Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study of endocrinologic changes in Parkinson's disease, Huntington's disease, and tardive dyskinesia may elucidate the pathophysiology of these disorders, especially the presence of hypothalamic lesions. There is probably a decrease in PRL concentrations in Parkinson's disease, and there may be an increase in TSH response to TRH stimulation. It is not clear if there is any change in GH concentrations in Parkinson's disease. There appears to be a robust increase in GH concentrations in Huntington's disease, and there may be a small increase in PRL as well. At present no endocrinologic abnormality has been well documented in tardive dyskinesia.
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PMID:The endocrinology of extrapyramidal system disorders. 296 53

The study of endocrinologic changes in Parkinson's disease, Huntington's disease, and tardive dyskinesia may elucidate the pathophysiology of these disorders, especially the presence of hypothalamic lesions. There is probably a decrease in PRL concentrations in Parkinson's disease, and there may be an increase in TSH response to TRH stimulation. It is not clear if there is any change in GH concentrations in Parkinson's disease. There appears to be a robust increase in GH concentrations in Huntington's disease, and there may be a small increase in PRL as well. At present no endocrinologic abnormality has been well documented in tardive dyskinesia.
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PMID:The endocrinology of extrapyramidal system disorders. 296 9

1. Nicotine, an important pharmacological component of cigarette smoke, is known to have significant effects on central nervous system (CNS) dopaminergic function. Although acute doses of nicotine have been shown to facilitate dopamine release, recent data indicate that chronic nicotine treatment may actually decrease CNS dopamine turnover in the striatum. 2. A number of epidemiological investigations have demonstrated that individuals who are or who have been smokers are less likely to develop idiopathic Parkinson's disease (a disorder involving a deficit in nigrostriatal dopaminergic neurotransmission). In addition, there is preliminary evidence that individuals with tardive dyskinesia (a hyperkinetic movement disorder observed in some cases of chronic neuroleptic treatment and thought by some to be associated with striatal dopamine receptor supersensitivity) are more likely to be smokers. 3. A unitary hypothesis is presented, proposing that smoking in early adult life may decrease CNS catecholamine turnover, thereby protecting against free radical formation from catecholamine oxidation that in turn damages striatal neurons. These individuals are thereby "protected" from the later development of Parkinson's disease. In this hypothetical scheme, individuals who are given neuroleptics and who also are smokers may develop a greater degree of dopamine receptor supersensitivity due to combined receptor blockade by neuroleptics and a decrease in CNS dopamine turnover caused by nicotine, resulting in an increased prevalence of tardive dyskinesia in this group.
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PMID:Hypothesis: a nicotine-dopamine interaction linking smoking with Parkinson's disease and tardive dyskinesia. 306 87

Tardive dyskinesia (TD) occurs in approximately 20% of patients treated chronically with antipsychotic drugs and constitutes a major public health problem. The cause of this disorder remains unknown, and no effective treatment has yet been found. The major etiologic theory (dopamine [DA] supersensitivity hypothesis) suggests that TD is the pharmacologic opposite of Parkinson's disease and implies that all patients with TD should respond uniformly to specific pharmacologic agents. Clinical research, however, has not borne this out. To evaluate pharmacologic response in TD syndromes, 15 patients underwent single dose acute administration of four different drugs: a DA agonist (bromocriptine 5 mg orally), a DA antagonist (haloperidol 5 mg intravenously), a cholinergic agonist (physostigmine 2 mg intravenously) and a cholinergic antagonist (benztropine 4 mg intravenously), individually in separate procedures at weekly intervals for four consecutive weeks in randomized order and under controlled double-blind conditions. Patients were evaluated for their clinical and endocrine responses. Pre- and post-drug administration TD exams were blindly rated. Results were not consistent with the DA supersensitivity theory; instead they demonstrated marked inter- and intrasubject variability in pharmacologic responses. Greatest uniformity in response was found among the tardive dystonic subjects, although this also was not consistent with a DA supersensitivity hypothesis. TD appears to be a pharmacologically heterogeneous condition, which may reflect the neurochemical complexity of the basal ganglia.
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PMID:Pharmacologic characterization of tardive dyskinesia. 320 17

We report two patients with dyskinesia responding to antidepressants. The first is a 70-year-old man with depression, Parkinsonism and neuroleptic-induced tardive dyskinesia who presented with hysterical mutism. After recovery from the mutism, he was started on desipramine for depression. One week later the dyskinesia improved markedly. The second patient is a 61-year-old man with Parkinson's disease, dementia, depression and L-dopa-induced oro-lingual-facial dyskinesias. He was taking levodopa, trihexyphenydil and bromocriptine. The depression was treated first with desipramine and later with trazodone. The dyskinesia improved significantly on both drugs. The response of the dyskinesias to antidepressant medication may be due to the fact that antidepressants decrease beta-adrenoreceptor sensitivity and density which in turn may result in a diminished release of dopamine since beta-adrenoceptors mediate the noradrenaline-stimulated release of dopamine.
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PMID:Response of tardive and L-dopa-induced dyskinesias to antidepressants. 369 Apr 36

Metoclopramide, a dopamine antagonist, is approved in the U.S. for the treatment of various gastrointestinal disorders. Its use has been investigated in a wide variety of diseases, including those not involving the intestinal tract. Although more study is required before routine clinical use of metoclopramide can be advocated, it may be effective in the treatment of tardive dyskinesia, in decreasing the risk factors associated with anesthetic-related aspiration, and as an adjunct in the treatment of gastric bezoars. It also may be used safely in patients with Parkinson's disease. The use of metoclopramide in the treatment of neurogenic bladder, orthostatic hypotension, tumor-associated gastroparesis, nonprolactinemic amenorrhea, failure to thrive, Tourette's syndrome, anorexia nervosa, and hiccups, as well as an adjunct to migraine therapy, has been investigated, but sufficient evidence has not been accumulated to advocate the use of metoclopramide in these disorders.
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PMID:Potential uses for metoclopramide. 390 32

Electrophysiological and pharmacological analysis of L-Dopa-induced dyskinesia and tardive dyskinesia (L.DD) due to neuroleptics was performed on 12 patients with Parkinson's disease and on 12 others with psychotic diseases. This analysis included the examination of spinal reflexes, monosynaptic H reflex, polysynaptic cutaneous reflex of the lower limb, muscular responses to passive movement [stretch reflex and shortening reaction (SR)] and the study of the motor response to a dopaminergic stimulus (I.V. injection of Piribedil (PBD), a dopamine agonist). There was no difference in EMG activity between L.DD and TD. Three EMG patterns can be distinguished: anarchic discharge pattern (ADA), tonic grouping discharge pattern (AST) and rhythmic burst pattern (ABR). PBD effects indicate a possible relationship between the EMG patterns and the sensitivity level of the motor dopamine receptors. During L-Dopa dyskinesia and tardive dyskinesia, the same changes in spinal reflexes were observed. Muscle tone tested by muscular responses to passive movement (shortening and myotatic reaction) was normal. Monosynaptic excitability explored by H/M ratio was within the normal range. In contrast, the polysynaptic nociceptive reflex was increased in every case. In Parkinsonian patients with L-Dopa dyskinesia, this pattern of the spinal reflexes was significantly different in comparison to the rigid phase. Intravenous infusion of PBD suppressed tremor and provoked the occurrence of dyskinetic activity in Parkinsonian patients with L-Dopa dyskinesia during the rigid phase. During the dyskinetic phase, as in tardive dyskinesia, PBD increases these phenomena and changes EMG activity in rhythmic pattern. It is suggested that L-Dopa dyskinesia and tardive dyskinesia can be determined by testing EMG activity, spinal reflexes and dopaminergic reactivity. There is evidence to suggest that the various types of involuntary abnormal movement represent a single entity, and that dopamine receptor supersensitivity may be involved.
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PMID:[Electrophysiological and pharmacological analysis of L-dopa-induced dyskinesia and tardive dyskinesia (author's transl)]. 611 68

Brain function can be affected by the availability of dietary precursors of neurotransmitters. This occurs because the rate-limiting synthetic enzymes are not "saturated" with substrate under normal circumstances. Tyrosine affects catecholaminergic neurons that fire rapidly, whether in the brain stem to decrease blood pressure in hypertension or in the adrenal gland to increase blood pressure in hypotension, and has been used in the treatment of Parkinson's disease and depression. Choline forms acetylcholine and has been used successfully in the treatment of tardive dyskinesia and memory disorders. Tryptophan, which forms serotonin, has been used for chronic pain therapy, sleep disorders, depression, and appetite control. Although these substances may lack the potency of traditionally used agonists, they offer an increase in specificity because the enzymes necessary to convert them to neurotransmitters are found only in neurons. Precursors are also "physiological"; they are consumed as foods and, therefore, should be relatively safe therapeutic agents.
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PMID:Neurotransmitter precursors and brain function. 612 95

Most classifications of movement disorders emphasize their differential diagnosis and epidemiology according to clinical history and neurological examination. This review of movement disorders is organized according to the hypothesis of basal ganglia neurotransmitter imbalance in order to emphasize current research based on the pharmacology of these disorders. Specifically, dopamine (DA) excess and acetylcholine (ACh) deficiency may characterize part of the pathology of several hyperkinetic movement disorders including tardive dyskinesia, Huntington disease, Gilles de la Tourette syndrome, l-dopa dyskinesias, tardive Tourette syndrome, and toxic Tourette syndrome. The mirror image of this paradigm, namely DA deficiency and ACh excess, may characterize several rigid-dystonic movement disorders including Parkinson disease, drug-induced dystonias, and dystonia musculorum deformans. Finally, the unique combination of DA excess with ACh excess may characterize idiopathic orofacial dyskinesia (also known as Meige dystonia, Brueghel syndrome, and blepharospasm-oromandibular dystonia). Evidence supporting this formulation of movement disorders is reviewed, the limitations of this hypothesis are discussed, and new data from our own studies are presented.
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PMID:The neuropharmacology of tardive dyskinesia, spontaneous dyskinesia, and other dystonias. 612 51

The authors compared the regions of motor involvement in levodopa-induced dyskinesia and neuroleptic-induced tardive dyskinesia. Significantly more patients with tardive dyskinesia than parkinsonian patients with levodopa-induced dyskinesia had lip and tongue movements. Patients with tardive dyskinesia had significantly higher mean AIMS scores in the orofacial region than parkinsonian patients with levodopa-induced dyskinesia. More patients with levodopa-induced dyskinesia than those with tardive dyskinesia demonstrated hyperkinesia in the lower extremities. Limb and truncal movements in levodopa-induced dyskinesia were worse in patients with more severe parkinsonism and correlated positively with the length of Parkinson's disease. These findings suggest that these dyskinesias may involve different pathophysiological mechanisms.
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PMID:A comparison of two iatrogenic dyskinesias. 613 63


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