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Biomedical subjects

J Vaamonde

Publications and source records attributed to J Vaamonde.

At least 37 records · Page 2Linked to original sources
PubMed1992

Acetazolamide improves action myoclonus in Ramsay Hunt syndrome.

The myoclonus of two patients with Ramsay Hunt syndrome was only partially controlled under treatment with clonazepam, sodium valproate, primidone, and piracetam. Acetazolamide (200 mg daily) was added to these drugs, resulting in a dramatic improvement. Placebo substitution (one patient) and withdrawal of acetazolamide in the other patient resulted in marked aggravation of the myoclonus. The mechanism of action of acetazolamide in myoclonus is unknown. Acetazolamide may be an additional therapeutic possibility for patients with severe action myoclonus.

Acetazolamide↗
PubMed1992

Abnormal muscle and skin mitochondria in family with myoclonus, ataxia, and deafness (May and White syndrome).

A mother and two of her daughters had deafness and cortical reflex myoclonus; the mother also had mild truncal ataxia. Muscle and skin biopsy specimens revealed abundant ragged-red fibres and abnormal mitochondria. The son of one of the daughters had sensorineural deafness. Three other grandchildren were asymptomatic. The two daughters also had diabetes mellitus, hypertension and cardiomyopathy. Another daughter died of renal failure. The mother lost her hearing in her 70s, one daughter in her 30s, and the other daughter and the grandson in their 20s. The mother has had transient episodes (24-48 hours) of temporal disorientation, severe action myoclonus, and ataxia for about eight years. This is the first reported family with inherited deafness, myoclonus, and ataxia with mitochondrial pathology.

Adolescent↗
PubMed1992

[Motor fluctuations in Parkinson disease: risk factors].

We studied the histories of 173 patients with Parkinson's disease (1985-1987) chronically treated with levodopa + dopa decarboxylase inhibitor. Ninety four patients had daily motor fluctuations and 79 showed stable motor response. The most significant differences between fluctuating and stable patients were given by age at disease onset and duration of levodopa therapy. Patient with disease onset before 60 had a greater risk (p less than 0.001) of developing fluctuations. Delaying the initiation of levodopa treatment was not associated with a smaller incidence of fluctuations.

Adult↗
PubMed1991

Hereditary paroxysmal ataxia with neuromyotonia.

The clinical manifestations of a patient with hereditary paroxysmal ataxia and neuromyotonia are described. Generalized tremor, triggered by sudden movements, and spasms of hand and foot muscles were the main clinical findings. Electromyogram (EMG) and nerve blocking studies led to the diagnosis of neuromyotonia. Treatment with acetozolamide was of no therapeutic value, confirming previous observations about the difference in response of paroxysmal ataxia with and without neuromyotonia.

Adult↗
PubMed1991

Subcutaneous lisuride infusion in Parkinson's disease. Response to chronic administration in 34 patients.

Thirty-eight parkinsonian patients with motor fluctuations and dyskinesias on chronic levodopa therapy were treated with subcutaneous lisuride infusion (SLI). Thirty-six were discharged from hospital on combined treatment with 24 h lisuride infusion (111.3 +/- 29.5 micrograms/h) and oral levodopa plus a decarboxylase inhibitor (729.6 +/- 452 mg/day); all obtained a marked initial improvement in mobility (mean reduction 'off' hours 87.5%); 34 were followed for a mean of 20.85 (range 6-45) months. Most patients continued to show improvement with respect to baseline assessment during chronic treatment but 23 developed dyskinesias, 'off' periods or both, which were difficult to control by changing the levodopa schedule, lisuride dose or both. In only 5 patients was lisuride treatment stopped because of inefficacy. The high incidence of psychiatric side-effects (18/38) was the major limiting factor for continuing lisuride infusion in this population of severe parkinsonian patients. Many complained about the inconvenience of the pump's technical requirements for long-term utilization, but only 4 patients abandoned SLI for this reason. These results indicate that motor function may be substantially improved in severe parkinsonian patients treated with SLI but increased dyskinesia or psychiatric adverse effects limited the long-term usefulness of this approach. It is suggested that continuous dopaminergic stimulation may be a particularly useful therapeutic strategy when applied in earlier stages of the disease.

Adult↗
PubMed1990

Generalized reflex myoclonus in a patient with alcohol-sensitive spontaneous myoclonus and an abnormal gait.

A patient with alcohol-sensitive spontaneous, action- and stimulus-sensitive generalized reflex myoclonus is reported. Gait was abnormal but could not be clearly classified as dystonic. No other neurological abnormality was present. The possible relationship between alcohol-sensitive myoclonic dystonia and this case is discussed. Reflex myoclonus may serve as an additional clinical marker in the study of families with alcohol-sensitive myoclonus, dystonia, or both.

Adult↗
PubMed1990

Dopaminergic responsiveness to apomorphine after chronic treatment with subcutaneous lisuride infusion in Parkinson's disease.

The aim of this study was to assess whether or not continuous infusion of lisuride in combination with intermittent levodopa-carbidopa administration was associated with tolerance. Intravenous apomorphine was given to four patients before initiation of chronic treatment with subcutaneous lisuride infusion and oral levodopa. The study was repeated under identical conditions after a mean of 18 months of treatment. In no case was the motor response induced by apomorphine infusion reduced as compared to baseline assessment. Choreic dyskinesias accompanying the "on" state were enhanced in all patients. These findings suggest that chronic continuous infusion of a dopamine agonist like lisuride, associated with oral levodopa, is not accompanied by tolerance or down-regulation of striatal dopaminergic receptors.

Administration, Oral↗
PubMed1989

Levodopa and 3-O-methyldopa plasma levels in parkinsonian patients with stable and fluctuating motor response.

Many parkinsonian patients with motor fluctuations in response to levodopa show a good response to initial morning doses but fail to respond in the afternoon and evening. We have studied levodopa and 3-O-methyldopa (3-OM-dopa) plasma profiles in 21 patients with fluctuations and eight patients with stable motor function throughout the day. Levodopa plasma peaks and valleys were similar for both group of patients. No significant difference for levodopa absorption index [defined as levodopa plasma levels after each dose divided by the quantity (mg) of ingested levodopa] was found between the first and the second levodopa-carbidopa dose in either group of patients. Even in patients who failed to improve after the second levodopa-carbidopa tablet (p.o.) on the day of the study, no significant variation in levodopa absorption index was observed. 3-OM-dopa values depended mainly upon levodopa consumption and were not different for patients with fluctuating or stable motor response. These findings provide further evidence of the prime role of central pharmacokinetic and pharmacodynamic factors in the pathogenesis of motor fluctuations in Parkinson's disease.

Aged↗
PubMed1989

Levodopa consumption reduces dopaminergic receptor responsiveness in Parkinson's disease.

In seven patients with Parkinson's disease with daily motor fluctuations, we found that the same subcutaneous apomorphine dose that improved motor function when given in the morning after a normal night without taking levodopa failed to turn patients "on" during afternoon and evening "off" periods, and on a different morning after receiving levodopa during the night. No significant changes in levodopa or 3-O-methyldopa plasma levels that could explain these variations were detected. These findings suggest that increased daily levodopa consumption may reduce striatal responsiveness to dopaminergic stimulation.

Aged↗
PubMed1989

[Orally administered lisuride in the treatment of complex fluctuations of motion in Parkinson disease].

Oral lisuride associated with the previous therapy (levodopa plus inhibitor) was given to 15 patients with complex fluctuations of mobility that were not controlled with usual therapy. In contrast with previous studies using this drug, in the present trial several lisuride doses (5-10 administrations) were distributed throughout the day. This therapeutic strategy permitted a greater control of the fluctuations, a significant reduction of the block hours and the disappearance or attenuation of biphasic dyskinesia and off dystonia. It is considered that the use of multiple doses of lisuride permits better therapeutic results than its usual administration schedule (3-4 times a day). Oral lisuride associated with levodopa may provide a definite improvement in motor function in patients with significant functional impairment. The general tolerance was very good using concomitant domperidone therapy.

Administration, Oral↗
PubMed1989

Motor complications associated with chronic levodopa therapy in Parkinson's disease.

Fluctuations and dyskinesias are the 2 main motor complications associated with chronic levodopa therapy. Striatal denervation following degeneration of the substantia nigra dopaminergic projections is probably the major pathophysiologic mechanism underlying motor fluctuations. In addition, pathologic modification of striatal receptors, partially related to the nonphysiologic delivery of levodopa in a discontinuous pulsatile mode, may be responsible for the various types of dyskinesias and sudden "off" episodes. Drugs capable of providing a stable dopaminergic stimulation should be particularly useful for preventing the development of motor complications in patients not yet treated. At the other end of the clinical spectrum, patients with complex fluctuations are the least likely to improve with slow-release levodopa preparations.

Dementia↗
PubMed1988

Subcutaneous administration of lisuride in the treatment of complex motor fluctuations in Parkinson's disease.

28 patients with Parkinson's disease showing complex "on-off" fluctuations in response to chronic levodopa plus dopa decarboxylase inhibitor (po) were treated with subcutaneous lisuride using a portable infusion pump. All patients improved initially during the first weeks of treatment. Four patients abandoned the trial within the first few weeks as a consequence of psychiatric complications (2 cases), inability to understand how to use the pump (one case) and subcutaneous nodule formation plus psychological rejections to wearing a pump (one case). All other 24 patients were treated for a minimum periods of 3 months (mean 9.6 months, maximum 24 months). The average daily dose of lisuride was 2.80 mg. The levodopa dose was reduced by 37%, but total withdrawal was not possible in any patient. Among the 18 patients who continued treatment at present, about 50% are independent and capable of undertaking most daily life activities. Psychiatric side-effects were present in 9 patients leading to permanent withdrawal in five. Subcutaneous lisuride infusions added to oral levodopa are clearly effective in patients with severe motor fluctuations. Careful selection of suitable patients and close monitoring is mandatory in order to obtain the best therapeutic results while reducing the risk of psychiatric adverse effects.

Drug Eruptions↗
PubMed1988

Piracetam in the treatment of different types of myoclonus.

Forty patients with different clinical and electrophysiological types of myoclonus were treated with piracetam (18-24 g per day, p.o.) alone, or with other drugs (clonazepam, sodium valproate, and primidone) in different combinations. Piracetam in monotherapy improved the electrophysiological abnormalities in patients with cortical reflex myoclonus, but had no useful clinical effect. Sixteen patients obtained benefit from piracetam when given in combination with other antimyoclonic drugs; improvement was dramatic in two patients, moderate in seven and mild in seven. All patients showing some response to piracetam had myoclonus of cortical origin; however, five other patients with similar cortical myoclonus failed to improve when piracetam was added. Tolerance was excellent and side effects were minimal and transient. It is concluded that piracetam probably has an antimyoclonic action, but its potential value as a therapeutic tool for disabling myoclonus requires further study.

Adolescent↗