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)

GI motility changes little--if at all--with age in healthy patients. However, a variety of diseases, including diabetes and Parkinson's disease, may cause autonomic neuropathy that is manifest as a motility disorder in the GI tract. Autonomic neuropathy can cause dysmotility in the esophagus, stomach, and gut. Symptoms are often nonspecific, including difficulty in swallowing, nausea, vomiting, heartburn, indigestion, diarrhea, and constipation. Nonpharmacologic treatment includes management of underlying diseases, avoidance of anticholinergic medications, and dietary changes. Agents with prokinetic action are the therapy of choice when drug treatment is indicated.
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PMID:GI motility disorders: diagnostic workup and use of prokinetic therapy. 790 Nov 29

We describe our clinical experience in the evaluation of gastrointestinal symptoms in patients with Parkinson's disease. Dysphagia, heartburn, medication-related nausea, and constipation were the predominant symptoms. Although all of the patients localized their dysphagia to the oropharynx and although oropharyngeal dysfunction was common, evaluation revealed significant dysfunction in either the esophageal body or lower esophageal sphincter in many--gastroesophageal reflux-related disease being especially common. Studies of anorectal sphincter and pelvic floor function in those patients with constipation demonstrated a high incidence of abnormal external anal sphincter dysfunction. We conclude, first, that dysphagia in patients with Parkinson's disease should not be assumed to result solely from oropharyngeal dysfunction but deserves detailed evaluation and, second, that constipation in Parkinson's disease is commonly consequent on anorectal sphincter and pelvic floor dysfunction.
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PMID:Gastrointestinal dysfunction in Parkinson's disease. A report of clinical experience at a single center. 793 Apr 24

In a recent study we identified abnormal salivation, dysphagia, nausea, constipation, and defecatory dysfunction as those gastrointestinal (GI) symptoms associated with Parkinson disease (PD) and characterized their relationship to PD severity and therapy. In this study, we re-evaluated these symptoms and their relationship to parameters of PD 18 months later. Sixty-six percent of the original participants responded. Over the 18 months, 68% of originally untreated PD subjects commenced anti-PD therapy. Abnormal salivation, dysphagia, nausea, constipation, and defecatory dysfunction were again identified as those GI symptoms more common in PD. Constipation increased both in severity and frequency. Comparison of GI symptom scores and parameters of PD dysfunction failed to reveal significant progression of either GI symptomatology or PD dysfunction, or the development of new GI symptoms over the 18-month period. This study validates our GI dysfunction assessment system and confirms abnormal salivation, dysphagia, nausea, constipation, and defecatory function as those GI symptoms truly associated with PD. A direct relationship between PD and its related GI symptoms is again supported.
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PMID:Gastrointestinal symptoms in Parkinson disease: 18-month follow-up study. 809 49

Several factors place older patients at increased risk for malnutrition. The physiologic effects of aging itself are considered risk factors, as are systemic diseases such as Parkinson's disease, diabetes, infection, and cancer; depression, and other psychiatric disorders; abnormal chemical values; and effects of various medications. Many of these factors are reversible if recognized and assessed early. Cholesterol and albumin measurements may help confirm the diagnosis of malnutrition. Nutrition-promoting interventions that you can recommend include increasing exercise, raising levels of fluid and nitrogen intake, avoiding constipation through dietary and lifestyle changes, and recommending routine dental examinations.
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PMID:The malnourished older patient: when and how to intervene. 832 14

A case of familial juvenile parkinsonism with dementia, orthostatic hypotension, neurogenic bladder and constipation was reported. He had been in a good health until the age of 28 when a finger tremor occurred on effort to hold hands in a definite position, and disturbances in gait and speech were noted. These symptoms were relieved by levodopa treatment followed by dyskinesia and motor fluctuations. Three years later, he complained of faintness, constipation and urinary frequency. The neurological examination revealed mentally sound male with masked face, tremor and rigidity in his extremities, and short step gait with lateropulsion. Urodynamic study showed uninhibited bladder. In the following years, orthostatic hypotension, dysuria and urinary retention developed gradually. He became mentally loose and was unable to take medicines appropriately. When in the Nishiojiya Byoin National Sanatorium, he tried to snake out the hospital many times. His parents and a brother suffered from Parkinson's disease and juvenile parkinsonism, respectively, suggesting an autosomal dominant inheritance. On admission to our hospital, he was apathetic. He had masked face, bilateral postural tremor, frozen gait and dyskinesia in the right lower extremity. Little bradykinesia or rigidity was noted. His muscle tone and deep tendon reflexes were decreased but neither muscular wasting, weakness, ataxia nor sensory disturbance was observed. Laboratory data including ceruloplasmin, copper, dopamine-beta-hydroxylase and lysosomal enzyme activities were normal except for mild anemia. A cranial CT scan revealed mild cortical atrophy in the frontal and temporal lobes, but nerve conduction study and cortical evoked potentials showed no abnormality. While in the hospital, his mental functions deteriorated to the state of dementia and orthostatic hypotension became apparent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Familial juvenile parkinsonism with dementia and autonomic failure--a case report]. 833 79

Constipation, a frequent symptom in Parkinson's disease (PD), is probably caused by degeneration of the autonomic nervous system, particularly the myenteric plexus. Cisapride is a drug that causes increased release of acetylcholine in the myenteric plexus. In a pilot study, cisapride therapy was investigated in 20 PD patients, 10 women and 10 men, who suffered from delayed intestinal transit. In all cases, cisapride therapy was associated with a significant acceleration of colonic transit, as measured by radioopaque pellets viewed on radiographs. Pellet count fell from a mean of 53.8 pretreatment to 30.4 after cisapride treatment. No adverse reaction and no "overshoot affects," such as diarrhea, were seen. Our findings suggest that cisapride may alleviate the constipation associated with Parkinson's disease.
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PMID:Cisapride treatment of constipation in Parkinson's disease. 834 Dec 99

We investigated autonomic function in patients with idiopathic Parkinson's disease (PD) by measuring sympathetic skin response (SSR) and R-R interval variation (RRIV). Sixty-two PD patients and 62 age-matched normal subjects were recruited. Abnormal SSR was noted in nine (14.5%) PD patients, including three in Stage II, three in Stage III, and three in Stage IV, but not in Stage I patients or normal subjects. Four of these nine patients had postural hypotension. Abnormal SSR was correlated with duration of illness and impotence. In PD patients, abnormal SSR may be due to intermediolateral column dysfunction. After logarithmic transformation and age adjustment, 19 (31.6%) of 60 PD patients had abnormal RRIV during rest and deep breathing. Abnormal RRIV was not related to staging or duration of illness. Patients with constipation had significantly lower RRIV, indicating parasympathetic dysfunction. RRIV was not affected by acute or chronic L-dopa treatment. The agreement between RRIV and SSR in PD patients was poor (kappa = -0.07). It appears that abnormal SSR, but not RRIV, may be associated with more autonomic disturbances in PD patients.
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PMID:Sympathetic skin response and R-R interval variation in Parkinson's disease. 847 81

Anorectal dysfunction and constipation are well recognized in Parkinson's disease and may reflect the direct involvement of the gastrointestinal tract by the primary Parkinson's disease process. We hypothesized, therefore, that anorectal function would alter in parallel with fluctuations in motor function related to on- and off-periods in Parkinson's disease, and employed combined anorectal manometry and electromyography to investigate anorectal function during both on- and off-periods in patients with Parkinson's disease. Manometric recordings revealed a deterioration in voluntary sphincter squeeze during off-periods (squeeze index, on versus off, mean +/- SEM: 46.4 +/- 11.1 versus 29.6 +/- 7.9 mm Hg, p < 0.05); correspondingly, simultaneous electromyographic (EMG) recordings showed poor recruitment of external anal sphincter and puborectalis muscles during off-periods. A hypercontractile ("paradoxical") rectosphincteric reflex response occurred during both on- and off-periods, and was associated with an increase in EMG activity in the external sphincter and/or the puborectalis muscle. These changes in manometric and EMG parameters paralleled changes in overall motor function. These findings provide further support for the involvement of the pelvic floor musculature in the Parkinson's disease process and also provide EMG correlates for some of the manometric abnormalities described in Parkinson's disease.
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PMID:Anorectal function in fluctuating (on-off) Parkinson's disease: evaluation by combined anorectal manometry and electromyography. 855 19

The patient with Parkinson's disease often needs concomitant treatment for disorders that accompany the disease, such as depression, insomnia or constipation, or for frequent concomitant alterations such as dizziness, high blood pressure or heart disease. The many drugs that can worsen motor symptoms in Parkinson's disease must be avoided, especially if use will be prolonged. Not all drugs that induce or aggravate parkinsonism have the same potency. We describe 3 groups: 1) drugs that invariably induce or aggravate parkinsonism if taken long enough or at high enough doses; 2) drugs that only provoke parkinsonism in some individuals, and 3) drugs that interfere with the action of levodopa. Knowledge of these drugs is essential for all doctors who treat patients with Parkinson's disease.
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PMID:[Drug treatment of frequent disorders in patients with Parkinson's disease]. 869 42

Patients with idiopathic Parkinson's disease (IPD) often show signs and symptoms of autonomic involvement, related to the disease itself or to its progression. The more frequently disturbances reported are connected with loss of extrapyramidal motor control, i.e. dysphagia, gastric emptying and the most common constipation. They concern about 73% of the patients. A high frequency of urinary symptoms, ranging from 37% to 71%, is also reported in IPD, in particular detrusor hyperreflexia causing urgency, frequency of micturing or urgency incontinence. Another autonomic groups of symptoms are related to the failure of cardiopressor adaptability which involve 15% of the subjects and are more typical of late onset cases or forms bordering with the Multiple System Atrophy, finally resulting in orthostatic hypotension (OH).
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PMID:Autonomic disorders in Parkinson's disease. 874 4


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