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)

Nursing interventions for each of the symptoms of Parkinson's disease, muscle rigidity, bradykinesia, tremors at rest and postural reflex abnormalities, are designed to increase the patient's quality of life by minimizing symptoms. Nurses are responsible for planning patient medication schedules to maximize drug effectiveness. Dietary implications include a low-protein regimen for the patient during the day, eliminating foods high in Vitamin B6, high caloric foods, and soft-solid foods offered at frequent feedings. Constipation is addressed by increasing the patient's fiber and fluid intake and by increasing the patient's mobility. Patient mobility is increased when the patient is taught purposeful activities and to concentrate on the way he walks. Communication is facilitated if the patient takes deep breaths before speaking and uses diaphragmatic speech. A telephone receiver which amplifies the patient's voice is also available. Interventions are good only if the patient chooses to implement them; he is the head of the health team planning his care.
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PMID:Nursing care of patients with Parkinson's disease. 322 57

Systolic blood pressure, mean R-R interval, and R-R interval variance were studied in patients with Parkinson's disease, spinocerebellar degeneration, and Shy-Drager syndrome. Postural hypotension correlated with anhidrosis (p less than 0.05), indicating sympathetic vasomotor dysfunction. Reduction of R-R interval variance while resting supine correlated with bladder-bowel dysfunction (p less than 0.05), indicating parasympathetic impairment. Reduction of R-R interval variance after postural changes correlated with constipation (p less than 0.005), postural hypotension (p less than 0.05), and anhidrosis (p less than 0.05), indicating both parasympathetic and sympathetic involvement. Dynamic study of the R-R interval provides objective information about autonomic function in neurologic disease.
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PMID:Postural hypotension and low R-R interval variability in parkinsonism, spino-cerebellar degeneration, and Shy-Drager syndrome. 668 92

KW-5338 (domperidone), a new dopamine antagonist, is considered to be an agent to cross the blood-brain barrier with difficulty. The antagonistic activities of KW-5338 against L-DOPA were investigated, KW-5338 showed a strong anti-emetic action against L-DOPA induced emesis in beagle dogs (ED50=0.056 mg/kg (p.o.)) and restored the L-DOPA induced depression of intestinal motility to some extent, while it did not antagonize anti-tremorine activities of L-DOPA and trihexyphenidyl in mice. These results suggest that KW-5338 prevents side effects of L-DOPA such as nausea, vomiting and constipation, without reduction in therapeutic effects of L-DOPA in Parkinson's disease.
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PMID:Antagonism of KW-5338 (domperidone) against emesis and depression of intestinal motility induced by L-DOPA. 727 86

Autonomic symptoms such as orthostatic hypotension, abnormal sweating and constipation occur frequently in Parkinson's disease. In our case, barium meal used for upper gastrointestinal study caused barium stone formation and a paralytic-ileus-like syndrome. Therefore, attention should be paid while using barium meal for diagnostic purpose in Parkinsonism.
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PMID:Barium stone impaction in parkinsonism. 747 96

Clinical studies suggest that gut disorders are common in Parkinson's disease, but the morphological basis is unknown. Depletion of dopamine-containing neurons in the central nervous system is a basic defect in Parkinson's disease. We compared colonic tissue from 11 patients with advanced Parkinson's disease, 17 with adenocarcinoma (normal tissue was studied), and five who underwent colectomy for severe constipation. Immunohistochemistry was used to stain myenteric and submucosal neurons for dopamine, tyrosine hydroxylase, and vasoactive intestinal polypeptide (VIP). Each class of neurons was quantified as a percentage of the total neuronal population stained for the marker protein gene product 9.5. Nine of the 11 Parkinson's disease patients had substantially fewer dopaminergic myenteric neurons than the other subjects (mean 0.4 [SE 0.2] vs 6.9 [2.3] in controls and 5.7 [2.0] in constipated subjects). There was very little difference between the groups in numbers of tyrosine-hydroxylase and VIP neurons. Two Parkinson's disease patients had similar distributions of all types of neurons, including dopaminergic myenteric neurons, to the controls. High-performance liquid chromatography showed lower levels of dopamine in the muscularis externa (but not mucosa) in four Parkinson's disease patients than in four controls (7.3 [5.1] vs 24.2 [4.6] nmol per g protein), but levels of dopamine metabolites were similar in the two groups. The identification of this defect of dopaminergic neurons in the enteric nervous system in Parkinson's disease may lead to better treatment of colorectal dysfunction in this disease.
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PMID:Dopaminergic defect of enteric nervous system in Parkinson's disease patients with chronic constipation. 756 69

We report one case of parkinsonism induced by cisapride and one case of Parkinson's disease whose symptoms were worsened by cisapride. Case 1. A 75-year-old female who had suffered from constipation and loss of appetite, was treated with cisapride for her gastro-intestinal symptoms. One year later, she developed progressive parkinsonian gait, cogwheel rigidity She showed parkinsonian gait, cogwheel rigidity and slowness in motion. Two months after cisapride was discontinued, her parkinsonism and depression disappeared. Case 2. A 66-year-old female with Parkinson's disease was given cisapride for constipation. Two months after starting cisapride, her akinesia and rigidity deteriorated gradually, and she became bed-ridden with dysphagia and dyspnea. After cisapride was discontinued, her parkinsonian symptoms improved gradually, and she became ambulant three months later. Cisapride is a benzamide derivative with a prokinetic action. Experimental studies have revealed that it has indirect cholinomimetic effects and potentially stimulates the gastrointestinal motor activity without blocking dopamine receptors or activating muscarinic cholinergic receptors. However, the present cases showed that cisapride could be a dopamine receptor blocker, and either induce or worsen parkinsonism. Therefore, cisapride should be avoided or very carefully used in parkinsonian patients and old people.
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PMID:[Parkinsonism induced or worsened by cisapride]. 772 93

Disorders of autonomic regulation are common in patients with Parkinson's disease (PD). Patients most frequently complain of dysphagia and therapy resistant constipation, as far as the gastrointestinal tract is concerned. These symptoms have to be attributed to a neuronal degeneration. In a pilot study we therefore investigated the effect of stimulation of the myenteric plexus by cisapride. 11 women and 13 men were examined, the average age was 67.3 years, the Webster rating 17 points. In 2 out of 24 patients, colonic transit was prolonged up to the limit, both with and without therapy. The other 22 patients showed an acceleration in transit on response to cisapride. On average the colonic transit of 130 hours was reduced to 79 hours. This objective improvement was associated with a subjective improvement. Central side effects or a worsening of Parkinsonian symptoms were not found. We conclude that cisapride is effective in the treatment of constipation in idiopathic PD.
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PMID:The effect of cisapride on delayed colonic transit time in patients with idiopathic Parkinson's disease. 781 Jan 53

We investigated the role of anorectal manometry in evaluating constipation and anorectal function in 15 patients with Parkinson's disease (PD) and compared results with those of 9 patients with idiopathic constipation (IC) and 8 control (C) subjects. Anal sphincter pressures on voluntary squeeze were lower in the PD patients. Sustained squeeze pressures (mm Hg C versus IC versus PD: 46.8 +/- 5.2 versus 31.2 +/- 3.6 versus 26.6 +/- 3.9; p < 0.05 PD versus C), squeeze duration (seconds: 53.6 +/- 2.5 versus 48.5 +/- 4.1 versus 33.6 +/- 9; p < 0.05 PD versus C) and squeeze index (area under the squeeze curve: 44.0 +/- 2.9 versus 34.5 +/- 3.3 versus 21.4 +/- 2.9; p < 0.001 PD versus C) were significantly lower in the PD group in comparison to the control group. In contrast, none of the parameters of anorectal manometry differed between controls and patients with idiopathic constipation. Some Parkinson's disease patients demonstrated an abnormal, hypercontractile response on testing of the rectoanal inhibitory reflex. Anal sphincter length, basal sphincter pressures, maximal squeeze pressures, extent of relaxation on rectoanal inhibitory reflex and threshold volume for rectal sensation were similar in the three groups. We conclude that an impaired squeeze response is a specific feature of anorectal function in Parkinson's disease. This may indicate direct involvement of the pelvic floor musculature by the parkinsonian disease process.
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PMID:Anorectal manometry in the assessment of anorectal function in Parkinson's disease: a comparison with chronic idiopathic constipation. 784 7

Constipation is well known to be a frequent symptom in idiopathic Parkinson's disease. In this study, colonic transit time was measured in 16 patients with nonidiopathic Parkinson's syndrome (non-IPS). These patients all had lacunar infarcts in the caudate, putamen, or globus pallidus, as a cause of the disease, as demonstrated by MRI. In comparison with the control group there was only a slightly longer transit time with, on the whole, a normal transit time (about 59 h). In only five cases was the transit time significantly decreased. Our results suggest that colonic transit is only prolonged in patients with idiopathic PD, whereas it is normal in non-IPS. This seems to be cause by a multi-degenerative process in the idiopathic disease.
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PMID:Colonic transit time in nonidiopathic Parkinson's syndrome. 785 54

Cisapride (CIS) is a prokinetic agent that increases gastrointestinal motility in normal individuals and improves constipation in Parkinson's disease (PD). We studied the effects of CIS on the clinical response and the peripheral pharmacokinetics of orally administered L-dopa given to patients with PD. Twenty patients with idiopathic PD and chronic constipation, whose response to L-dopa was suboptimal or characterized by fluctuations, agreed to participate in an open study that lasted for 2 weeks. Fourteen patients completed the study (mean age 65 +/- 9.3 years, mean duration of treatment 5.7 +/- 4.2 years, mean L-dopa daily doses 658.9 +/- 269.9 mg); six patients were excluded due to lack of compliance or changes in medication during the study. The end points of the study included the mean levels of L-dopa, the height of the peak of L-dopa in plasma, mean plasma levels of 3-OM-dopa, and the speed and quality of gait and visuomanual coordination before and during treatment with CIS. CIS increased peak plasma levels of L-dopa by 37% and the mean plasma levels of L-dopa by 13% with respect to those obtained with the same dose of L-dopa before the addition of CIS. Therefore, CIS appears to increase early absorption of L-dopa through acceleration of gastric emptying. CIS also increased plasma 3-OM-dopa levels, improved visuomanual coordination, and reduced gait disability. CIS improves gastrointestinal function and response to L-dopa in patients with PD and could be a helpful add-on medication in these patients.
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PMID:The effects of cisapride on plasma L-dopa levels and clinical response in Parkinson's disease. 788 57


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