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Biomedical subjects

D B Calne

Publications and source records attributed to D B Calne.

At least 181 records · Page 10Linked to original sources
PubMed1986

Dementia in movement disorders.

Of all the movement disorders, Huntington's disease has been most consistently associated with dementia, while it is only over the last decade that intellectual cognitive decline have been recognized as common features of Parkinson's disease. It is now known that the pathology in these two conditions reflects differential involvement of the striatum. The Huntington lesion is primarily in the caudate, while the Parkinson lesion preferentially affects the putamen. Both conditions have more diffuse pathology, and dementia may also occur in a wide range of other extrapyramidal diseases, such as progressive supranuclear palsy, the parkinsonism-dementia complex of Guam, and certain spinocerebellar degenerations. Clinicopathological correlations will be reviewed in these disorders of primarily subcortical pathology, and comparisons will be made with Alzheimer's disease, a disorder of predominantly cortical pathology.

Alzheimer Disease↗
PubMed1986

A case-control study of twin pairs discordant for Parkinson's disease: a search for environmental risk factors.

A previous study of twins with Parkinson's disease (PD) revealed low concordance, suggesting that genetic factors play a minor role in the etiology of PD. To identify possible environmental determinants of PD while maximally controlling for hereditary factors, 31 monozygotic twin pairs discordant for PD were interviewed by telephone. Information about possible risk factors was obtained from systematic and uniform interviews with cases and controls. The only statistically significant result was less cigarette smoking by PD patients (p less than 0.05). Thirteen dizygotic discordant twin pairs were evaluated with the same techniques, but there were no statistically significant differences between affected and unaffected twins.

Female↗
PubMed1986

Early parkinsonism.

The early clinical diagnosis of parkinsonism has been reviewed, together with consideration of investigations that may be helpful in certain cases. The controversial issues of management in early Parkinson's disease have been addressed, and some newer concepts of early diagnosis and management have been discussed, deriving from the study of a population of patients exposed to MPTP.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

(+)-4-Propyl-9-hydroxynaphthoxazine (PHNO), a new dopaminomimetic, in treatment of parkinsonism.

PHNO is a naphthoxazine compound with selective D2 agonist properties and a molecular structure unrelated to the morphine and ergot derivatives that have been used to treat Parkinson's disease. A double-blind, dose-ranging study on 8 patients showed that it is effective in the treatment of parkinsonism; its duration of effect of up to 6 h could make it useful for patients who experience wearing-off reactions with levodopa.

Adult↗
PubMed1985

A pilot study on the use of botulinum toxin in spasmodic torticollis.

Dystonic torticollis has been treated with local injections of botulinum toxin in a single blind study of 12 patients. A significant decrease of abnormal movements was recorded, and pain improved. Further studies are desirable to define the optimum dosage and site for injections, and the long term effects of repeated injections.

Adult↗
PubMed1985

Dystonia and calcification of the basal ganglia.

We studied a family with dominantly inherited dystonia and intracranial calcification. Thirty-seven members were examined; 13 were affected by dystonia that was segmental in most patients, affecting especially the voice, face, neck, and limbs. Intracranial calcification involved the putamen, pallidum, cerebral white matter and cortex, and cerebellar nuclei. Several patients had both dystonia and calcification, but others had either dystonia or calcification alone.

Adult↗
PubMed1985

Motor function in the normal aging population: treatment with levodopa.

In normal elderly humans there is progressive motor dysfunction and loss of nigrostriatal neurons and brain dopamine similar to, although of a milder degree than, that seen in Parkinson's disease. Ten healthy elderly volunteers were given carbidopa/levodopa or placebo in a double-blind crossover study. We measured movement velocity, reaction time, tremor, visual evoked response (VER), and electroretinography (ERG). Significant changes were seen only in ERG. Motor functions and VER were unchanged. Although there appeared to be pharmacologic activity (ie, changes in ERG), levodopa, in adequate antiparkinson dosage, had no impact on the mild extrapyramidal impairment of normal elderly subjects.

Aged↗
PubMed1985

Parkinson's disease: a comparison of mesulergine and bromocriptine.

Previous studies with mesulergine (CU 32-085) demonstrated safety and efficacy in short-term observations of patients with Parkinson's disease. We compared mesulergine with bromocriptine in 20 patients with Parkinson's disease. Eighteen patients completed the randomized, double-blind, crossover study. Clinical assessments employed the UBC scale and "Mini-Mental State" examination; neurophysiologic measurements were undertaken on wrist rigidity and speed and accuracy of hand movement, and toxicity screening tests were compared. There were no significant differences between the effects of mesulergine (mean dosage, 27.4 mg/d) and bromocriptine (mean dosage, 40.8 mg/d).

Adult↗
PubMed1985

Dystonia: treatment with bromocriptine.

As with parkinsonism, certain dystonias may involve disturbances in dopaminergic neurotransmission. The effects of bromocriptine, 18-150 mg/day (mean, 72.5), were studied in 15 patients with a variety of dystonic disorders, using a double-blind, crossover format. Of the 13 patients completing several weeks of medication, seven improved more than 10% and two worsened, on clinical ratings, while five recognized improvement in disability. Dopaminomimetic agents such as bromocriptine, used in the dose range effective for treating parkinsonism, may yield symptomatic improvement with several patterns of dystonia.

Adult↗
PubMed1984

Dopamine agonists and Parkinson's disease.

The therapeutic use of dopamine agonists for Parkinson's disease, clinical guidelines for their introduction into antiparkinson regimens, and their range of adverse effects are reviewed. The role played by the dopaminomimetic ergots in elucidating dopamine receptor function, and laboratory methods that identify dopamine agonists, are also examined.

Antiparkinson Agents↗
PubMed1984

Cerebral glucose metabolism in Parkinson's disease.

Local cerebral glucose utilization was measured in patients with predominantly unilateral Parkinson's disease using 18F-2-fluoro-deoxyglucose and positron emission tomography. Preliminary results indicate the presence of asymmetric metabolic rates in the inferior basal ganglia. The structure comprising the largest portion of basal ganglia at this level is globus pallidus. These findings are consistent with metabolic studies on animals with unilateral nigrostriatal lesions in which pallidal hypermetabolism on the lesioned side has been demonstrated. Increased pallidal activity is likely secondary to a loss of inhibitory dopaminergic input to the striatum from substantia nigra.

Aged↗
PubMed1984

Dopamine agonists in Parkinson's disease.

Dopamine agonists have yielded two important advances to our understanding of the basal ganglia--they have facilitated the subdivision of different classes of dopamine receptors, and they have established the fact that important dopaminergic effects can be achieved by activation of dopamine receptors in a manner that is unrelated to anoxal impulse traffic in dopaminergic neurons--a phenomenon similar in its diffuse, slow, characteristics to an endocrine effect. The tangible clinical benefit of dopamine agonists has been evident in patients with prominent dyskinesia or wearing off reactions. It is possible that earlier use of agonists, in low doses combined with similarly low doses of levodopa, may improve the long term treatment of Parkinson's disease, but as yet there is no firm evidence. In the future, we can expect to see agonists with more prolonged effects, deriving from the formation of active metabolites. We can also hope to gain further insight into the correlations between the various animal models of dopaminomimetic activity, and specific aspects of drug efficacy and toxicity in parkinsonian patients. Such information should allow the design of improved pharmacotherapy.

Bromocriptine↗
PubMed1984

Disposition of oral lisuride in Parkinson's disease.

The single and multiple oral dose plasma kinetics of lisuride were followed by a recently developed radioimmunoassay method in 11 patients with Parkinson's disease. A very wide range of plasma drug concentrations resulted from a single dose of 300 micrograms, as reflected in large interindividual differences in peak concentration (0.27 to 3.30 ng/ml) and AUC after the initial dose (43.1 to 617 ng X min/ml). Absorption was rapid, with a mean time to peak of 39 min. Only 0.05% of the dose was excreted unchanged in urine in 24 hr. There was a 110% increase in apparent oral clearance after 2 to 4 wk of treatment.

Administration, Oral↗
PubMed1984

Assessment of Parkinson's disease.

The quantitative assessment of clinical deficits in Parkinson's disease has become more difficult due to such factors as the introduction of therapy that induces involuntary movements, the recognition of marked fluctuations in response to treatment, and an increasing of memory disturbance in patients. An attempt to take these problems into account using a brief and simple scale of evaluation is presented.

Activities of Daily Living↗
PubMed1984

L-dopa decarboxylation in chronically treated patients.

We measured decarboxylation of oral L-dopa in patients chronically treated with L-dopa, and in untreated controls. Chronic L-dopa and carbidopa administration did not affect the extent of whole-body decarboxylation, and it is therefore unlikely that on-off fluctuations are related to chronic changes in the activity of L-aromatic amino acid decarboxylase. The observed duration of action and dose-response properties of carbidopa suggested that current empirically based dose schedules are optimal and supported the concept that decarboxylase inhibitors enhance the clinical effect of L-dopa largely by reducing the extent of first-pass metabolism rather than through an action on the decarboxylase enzyme in cerebral capillaries.

Adult↗