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Biomedical subjects

J D Parkes

Publications and source records attributed to J D Parkes.

At least 19 recordsLinked to original sources
PubMed1992

The delayed sleep phase syndrome: clinical and investigative findings in 14 subjects.

Fourteen subjects are described in whom a clinical diagnosis of the delayed sleep phase syndrome was made. The condition is multi-factorial, dependent on lifestyle, mood and personality, as well as on familial factors but no single factor in isolation is sufficient to explain the delay in sleep timing. Refusal to attend school may be important in some instances but will not explain cases with delayed age of onset. In half the subjects the delay in sleep phase started in childhood or adolescence. The syndrome causes severe disruption to education, work and family life. Polysomnography, motor activity monitoring of rest-activity cycles, plasma melatonin profiles and urinary melatonin metabolite excretion are normal. Different patterns of sleep phase delay seen in the syndrome include stable, progressive, irregular and non-24 hour sleep-wake cycles. These patterns may result from different social and other Zeitgebers ("time-markers", for example sunrise, sunset) in the normal environment. Treatment by forced sleep-wake phase advance or with melatonin resulted in a partial sleep-phase advance but this was not maintained on stopping treatment.

Adolescent↗
PubMed1991

Delayed sleep phase syndrome response to melatonin.

The actions of melatonin on the sleep-wake cycle were investigated by means of a randomised, double-blind, placebo-controlled trial in 8 subjects with a delayed sleep phase syndrome attending a sleep disorders clinic. In randomised order the subjects received placebo or melatonin 5 mg daily for 4 weeks with a 1 week washout period between the treatments. Drug or placebo was given at 2200 h, 5 h before the mean time of sleep onset determined by pretrial sleep logs. In all 8 subjects sleep onset time (mean advance 82 [range 19-124] min; p less than 0.01) and wake time (117 [10-187] min; p less than 0.01) were significantly earlier during melatonin treatment than during placebo. Mean total sleep time was slightly less on melatonin (8 h 12 min) than on placebo (8 h 46 min). Alertness acrophase calculated from the subjects' ratings of alertness made every 2 h while awake was unaltered. Melatonin may act as a phase-setter for sleep-wake cycles in subjects with a delayed sleep phase syndrome.

Administration, Oral↗
PubMed1979

Mazindol in the treatment of narcolepsy.

Thirty-four subjects with the narcoleptic syndrome were treated with mazindol 3--8 mg daily for 1 year. Treatment cuased a sustained improvement in narcolepsy, but had no effect on cataplexy or sleep paralysis. The response to mazindol was excellent in six subjects, good in 14, moderate in 12 and poor in two. No cardiovascular effects, haematological toxicity, tolerance or dependence occurred. Mazindol 6 mg had the same effect on narcolepsy as d-amphetamine 50 mg, but caused less side effects.

Adolescent↗
PubMed1979

Bromocriptine in the treatment of parkinsonism.

Bromocriptine alters the motor behaviour of animals and improves the motor defect of parkinsonism. Changes in movement are accompanied by biochemical changes in the central nervous system, consistent with the idea that bromocriptine has a dopamine agonist action in the basal ganglia and also in the mesolimbic system and hypothalamus. The overall anti-parkinsonian effect of bromocriptine is similar to that of l-dopa alone or with benserazide (a decarboxylase inhibitor) when optimum doses are used, although individual patients may respond better to 1 drug than to the other.

Apomorphine↗
PubMed1978

Effect of new dopamine-blocking agent (oxiperomide) on drug-induced dyskinesias in Parkinson's disease and spontaneous dyskinesias.

Oxiperomide, a new dopamine-receptor antagonist, was found to decrease dyskinesias in patients with Parkinson's disease receiving levodopa or other dopamine agonists without necessarily increasing Parkinsonian symptoms. Oxiperomide also decreased spontaneous dyskinesias in those with tics and chorea and to a less extent in those with torsion dystonia, without necessarily causing Parkinsonism. These results provide evidence that more than one population of dopamine receptors exist in the extra pyramidal system, and encourage the search for selective dopamine antagonists.

Aged↗
PubMed1978

Plasma bromocriptine levels, clinical and growth hormone responses in Parkinsonism.

1. Plasma bromocriptine levels following separate oral doses of bromocriptine 12.5, 25, 50 and 100 mg have been determined in ten subjects with parkinsonism. 2. There was considerable variation between peak plasma bromocriptine levels in individual subjects after similar doses of bromocriptine. Peak levels occurred 30--210 min after dosage (mean 102 min). Peak clinical response, peak rise in plasma growth hormone level and fall in blood pressure followed shortly after peak bromocriptine levels occurred. 3. The shape of the plasma-time curve for bromocriptine was similar with all dosages. 4. There was no significant relationship between peak plasma bromocriptine levels, peak clinical response, peak increase in growth hormone and peak fall in blood pressure. However, the degree of improvement in the signs of parkinsonism was related to plasma bromocriptine levels was achieved. 5. Metoclopramide 60 mg pretreatment had no consistent effect upon plasma bromocriptine levels, the clinical or hormonal response.

Aged↗
PubMed1978

Genetic study of narcoleptic syndrome.

In this family study of the narcoleptic syndrome, 52% of the probands had an affected first degree relative, 41.9% of the sibs of those probands with an affected parent were similarly affected, 33.3% of the parents of 2 affected sibs and 41.2% of the children (after a correction for age) had narcolepsy, cataplexy, or both.

Age Factors↗
PubMed1978

Sodium valproate in the treatment of levodopa-induced dyskinesia.

The effect of sodium valproate 1200 mg daily on the disability of Parkinsonism and on levodopa-induced dyskinesia was assessed in a double-blind crossover trial with matched placebo in 12 patients with Parkinson's disease. No objective change in the severity of Parkinsonism or dyskinesias was noted. However, six out of nine patients who completed the trial noted a slight to moderate improvement in their dyskinesias with no change in their Parkinsonism. Excess salivation improved in four subjects on sodium valproate.

Clinical Trials as Topic↗
PubMed1977

Success and problems of long-term levodopa therapy in Parkinson's disease.

The patient with Parkinson' disease on chronic levodopa therapy, like the diabetic on insulin, is dependent on the drug. Like the diabetic, the patients with Parkinson's disease may run into problems during long-term treatment. Two have emerged as frequent and serious, an insidious and progressive loss of benefit and the appearance of progessively more severe fluctuations in disability. It is concluded that progression of the underlying pathology of the disease is probably responsible. Discovery of the exact causes for loss of benefit may provide a rational basis for new therapy.

Brain↗