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)

Several tests of cardiovascular and gastrointestinal function have been approved for the diagnosis of autonomic regulation dysfunction in Parkinson's disease. In the present study we compared the diagnostic value of the sympathetic skin response (SSR) with the established methods. Ninety percent of the 20 patients we examined (10 women, 10 men, 46 to 80 years) showed pathological results in the cardiovascular function test. Fifty-five percent had a prolonged colon transit, indicating a gastrointestinal dysfunction. We saw pathologically prolonged latencies of the SSR in 35% of the patients, 55% had borderline results. Three of the 20 patients had pathological results in all of the functions examined. Half of the patients had two pathological results, whereas 7 patients were pathological in only one of the three examinations. We were unable to establish any correlation between the SSR and other results, and we also found no relationship between prolonged SSR and the duration of the disease.
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PMID:[Sympathetic skin response in Parkinson syndrome]. 750 Oct 94

Electrogastroenterography (EGEG) is a method to record electrical activities of the stomach and the intestine using skin electrodes. We investigated whether this method could be used to detect gastrointestinal dysfunction in patients with idiopathic Parkinson's disease. EGEG recordings were done with ten patients with idiopathic Parkinson's disease and ten control subjects before and after a meal. The patients showed changes in EGEG that were markedly similar to those of acute stage of vagotomized patients reported previously. Patients' increase rate in amplitude of gastric activity after the meal (median: 1.19) was significantly (P < 0.05, Mann-Whitney test) smaller than that of the controls (median: 2.84), and normal temporal frequency decrease of gastric activity after the meal was not seen in the patient group. These results suggest vagal nerve dysfunction of patients with Parkinson's disease, though other possibilities could not be denied. EGEG may be useful to assess patients' gastrointestinal dysfunction though we need further study to elucidate the relation between pathophysiology of their symptoms and EGEG findings.
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PMID:Gastrointestinal dysfunction in Parkinson's disease detected by electrogastroenterography. 771 22

Gastrointestinal dysfunction is a frequent and occasionally dominating symptom of Parkinson's disease (PD). Features of gastrointestinal dysfunction include disordered control of saliva, dysphagia, gastroparesis, constipation in the sense of decreased bowel movement frequency, and defecatory dysfunction necessitating increased straining and resulting in incomplete evacuation. Excess saliva accumulates in the mouth because of decreased swallowing frequency. Dysphagia develops in approximately 50% of patients and may be a reflection of both central nervous system and enteric nervous system derangement. Gastroparesis may produce a variety of symptoms, including nausea, and also may be responsible for some of the motor fluctuations seen with levodopa therapy. Bowel dysfunction in PD may be the result of both delayed colon transit and impaired anorectal muscle coordination.
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PMID:Gastrointestinal dysfunction in Parkinson's disease. 1078 40

There is growing recognition that gastrointestinal dysfunction is common in Parkinson's disease (PD). Virtually all parts of the gastrointestinal tract can be affected, in some cases early in the disease course. Weight loss is common but poorly understood in people with PD. Dysphagia can result from dysfunction at the mouth, pharynx, and oesophagus and may predispose individuals to aspiration (accidental inhalation of food or liquid). Gastroparesis can produce various symptoms in patients with PD and may cause erratic absorption of drugs given to treat the disorder. Bowel dysfunction can consist of both slowed colonic transit with consequent reduced bowel-movement frequency, and difficulty with the act of defecation itself with excessive straining and incomplete emptying. Recognition of these gastrointestinal complications can lead to earlier and potentially more effective therapeutic intervention.
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PMID:Gastrointestinal dysfunction in Parkinson's disease. 1284 67

Neuroplastic changes in the enteric nervous system (ENS) may be observed in physiological states, such as development and aging, or occur as a consequence of different pathological conditions, ranging from enteric neuropathies (e.g., Hirschsprung's disease) to intestinal (e.g., inflammatory bowel disease) or extra-intestinal diseases (e.g., Parkinson's disease). Studying ENS plasticity may help to elucidate the pathophysiology of several diseases and have a bearing on the development of new pharmacological interventions. In the present review, we would like to focus on neuronal plasticity evoked by gastrointestinal inflammation occurring in inflammatory bowel disease and in a subset of patients with severe derangement of gut motility due to an enteric neuropathy characterized by an inflammatory infiltrate of the enteric plexuses. Major features of neuroplasticity within the enteric microenvironment encompass structural abnormalities ranging from nerve re-arrangement (e.g., hypertrophy and hyperplasia) to degeneration and loss of enteric ganglion cells; altered synthesis, content and release of neurotransmitters as well as up- or down-regulation of receptor systems; gastrointestinal dysfunction characterized by sensory-motor and secretory impairment of the gut. Interestingly, neuronal changes may also occur in segments of the gastrointestinal tract remote from the site of the original inflammation, e.g. the ileum may show neuroplastic changes during colitis. Sometimes, the inflamed site may even be outside the gut. Among potential mechanisms underlying ENS plasticity, neurotrophins and enteric glia deserve special attention. A better comprehension of ENS plasticity during inflammation could be instrumental to develop new therapeutic options for patients with IBD and inflammatory enteric neuropathies.
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PMID:Enteric neuroplasticity evoked by inflammation. 1662 34

Weight loss is frequent in patients with Parkinson's disease (PD). Reduced energy intake and/or increased energy expenditure have been postulated as the cause. Dysphagia, anorexia, and gastrointestinal dysfunction may be possible causes of reduced energy intake; whereas, rigidity, tremor, and levodopa-induced dyskinesia may increase energy expenditure. Levodopa may enhance glucose metabolism resulting in enhanced energy expenditure. Depression, anti-parkinsonian drugs, and medical complications such as pneumonia and malignancies also may facilitate weight loss in PD. Combinations of various degrees of these factors, especially in advanced PD, may produce weight loss. Such weight loss is associated with malnutrition which may precipitate infection and decubitis; accelerate motor, behavioral, and autonomic impairment; consequently spoiling one's quality of life. Attention must be paid as well to motor symptoms to prevent or reverse weight loss in PD patients.
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PMID:Weight loss in Parkinson's disease. 1713 Dec 27

Current dopaminergic therapies for the treatment of Parkinson's disease are associated with the development of long-term motor complications. Abnormal pulsatile stimulation of dopamine receptors is thought to underlie the development of motor complications. There is thus a need for therapies that mimic the normal physiological state more closely by resulting in constant dopaminergic stimulation (CDS). Several studies support the hypothesis that CDS can reverse levodopa-induced motor complications. Other potential benefits of CDS include alleviating nocturnal disturbances, minimizing daytime sleepiness, avoiding priming for motor fluctuations and dyskinesia, preventing the development of gastrointestinal dysfunction and reducing the risk of developing psychosis or behavioural disturbances. Continuous infusion of dopaminergic therapies is impractical for the routine treatment of large numbers of patients. Although catechol-O-methyltransferase inhibitors or sustained-release preparations of levodopa may be beneficial, they do not entirely eliminate pulsatile stimulation of dopamine receptors. A new dopamine agonist (rotigotine), delivered over 24 h by a once-daily transdermal patch, has been investigated in several clinical trials. Continuous delivery of rotigotine has been shown to provide 'true' CDS in animal models. The potential of true CDS therapy to prevent or reduce long-term motor and non-motor complications requires investigation in appropriately designed clinical trials.
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PMID:Constant dopaminergic stimulation by transdermal delivery of dopaminergic drugs: a new treatment paradigm in Parkinson's disease. 1804 45

Gastrointestinal disorders, particularly severe constipation and delayed gastric emptying, are core symptoms of Parkinson's disease that affect most patients. However, the neuropathological substrate and physiological basis for this dysfunction are poorly defined. To begin to explore these phenomena in laboratory models of PD, rats were treated with either vehicle or rotenone (2.0 mg/kg, i.p.; 5 days/week) for 6-weeks. Myenteric plexus alpha-synuclein aggregate pathology and neuron loss were assessed 3-days and 6-months after the last rotenone injection. Gastrointestinal motility was assessed at 3-days, 1-month and 6-months after the last rotenone injection. Rotenone treatment caused an acute reduction in alpha-synuclein-immunoreactivity, but this was followed 6 months later by a robust increase in aggregate pathology and cytoplasmic inclusions that were similar in appearance to enteric Lewy-bodies in idiopathic PD. Rotenone-treated rats also had a moderate but permanent loss of small intestine myenteric neurons and an associated modest slowing of gastrointestinal motility 6-months after treatment. Our results suggest that a circumscribed exposure to an environmental toxicant can cause the delayed appearance of parkinsonian alpha-synuclein pathology in the enteric nervous system and an associated functional deficit in gastrointestinal motility. The rotenone model may therefore, provide a means to investigate pathogenic mechanisms and to test new therapeutic interventions into gastrointestinal dysfunction in PD.
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PMID:Chronic rotenone exposure reproduces Parkinson's disease gastrointestinal neuropathology. 1959 68

As with other neurodegenerative diseases, neurologic and nutritional elements may interact affecting each other in Parkinson's disease (PD). However, the long-term effects of such interactions on prognosis and outcome have not been given much attention and are poorly addressed by current research. Factors contributing to the clinical conditions of patients with PD are not only the basic features of PD, progression of disease, and the therapeutic approach but also fiber and nutrient intakes (in terms of both energy and protein content), fluid and micronutrient balance, and pharmaconutrient interactions (protein and levodopa). During the course of PD nutritional requirements frequently change. Accordingly, both body weight gain and loss may occur and, despite controversy, it seems that both changes in energy expenditure and food intake contribute. Nonmotor symptoms play a significant role and dysphagia may be responsible for the impairment of nutritional status and fluid balance. Constipation, gastroparesis, and gastro-oesophageal reflux significantly affect quality of life. Finally, any micronutrient deficiencies should be taken into account. Nutritional assessments should be performed routinely. Optimization of pharmacologic treatment for both motor and nonmotor symptoms is essential, but nutritional interventions and counseling could and should also be planned with regard to nutritional balance designed to prevent weight loss or gain; optimization of levodopa pharmacokinetics and avoidance of interaction with proteins; improvement in gastrointestinal dysfunction (e.g., dysphagia and constipation); prevention and treatment of nutritional deficiencies (micronutrients or vitamins). A balanced Mediterranean-like dietary regimen should be recommended before the introduction of levodopa; afterward, patients with advanced disease may benefit considerably from protein redistribution and low-protein regimens.
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PMID:Major nutritional issues in the management of Parkinson's disease. 1969 Nov 25

Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease. It has been classically considered that the pathological hallmarks of Parkinson's disease, namely Lewy bodies and Lewy neurites, affect primarily the substantia nigra. Nevertheless, it has become increasingly evident in recent years that Parkinson's disease is a multicentric neurodegenerative process that affects several neuronal structures outside the substantia nigra, among which is the enteric nervous system. Remarkably, recent reports have shown that the lesions in the enteric nervous system occurred at a very early stage of the disease, even before the involvement of the central nervous system. This led to the postulate that the enteric nervous system could be critical in the pathophysiology of Parkinson's disease, as it could represent a route of entry for a putative environmental factor to initiate the pathological process (Braak's hypothesis). Besides their putative role in the spreading of the pathological process, it has also been suggested that the pathological alterations within the enteric nervous system could be involved in the gastrointestinal dysfunction frequently encountered by parkinsonian patients. The scope of the present article is to review the available studies on the enteric nervous system in Parkinson's disease patients and in animal models of the disease. We further discuss the strategies that will help in our understanding of the roles of the enteric nervous system, both in the pathophysiology of the disease and in the pathophysiology of the gastrointestinal symptoms.
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PMID:The second brain and Parkinson's disease. 1971 93


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