and personal history, the laboratory investigation of both patients revealed coagulation abnormalities compatible with a dysfibrinogenemia. The occurrence of a similar defect also in plasma of one of the propositi's asymptomatic relatives is suggestive of an inherited fibrinogen disorder.

Adult↗
PubMed1983

Prolactin secretion in man: a useful tool to evaluate the activity of drugs on central 5-hydroxytryptaminergic neurones. Studies with fenfluramine.

Acute oral administration of various doses of fenfluramine, a 5-HT releaser, induced a dose-related increase of PRL secretion in nine healthy volunteers. Fenfluramine reached the maximum effect on PRL secretion at 4 h after its administration. This effect was already significant at 2 h and lasted till 8 h. Metergoline, a 5-HT receptor blocker, when administered alone, decreased serum PRL levels in six healthy subjects. The pretreatment with this drug significantly antagonized the PRL-releasing action of fenfluramine (60 mg) suggesting that the effect of fenfluramine on PRL release may be mediated through a 5-HT mechanism in the brain. These findings suggest the possibility that serum PRL levels in humans may represent a useful tool to evaluate, in vivo, the activity of drugs possessing putative 5-hydroxytryptaminergic properties.

Adult↗
PubMed1981

Pharmacological evidence of supersensitivity of central serotonergic receptors involved in the control of prolactin secretion.

m-Chlorophenylpiperazine (m-CPP), a serotonin receptor agonist, induced dose-related increase in plasma prolactin levels in the rat. This effect was significantly prevented by pretreatment with metergoline, a serotonin receptor blocker. Long-term degeneration of hypothalamic serotonin nerve endings induced by intraventricular injection of 5, 7-dihydroxytryptamine, significantly enhanced the PRL-releasing action of m-CPP, as revealed by the shift to the left in the dose-response curve that relates the dose of m-CPP to plasma PRL levels. Thus the evidence suggests the possible development of supersensitivity of central serotonin receptors involved in the control of prolactin release.

5,7-Dihydroxytryptamine↗
PubMed1981

Carbamazepine, phenytoin and phenobarbital do not influence brain catecholamine uptake, in vivo, in male rats.

Desipramine (10 mg/kg, i.p.), a specific blocker of noradrenaline uptake, significantly antagonized the decrease of brain noradrenaline induced by an intraventricular injection of 6-hydroxydopamine (200 micrograms in 20 microliter) in rats. The depletion of brain dopamine, in 6-hydroxydopamine plus pargyline-treated rats was counteracted by nomifensine (10 mg/kg, i.p.), a drug which has been reported to markedly inhibit dopamine uptake both in vivo and in vitro. Carbamazepine (10 mg/kg, i.p.), phenytoin (200 mg/kg, orally) and phenobarbital (20 mg/kg, orally) were unable to significantly affect either the decrease of noradrenaline or the depletion of dopamine induced by 6-hydroxydopamine. These findings seem to suggest that these anticonvulsant drugs do not inhibit brain catecholamine uptake in vivo in male rats.

Animals↗
PubMed1979

Effect of midbrain raphe lesion or 5,7-dihydroxytryptamine treatment on the prolactin-releasing action of quipazine and D-fenfluramine in rats.

The role of brain serotonin in regulating prolactin (PRL) secretion has been investigated by studying the effect of quipazine and D-fenfluramine, two serotonin-like drugs, on plasma PRL levels under various experimental conditions. Quipazine (5, 10 and 20 mg/kg i.p.) and D-fenfluramine (5, 7.5 and 10 mg/kg i.p.) induced dose-related increases in plasma PRL levels in male rats. Intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) or electrolytic lesion of the nucleus raphe medianus (MR), which caused a marked and selective depletion of hypothalamic serotonin levels, significantly reduced the PRL-releasing effect of both quipazine and D-fenfluramine. These results suggest that the effect of these drugs on PRL release is mediated through a serotonergic mechanism in the brain.

5,7-Dihydroxytryptamine↗