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 present study analyses the relation of both the diminished cardiovascular reflexes and the diminished plasma noradrenaline (NA) response to standing to the severity of the autonomic nervous system (ANS) dysfunction in patients with Parkinson's disease (PD). 47 patients with PD were investigated. A clear correlation was established between the duration and the severity of PD (by the Webster rating scale) and the degree of autonomic dysfunction (ANS disability scale). Similarly, a significant negative correlation was found between the diminished cardiovascular reflexes and the clinical severity of the ANS disturbance. Furthermore, a slight correlation was shown between the clinical severity of ANS dysfunction and plasma NA concentrations in response to a standing-up stimulus.
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PMID:Correlation of the severity of autonomic dysfunction to cardiovascular reflexes and to plasma noradrenaline levels in Parkinson's disease. 359 58

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

Responses of serum noradrenaline (NA) levels to standing up were determined in patients with Parkinson's disease (PD) examining 15 patients and 13 healthy subjects of similar age in order to obtain information about autonomic failure in PD. Mild symptoms of autonomic dysfunction were found in all the patients. The mean (+/- SD) increment of serum NA levels as a response to standing up of patients was 0.11 +/- 0.29 nmol/l and that of the controls 1.09 +/- 1.15, the percentage rises being 5.4 +/- 12.1 and 38.2 +/- 35.0, respectively. These results indicate that serum NA responses to standing up in patients with PD are significantly diminished describing a sympathetic nervous system deficit in PD.
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PMID:Serum noradrenaline response to standing up in patients with Parkinson's disease. 378 Jul 79

In order to study the role of the neurotransmitter noradrenaline (NA) and its main brain metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) in autonomic failure in Parkinson's disease (PD), an analysis of the relation of cerebrospinal fluid (CSF) NA and MHPG levels and a rating of autonomic nervous system (ANS) impairment was carried out. The mean baseline NA level in CSF of PD patients was 220.0 +/- 110.0 pg/ml, and the mean baseline MHPG level 9.9 +/- 3.9 ng/ml. These levels did not differ from those of age-matched controls. Within the group of patients with PD neither the duration of the disease nor its medication influenced the results. No correlation could be found in patients with PD between the CSF NA levels and the severity of autonomic failure, but a clear correlation was found between the CSF MHPG concentrations and the severity of autonomic failure.
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PMID:Correlation of autonomic dysfunction to CSF concentrations of noradrenaline and 3-methoxy-4-hydroxyphenylglycol in Parkinson's disease. 381 83

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces a profound parkinsonian state when systemically administered in monkeys and man. Previous studies have shown MPTP to be toxic to only the dopamine (DA) cells in the substantia nigra pars compacta and not to other catecholamine (CA)-containing cells. The data presented here suggest that MPTP also has a specific neurotoxic effect on the DA-containing cells of the ventral tegmental area and the noradrenaline-containing cells of the locus coeruleus in macaque monkeys with a moderate-to-severe parkinsonian syndrome. The results suggest that MPTP-induced parkinsonism in the monkey more closely replicates the neurochemical changes seen in idiopathic Parkinson's disease than previously thought.
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PMID:Sites of the neurotoxic action of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the macaque monkey include the ventral tegmental area and the locus coeruleus. 387 82

The concentrations of 5-hydroxytryptamine (5HT), noradrenaline, and dopamine were estimated post mortem in brain stem, hypothalamus, and caudate nucleus in 33 patients who had been treated with isocarboxazid, clorgyline, or tranylcypromine and 11 controls. Similar and highly significant increases in 5HT and noradrenaline concentration occurred with all three drugs. The distribution was unimodal, but about a quarter of the patients showed only a small increase in brain amines. Tranylcypromine seemed to have a significantly greater effect on dopamine in caudate nucleus and hypothalamus compared with isocarboxazid and clorgyline. In the doses used chlorpromazine did not reduce the amine concentrations. Four patients with Parkinson's syndrome had low concentrations of dopamine in caudate nucleus in spite of monoamine oxidase inhibitor administration.
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PMID:Brain amine concentrations after monoamine oxidase inhibitor administration. 500 39

The integrity of the autonomic nervous system was assessed in 11 Parkinsonian patients with symptoms suggestive of autonomic dysfunction. Three had the additional clinical features of the Shy-Drager variant of idiopathic orthostatic hypotension and were found to have a gross disturbance of vasomotor, sudomotor, pilomotor, and bladder function; assessment indicated that a lesion was present at sympathetic ganglionic level or beyond in two cases, though a more centrally placed lesion may well have been present also, as in the third case. In the remaining eight patients with paralysis agitans no unequivocal functional disturbance was found except in the bladder; nevertheless, the low resting blood pressure and the supersensitivity to intravenously infused L-noradrenaline in the three patients in whom it was tested is taken to imply defective regulation from higher centres, with a consequent reduction in impulse traffic at sympathetic nerve terminals. Such a concept is supported by experimental studies in animals and would account for the low renin and aldosterone secretion rates and reduced noradrenaline formation reported by others in patients with paralysis agitans.
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PMID:Assessment of autonomic function in patients with a Parkinsonian syndrome. 509 25

The pupillary diameter of 11 patients with Parkinson's disease was significantly decreased four hours after ingestion of L-dopa. It is suggested that this miosis may be caused by diminished noradrenaline output at sympathetic nerve endings, or alternatively by an action on the central nervous system.
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PMID:Miosis during L-dopa therapy. 542 6

According to their mental status, patients with Parkinson's disease can be subdivided into three groups: (1) mentally normal patients; (2) patients with severe cognitive impairment and Alzheimer-type brain pathology (neuritic plaques, neurofibrillary tangles, granulovacuolar changes); and (3) demented patients without any evidence of Alzheimer changes. Neurochemically, irrespective of the presence or absence of Alzheimer-type brain pathology, demented Parkinson patients seem to have the same disturbance of cortical cholinergic neuron function as patients with Alzheimer-type dementia (Alzheimer's disease), namely, reduced levels of cortical acetylcholine esterase and choline acetyltransferase activity. At present, the question whether the "cortical cholinergic deficiency" is the only (or sufficient) neurochemical basis for the cognitive impairment in Parkinson patients with dementia cannot be answered with certainty; the additional role of other neurotransmitter changes known to occur in the Parkinson brain, especially loss of cortical, hippocampal and subcortical noradrenaline and/or dopamine cannot be ruled out.
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PMID:Neurochemical basis of dementia in Parkinson's disease. 614 10

1 Dopamine deficiency in the brain is the prime biochemical deficit in Parkinson's disease, but loss of noradrenaline and 5HT also may contribute. 2 In rats, 5HT-containing neurones originating from the dorsal and median raphe nuclei innervate forebrain dopamine-containing areas so as to impose an inhibitory regulatory tone on dopamine function. However, this interaction between brain dopamine and 5HT-containing neuronal systems is complex, and the effect produced appears dependent on the relative activity of each system. 3 Anatomical evidence for innervation of dopamine-containing brain regions by noradrenaline fibres in the rat is scanty, but functional studies suggest the existence of inputs which facilitate dopamine function. 4 Drug therapy designed to increase or decrease brain 5HT function has had no consistent effect in Parkinson's disease. 5 Manipulation of brain noradrenergic activity in Parkinson's disease had little effect, although the noradrenaline precursor L-threo-DOPS may reduce freezing attacks. 6 Until more specific drug molecules are available the role of brain noradrenergic and 5HT mechanisms in Parkinson's disease remains uncertain.
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PMID:Noradrenaline and 5-hydroxytryptamine modulation of brain dopamine function: implications for the treatment of Parkinson's disease. 633 12


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