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Biomedical subjects

R Mutani

Publications and source records attributed to R Mutani.

At least 55 records · Page 3Linked to original sources
PubMed1992

Magnetic brain stimulation: the silent period after the motor evoked potential.

In 25 normal subjects, we studied the EMG silent period following the magnetic motor evoked potential (MEP) when the target muscle was tonically contracted (post-EMP silent period [PMSP]). In the first dorsal interosseous muscle (FDI), PMSP duration increased in linear proportion to stimulus intensity, but not to the size of the preceding MEP. The PMSP was longer in hand and forearm muscles than in upper arm muscles. In the FDI, PMSP was longer than the peripheral silent period (PSP) even when multiple peripheral stimuli were used to get M responses whose twitch force was equivalent to that of MEPs. Weak magnetic stimuli evoked silent periods preceded by no MEP in several subjects. Spinal alpha-motoneurons (alpha-MNs) were partially inhibited during the first PMSP portion, but later this effect recovered. MEPs due to weak electrical stimuli to motor cortex were only slightly inhibited during the late PMSP. Segmental inhibitory loops evoked by the muscle twitch and inhibitory projections descending to alpha-MNs from the cortex predominantly underlie earlier PMSP portions, but recurrent intracortical inhibition may also contribute. Later portions are predominantly due to other stimulus-related cerebral inhibitory or suppressing phenomena.

Adult↗
PubMed1991

Multiple system atrophy-autonomic failure: a case with early laryngeal stridor and without orthostatic hypotension.

We report a case of multiple system atrophy-autonomic failure in which the most interesting features were the uncommon onset of a laryngeal stridor in the absence of orthostatic hypotension and the clinical-nosographic possibilities for the autonomic changes found. The differentiation between autonomic failure and pure autonomic failure and their relationship to multiple system atrophy are still under discussion. We agree with the authors who consider that the absence/presence of orthostatic hypotension may be taken as discriminant for this purpose.

Aged↗
PubMed1991

Perception and action in 'visual form agnosia'.

A single case study of a patient with 'visual form agnosia' is presented. A severe visual recognition deficit was accompanied by impairments in discriminating shape, reflectance, and orientation, although visual acuity and colour vision, along with tactile recognition and intelligence, were largely preserved. Neuropsychological and behavioural investigations have indicated that the patient is able to utilize visual pattern information surprisingly well for the control of hand movements during reaching, and can even read many whole words, despite being unable to make simple discriminative judgements of shape or orientation. She seems to have no awareness of shape primitives through Gestalt grouping by similarity, continuity or symmetry. It is proposed that many of these perceptual disorders might be the combined result of (1) a selective loss of the cortical elaboration of the magnocellular visual processing stream, and (2) a selective output disconnection from a central processor of visual boundaries and shape primitives in the occipital cortex.

Adult↗
PubMed1991

Parkinson's disease rigidity: magnetic motor evoked potentials in a small hand muscle.

We studied the EMG potentials evoked in the bilateral first dorsal interosseus muscle by electromagnetic stimulation of the corticomotoneuronal descending system in 10 Parkinson's disease patients and in 10 age- and sex-matched normal controls. We selected patients who did not have tremor but had predominant rigidity with asymmetric body involvement. On the rigid side of the PD patients, the threshold to cortical stimulation was lower than on the contralateral side or than normal values. On average, patients had normal central conduction times, but their motor evoked potentials (MEPs) on the rigid side were larger than those of controls when the cortical stimulus was at rest or during slight tonic contraction of the target muscle. In the latter condition, a silent period shorter than that of controls followed MEPs, whereas the peripheral silent period following ulnar nerve stimulation at the wrist was prolonged. Alpha motor neuron excitability, tested by the F-wave method, was enhanced on the rigid side at rest. In rigidity, spinal motor nuclei may be more responsive than normal to descending inputs from motor cortex, or the entire corticomotoneuron system may prove hyperexcitable under given conditions.

Aged↗
PubMed1990

A simple and disposable visual measuring device to assay antiepileptic drugs from whole blood samples.

This study evaluated a new, simple, disposable visual measuring device (AccuLevel), which uses enzyme immunochromatography to indicate visually, without any instrument, the concentrations of three major antiepileptic drugs (AEDs) in small blood samples. Drug levels (30 values for diphenylhydantoin, 41 for phenobarbital, and 40 for carbamazepine) obtained by AccuLevel were compared with those obtained with the enzyme-multiplied immunoassay technique (EMIT). Results showed an excellent correlation between EMIT and AccuLevel data for the three major AEDs. The method appears to be particularly suitable in outpatients and in case of emergency.

Anticonvulsants↗
PubMed1990

Conventional vs controlled-release carbamazepine: a multicentre, double-blind, cross-over study.

The tolerability and pharmacokinetics of a new controlled-release (CR) formulation of carbamazepine (CBZ), were assessed in a multicentre, double-blind, cross-over trial, carried out in 48 epileptic patients (21 men, 27 women; mean age 34.2 years) on conventional CBZ monotherapy, but without complete seizure control (n = 22) or with intermittent side effects (n = 4), or with both (n = 22). Eligible patients were randomized to conventional CBZ or CR CBZ, each given in sequence at individualized daily doses, subdivided into the lowest number of administrations. Each period of the cross-over consisted of a first phase of optimal dose finding (lasting up to two months) and a second one of maintenance (lasting one month) used for evaluation. At the end of each period, a 10-h plasma CBZ and CBZ-epoxide concentration profile, as well as the tolerability and the efficacy of the drugs, were evaluated. The mean CBZ daily dose increased by 16% during the administration of the CR formulation. Fluctuations of total CBZ and 10, 11-epoxide plasma level daily profiles at steady-state were significantly (p less than 0.001) lower during CR CBZ treatment, leading to a significant (p less than 0.001) decrease in intermittent side effects (6 patients on CR CBZ vs 26 on conventional CBZ). Finally, 38 patients on CR CBZ (vs 15 patients on conventional CBZ) were treated with a b.i.d. regimen.

Adolescent↗
PubMed1989

Major depression in Parkinson's disease and the mood response to intravenous methylphenidate: possible role of the "hedonic" dopamine synapse.

The euphoric response to equivalent doses of intravenous methylphenidate (MTP) was assessed in a group of 13 Parkinsonian patients affected by major depression, in a group of 11 nondepressed Parkinsonians, in a group of 14 nonparkinsonian subjects suffering from major depression, and finally in a group of 12 controls with no CNS or psychiatric disease. Subjects of all four groups were matched for age, sex and other main characteristics. Depressed and nondepressed Parkinsonians were also matched for duration and severity of illness, and for the type of antiparkinsonian treatment. The response to MTP was evaluated in the context of a double-blind, placebo-controlled study. Parkinsonian patients with major depression exhibited a significant lack of sensitivity to the euphoriant effects of MTP, in comparison with the other three groups. Euphoria produced by central stimulants has been shown to depend on the activity of a dopamine synapse in humans, which is thought to be situated at the limbic terminals of dopamine neurons located in the ventral tegmental area. Degeneration of this system may have predisposed our Parkinsonian patients to major depression.

Adult↗
PubMed1988

Analgesic action of methylphenidate on parkinsonian sensory symptoms. Mechanisms and pathophysiological implications.

Intravenous administration of methylphenidate hydrochloride, a central stimulant, was unexpectedly found to exert a potent analgesic effect on primary sensory symptoms in a group of patients with Parkinson's disease. This effect, which has now been studied in a short-term, double-blind, placebo-controlled experiment, subsequently disappeared if patients were pretreated with a beta-blocker or with a serotonin antagonist. Cerebrospinal fluid monoamine metabolites were determined in some of these patients, and the 5-hydroxyindoleacetic acid level was found to be significantly lower than in parkinsonian patients without pain and in normal volunteers. Given the mechanism of action of methylphenidate on the central nervous system, the adrenergic and serotoninergic mediation of its analgesic effect, and the demonstration of impaired central serotonin metabolism in the patient group, it is concluded that not only central dopaminergic deficiency but also altered noradrenergic and serotoninergic transmission in the spinal cord are quite likely to play a role in the pathophysiology of pain in Parkinson's disease.

Aged↗
PubMed1988

Free drug levels monitoring as a detector of false metabolic refractory epilepsy.

Unbound and total plasma levels of carbamazepine (CBZ) and phenobarbital (PB) were evaluated in a group of 12 refractory patients out of 397 subjects, with normal values of total drug concentration and unbound levels below the expected ones. We established a minimal acceptable 'subtherapeutic' free drug level, i.e. less than 9.62 micrograms/ml for PB and 1.36 micrograms/ml for CBZ. PB and CBZ dosages were increased during a 3-month period. We observed a normalization of free levels, unaccompanied by a significant decrease in seizure frequency. Free drug level monitoring may prove to be an unchallenged detector of false metabolic refractory epilepsy.

Adolescent↗
PubMed1987

Distribution of diphenylhydantoin in the brain during experimental status epilepticus of the cat.

The distribution of diphenylhydantoin (PHT) (40 mg/kg i.p.) in the brain was investigated in cats with convulsive generalized (group 1) and focal penicillin-induced status epilepticus (group 2), and in controls. A significant increase in the amount of PHT entering the brain during the convulsive status was found, with peak brain levels at 45 min (12 +/- 3.2 micrograms/g vs. 6.0 +/- 0.8 in normal cats, P less than 0.05). In the focal status brain concentrations of PHT reached levels intermediate between controls and group 1 cats. At 15 min, elevated blood levels of the drug were paralleled by increased concentrations in the brain, whereas at 30 and 45 min other factors, such as changes in cerebral blood flow, cerebral pH, vascular resistance, metabolic derangement and blood-brain barrier disruption were presumably responsible for the altered brain PHT uptake. The relevance of these data to clinical practice is discussed, in relation to the treatment of human status epilepticus and the potentially neurotoxic effects of the drug.

Animals↗
PubMed1985

Cardiac side effects of phenytoin and carbamazepine. A dose-related phenomenon?

Three patients with dystrophia myotonica and echocardiographic signs of subclinical cardiopathy had cardiac side effects during oral treatment with phenytoin sodium or carbamazepine. These side effects were dose related: ventricular tachycardia appeared at a toxic serum phenytoin level in one patient and disappeared as the concentration fell within the therapeutic range, and atrioventricular block grade 1 developed in two patients at low serum carbamazepine levels, its severity increasing with the drug level. Given the risk of dangerous side effects, cardiac status needs to be carefully assessed before administration of phenytoin or carbamazepine in the treatment of dystrophia myotonica.

Adult↗
PubMed1984

A longitudinal study of valproate free fraction in the specific age group at greatest risk for febrile convulsions (children below 3 years).

The behavior of the free fraction of valproic acid (VPA) was evaluated during long-term treatment of 24 children (9-18 months of age) with febrile convulsions. A series of relevant hematological parameters was monitored for the entire observation period (12 months). VPA plasma levels ranged from 54.3 +/- 26 to 66.6 +/- 32.8 micrograms/ml. The unbound fraction of the drug was determined in tears, which has been shown to be the best practical indicator of the free portion of an anticonvulsant drug, and ranged from 5.1 +/- 4.0 to 6.1 +/- 4.3 micrograms/ml. The tear/plasma ratio (and hence the free/total ratio) ranged from 9.3 to 9.7, in agreement with literature data. No significant variations of VPA plasma and tear levels, and therefore of the tear/plasma ratios, were ever observed. The hematological data revealed no significant alterations during the entire observation time, although some of the variables did fluctuate. Side effects were mild and temporary. The present report indicates that VPA has no particular toxic effect in young children treated for the prevention of febrile convulsions.

Female↗
PubMed1984

Fatal hyperpyrexia after withdrawal of levodopa.

We studied a patient affected with idiopathic Parkinson's disease and levodopa-induced dyskinesias. Fatal hyperpyrexia followed simultaneous levodopa withdrawal and a decrease in the dosage of diphenhydramine. The clinical features were those of the neuroleptic malignant syndrome. The rapid decrease in dopaminergic activity may have been important in causing the syndrome.

Basal Ganglia Diseases↗
PubMed1983

Brain atrophy, peripheral neuropathy and folic acid deficiency.

A woman with peripheral neuropathy and cerebral atrophy, both secondary to a selective folic acid deficiency caused by severe gastrointestinal disturbances, was given folic acid replacement therapy, which improved her clinical, blood and neurophysiological status.

Atrophy↗
PubMed1983

The quantification of myotonia. A problem in the evaluation of new antimyotonic drugs.

The evaluation of an antimyotonic drug is often difficult since the severity of myotonia is itself hard to assess. The rise in arterial potassium level produced by the infusion of increasing concentrations of potassium chloride brought about reproducible changes in the excitability level of myotonic muscles proportional to the plasma potassium concentration. The excitability changes were assessed by three methods commonly used for evaluating antimyotonic drugs. The duration of the electromyographic relaxation time after maximal voluntary effort proved to be the only test which reliably assessed the variations of muscular excitability proportional to the increased plasma potassium. By contrast, the duration of percussion- or electrically-induced myotonic after-discharges was extremely variable and independent of plasma potassium.

Electric Stimulation↗
PubMed1983

The current status of taurine in epilepsy.

The part played by taurine in epileptogenesis is still controversial. A cortical deficit of the amino acid has been confirmed only in certain types of human and animal epilepsy, and the effects of an artificial change of taurine cortical concentration are inconclusive. An increase is associated with a reduced susceptibility to epileptogenic agents but not with the prevention of epilepsy, while a decrease may precipitate seizure activity in genetically susceptible rats but does not bring about spontaneous epileptic activity in normal animals. The role of taurine in synaptic transmission is uncertain (specific inhibitory neurotransmitter, indirect modulator of membrane excitability), and its antiepileptic action, confirmed in several models of experimental epilepsy and in short-term clinical studies, does not seem to possess major clinical relevance since trials with a longer follow-up gave unsatisfactory results. Taurine's limited diffusibility across the blood-brain barrier may be the main factor restricting the antiepileptic effect of this compound.

Animals↗