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Biomedical subjects

C M Tanner

Publications and source records attributed to C M Tanner.

122 records · Page 7Linked to original sources
PubMed1982

Pharmacology of hallucinations induced by long-term drug therapy.

The authors studied 20 patients with Parkinson's disease and prominent hallucinations related to dopaminergic or anticholinergic therapy. The character of the hallucinations appeared distinct from the classic description of either acute anticholinergic or acute aminergic hallucinatory states. Manipulation of either kind of drug could precipitate or relieve hallucinations in a given patient, which suggests that the dopaminergic/cholinergic systems are reciprocally active in the pathophysiology of long-term drug-induced hallucinatory states in this population.

Antiparkinson Agents↗
PubMed1982

Pergolide mesylate and idiopathic Parkinson disease.

We studied the effects of pergolide mesylate in an open trial of 23 patients with idiopathic Parkinson disease (PD). All had suffered from loss of efficacy or dose-limiting side effects on current antiparkinsonian regimens. On pergolide therapy, improvement, which was maintained for 6 months, was noted in some parkinsonian features in all 23 patients. All patients suffering from on-off phenomenon were helped by pergolide. Significant side effects were not encountered. Pergolide is useful in the treatment of PD.

Adolescent↗
PubMed1982

Cholinergic mechanisms in Tourette syndrome.

To examine the role of the cholinergic system in Tourette syndrome, we administered intramuscular physostigmine and scopolamine hydrobromide to 10 patients, evaluating both motor tics and involuntary vocalizations. Patients showed a consistent abatement of motor tics and exacerbation of vocal tics after scopolamine injection. The scopolamine effect was reversed by physostigmine. These data suggest that the cholinergic system plays a role in the pharmacologic pathophysiology of Tourette syndrome. The pharmacology of vocal and motor tics may differ, and cholinergic manipulation may benefit some patients.

Adolescent↗
PubMed1982

Primary writing tremor: a selective action tremor.

Progressive difficulty in handwriting due to jerking movements precipitated by the act of writing beginning between the ages of 8 to 54 is reported in six patients. There was no rest tremor, but three had mild postural tremor. Specific muscle activity (especially pronation of the wrist or abduction of the fingers) elicited the tremors that persisted as long as the evocative posture or muscle activity was maintained. None had a family history of tremors, but two had a history suggestive of hypoxia at birth. Unlike benign essential tremor, the movements did not respond to propranolol HCl, but most patients were benefited both acutely and chronically by centrally active anticholinergic agents.

Adolescent↗
PubMed1982

Meige disease: acute and chronic cholinergic effects.

We studied central cholinergic systems in 13 patients with idiopathic adult-onset blepharospasm/oromandibular dystonia (Meige syndrome). Six patients studied acutely, and 12 of 13 patients studied chronically, improved after administration of centrally acting anticholinergic agents. These data suggest that Meige syndrome is pharmacologically similar to other dystonic disorders, in which central cholinergic antagonism is more consistently of benefit than manipulation of central dopaminergic systems.

Adult↗
PubMed1981

Weekly drug holiday in Parkinson disease.

Patients with Parkinson disease and drug-related side effects entered an open-trial study in which they stopped all dopaminergic medications for 2 consecutive days each week. Nine of 17 patients could tolerate the cessation of dopaminergic medication, and all of them showed improvement of side effects during the drug holiday and often throughout the week. Patients who could not tolerate withdrawal of medication were identified within 3 weeks by increased tremor or bradykinesia. This at-home drug holiday offers a potential therapy applicable to large numbers of parkinsonian outpatients who suffer progressive drug-related side effects.

Adult↗
PubMedDate not supplied

Association of coffee and caffeine intake with the risk of Parkinson disease.

CONTEXT: The projected expansion in the next several decades of the elderly population at highest risk for Parkinson disease (PD) makes identification of factors that promote or prevent the disease an important goal. OBJECTIVE: To explore the association of coffee and dietary caffeine intake with risk of PD. DESIGN, SETTING, AND PARTICIPANTS: Data were analyzed from 30 years of follow-up of 8004 Japanese-American men (aged 45-68 years) enrolled in the prospective longitudinal Honolulu Heart Program between 1965 and 1968. MAIN OUTCOME MEASURE: Incident PD, by amount of coffee intake (measured at study enrollment and 6-year follow-up) and by total dietary caffeine intake (measured at enrollment). RESULTS: During follow-up, 102 men were identified as having PD. Age-adjusted incidence of PD declined consistently with increased amounts of coffee intake, from 10.4 per 10,000 person-years in men who drank no coffee to 1.9 per 10,000 person-years in men who drank at least 28 oz/d (P<.001 for trend). Similar relationships were observed with total caffeine intake (P<.001 for trend) and caffeine from non-coffee sources (P=.03 for trend). Consumption of increasing amounts of coffee was also associated with lower risk of PD in men who were never, past, and current smokers at baseline (P=.049, P=.22, and P=.02, respectively, for trend). Other nutrients in coffee, including niacin, were unrelated to PD incidence. The relationship between caffeine and PD was unaltered by intake of milk and sugar. CONCLUSIONS: Our findings indicate that higher coffee and caffeine intake is associated with a significantly lower incidence of PD. This effect appears to be independent of smoking. The data suggest that the mechanism is related to caffeine intake and not to other nutrients contained in coffee. JAMA. 2000;283:2674-2679.

Aged↗
PubMedDate not supplied

Occupational and environmental causes of parkinsonism.

Occupational causes of parkinsonism have usually been identified by direct temporal association of an exposure with disease symptoms, although recently a latent period between exposure and disease causation is being investigated. This review presents the definition of parkinsonism as contrasted with Parkinson's disease, notes the general concepts important to the consideration of toxic effects on the central nervous system, and addresses each group of agents known to cause parkinsonism, including common sources of exposure, clinical course, and proposed mechanisms of toxicity. Agents discussed include manganese, carbon disulfide, organic solvents, carbon monoxide, and MTPT and similar agents.

Environmental Exposure↗