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)

This investigation was conducted to clarify the epidemiology of ALS disease in Sardinia. During the years 1965-1974, the average annual incidence was found to be 0.64/100,000 inhabitants. On prevalence day, October 24th, 1974, the prevalence rate was 1.56/100,000 inhabitants. A significant male predominance was found, the average annual incidence rates for men and women being 0.88 and 0.40, respectively. The peak in both sexes was reached between 60 and 69 years. ALS distribution in the study area was uniform but its occurrence was significantly higher among agricultural workers (5.28/100,000). ALS started on average at 56.58 years and its duration was 2.5 years, being significantly longer in patients under 40-years-old. The distribution of the various clinical forms was: 66 per cent conventional forms, 20 percent bulbar and 14 per cent pseudo-polyneuritic. In the bulbar type, a female predominance was found. About 96 percent of cases were sporadic and 4 per cent familial. Familial cases presented no difference from sporadic cases. Trauma was present in 10.5 percent of the cases and gastrointestinal disfunction in 13 per cent. This probably reflects some relationship between trauma and ALS, and between malnutrition and ALS. No combination of ALS, dementia and parkinsonism was observed. Dementia was associated with ALS in four cases and Parkinson's disease in one case, separately. The combination of other disease states with ALS in the present study may be simple coincidence.
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PMID:Studies on epidemiological, clinical, and etiological aspects of ALS disease in Sardinia, Southern Italy. 84 75

Some elderly patients with chronic illness such as stroke, or Parkinsonism cannot take food orally because of dysphagia. In such cases, tube feeding can be used as a supplement to oral intake when malnutrition is present. This route allows for easier nursing care and decreases the frequency of aspiration pneumonia. Complications of tube feeding include nutrient deficiency states, pulmonary aspiration, gastrointestinal and metabolic disorders. We report two cases with complications of acute gastric ulcer which was thought to be induced with long-term tube feeding. Case 1 was a 61-year-old male patient with Parkinson's disease for ten years. L-DOPA had been administered with good control of his condition. However, his ability to swallow has deteriorated gradually. As he often suffered from aspiration pneumonia, nasogastric tube feeding was performed. After three years of tube feeding, he suddenly vomited much bloody material. He died from massive bleeding with acute gastric dilatation. Autopsy showed giant acute gastric ulcer covered with coagulated blood. UL3, 50 mm in maximum diameter, was observed in the middle portion of the greater curvature, where the top of tube probably came in contact with the gastric wall. Case 2 was an 83-year-old female patient with stroke and chronic heart failure. She had been hospitalized for about one year because of the intermittent deterioration of her cardiac condition. Furthermore, her inability to swallow increased during her hospitalization. She also suffered from aspiration pneumonia. Nasogastric tube feeding was performed to prevent aspiration pneumonia and malnutrition. She died of acute heart failure after twelve months. Autopsy revealed heart dilatation, old myocardial infarction and stroke. In addition, two acute gastric ulcers (UL3.10 and 30 mm in diameter) were recognized; one was in the upper portion of the greater curvature, the other in the lower portion of the greater curvature. The location of these gastric ulcers was unusual. Moreover, they coincided with location of top of the nasogastric tube. From these two cases, we conclude that in long-term tube feeding the tip of the tube often comes in contact with the gastric wall, and gastric ulcer could be produced by repeated mechanical stimulus of the wall. Reports of acute gastric ulcer induced by tube feeding have not been published previously. Therefore, we should pay much attention to this complication in the care of the elderly people with long-term tube feeding.
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PMID:[Long-term nasogastric feeding and complications of acute gastric ulcer in two elderly patients]. 143 62

Neuropsychological test performance was compared in 37 neuroleptic treated DSM-III schizophrenic patients, 27 untreated schizophrenic patients, and 27 normal controls. Neuroleptic treated patients performed significantly less well than untreated patients at recalling a complex figure, at planning on a mazes test, and had poorer fine motor coordination. Controls and untreated patients performed equally well on these tests. The results were not altered in 16 neuroleptic treated patients who had been prescribed low doses of benztropine, nor 38 patients who reported prior substance abuse. Similar cognitive impairments are observed in Parkinson's disease and are associated with dopaminergic antagonist drugs in schizophrenics. Therefore, they do not comprise part of the Schizophrenic Deficit State. Two tests were better performed by controls than patients. Reaction time was slower and more variable in both treated and untreated patient groups than controls. The recall of paraphrased passages was significantly poorer in both patient groups than controls, a finding that is robust in subgroups matched for IQ. Neuroleptic treatment was associated with significantly better performance on this test.
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PMID:Neuroleptic drug effects on cognitive function in schizophrenia. 198 Jun 13

Mortality rates for deaths "due to" and "with" motor neuron disease are presented for the first time. Age-specific mortality rates increase with age until 70 to 74 years and then decline. There appear to be no major differences by race in the age-adjusted mortality rates, but these rates are higher for males both white and nonwhite. A case-control study of all deaths with amyotrophic lateral sclerosis (ALS) was conducted for deaths due to ALS in the year 1971. Conditions associated with ALS at the time of death include pneumonia and bronchopneumonia, symptoms referable to respiratory system, superficial injury to shoulder and upper arm, essential benign hypertension, chronic skin ulcer, and malnutrition. No association was found between ALS and malignancies, Parkinson's disease, or dementia.
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PMID:Motor neuron disease in the United States, 1971 and 1973-1978: patterns of mortality and associated conditions at the time of death. 361 53

To determine which conditions may be associated with reduced survival in patients with Alzheimer's disease, we studied all death certificates in the United States for 1978 on which senile and presenile dementia (ICDA 290, N = 7,195) was mentioned. Each case was compared with two control deaths. Differences in the frequency of listing on the death certificates for the following conditions reached statistical significance: infections, trauma, nutritional deficiency, chronic ulcer of skin, foreign body in pharynx, cataract, glaucoma, blindness, deafness, Parkinson's disease, and epilepsy. There seem to be many preventable and treatable disorders in patients with senile and presenile dementia.
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PMID:Conditions associated with Alzheimer's disease at death: case-control study. 394 92

Neurogenic dysphagia results from sensorimotor impairment of the oral and pharyngeal phases of swallowing due to a neurologic disorder. The symptoms of neurogenic dysphagia include drooling, difficulty initiating swallowing, nasal regurgitation, difficulty managing secretions, choke/cough episodes while feeding, and food sticking in the throat. If unrecognized and untreated, neurogenic dysphagia can lead to dehydration, malnutrition, and respiratory complications. The symptoms of neurogenic dysphagia may be relatively inapparent on account of both compensation for swallowing impairment and diminution of the laryngeal cough reflex due to a variety of factors. Patients with symptoms of oropharyngeal dysphagia should undergo videofluoroscopy of swallowing, which in the case of neurogenic dysphagia typically reveals impairment of oropharyngeal motor performance and/or laryngeal protection. The many causes of neurogenic dysphagia include stroke, head trauma, Parkinson's disease, motor neuron disease and myopathy. Evaluation of the cause of unexplained neurogenic dysphagia should include consultation by a neurologist, magnetic resonance imaging of the brain, blood tests (routine studies plus muscle enzymes, thyroid screening, vitamin B12 and anti-acetylcholine receptor antibodies), electromyography/nerve conduction studies, and, in certain cases, muscle biopsy or cerebrospinal fluid examination. Treatment of neurogenic dysphagia involves treatment of the underlying neurologic disorder (if possible), swallowing therapy (if oral feeding is reasonably safe to attempt) and gastrostomy (if oral feeding is unsafe or inadequate).
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PMID:Dysphagia associated with neurological disorders. 820 77

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

Achalasia is an uncommon esophageal motility disorder of unknown etiology. To gain insights into possible etiologic risk factors, demographic and comorbidity data were obtained from Medicare hospital discharge data files from 1986-1989 on patients aged 65 and older. Age-adjusted sex- and race-specific occurrence rates were calculated for each US state. The rate of comorbid illness occurrence in achalasia patients was compared to that of the entire hospitalized Medicare population. Records of 15,000 achalasia discharges were available for analysis. Achalasia discharge rates increased linearly from age 65 to 94 years. They were similar in males and females as well as whites and nonwhites. High rates were observed in the South and low rates in most states of the East North Central region around the Great Lakes and in the Pacific region. The same geographic pattern was observed in men and women as well as in the two separate subsets of data representing the periods 1986-1987 and 1988-1989. Achalasia was associated with a significantly increased risk for pulmonary complications, malnutrition, and gastroesophageal cancer. The concordant occurrence of achalasia in patients with Parkinson's disease, depressive disorder, and various other myoneural disorders indicated a possible etiologic relationship. Achalasia appears to represent the clinical end point of several different pathways. Besides aging, different neurologic diseases may contribute to a loss in control of esophageal motility. The geographic pattern could suggest the influence of environmental factors.
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PMID:Epidemiology of hospitalization for achalasia in the United States. 842 36

Coined by Sifneos in 1972, alexithymia refers to a relative narrowing in emotional functioning, an inability to find appropriate words to describe their emotions and, a poverty of fantasy life. Although initially described in the context of psychosomatic illness, alexithymic characteristics may be observed in patients with a wide range of medical and psychiatric disorders: Parkinson disease, depression, anxiety, substance abuse and eating disorders. Flattening of affect and poverty of speech, major negative symptoms, referred to chronic schizophrenia: there is a lack of outward display of emotion. Accordingly, some disturbances of alexithymia's scores would be expected in schizophrenic patients. The purpose of this study was to estimate and compare the prevalence of alexithymia in deficit and non-deficit schizophrenia. The term "deficit symptoms" may be used as Carpenter, to refer specifically to those negative symptoms that are not considered secondary. The influence of patients' symptoms has also been studied on alexithymia scores: negative and positive symptoms of schizophrenia, depression, anxiety, anhedonia and effects of neuroleptics. Twenty-five patients, meeting DSM III-R criteria for schizophrenia have been studied. All of them treated by neuroleptics, were in a stable clinical status for at least one month. The patients have been categorized into deficit (n = 12) and non-deficit (n = 13) subgroups by one trained psychiatrist (SD), using the Schedule for the Deficit Syndrome. The subjects have been assessed by the same rater (IN), blind to deficit status, using six rating scales: Beth Israel Questionnaire (BIQ) and Toronto Alexithymia Scale (TAS) for alexithymia, Positive and Negative Syndrome Scale (PANSS), Montgomery and Asberg Depression Rating Scale (MADRS), revised Physical Anhedonia Scale (PAS), and finally, Extrapyramidal Symptom Rating Scale (ESRS). Using TAS, alexithymic characteristics were more prevalent in the deficit subgroup as compared to non-deficit subgroup (83% versus 30.76%; p < 0.01). Significant correlations were observed in the non-deficit subgroup between: TAS and anxiety (r = 0.743; p < 0.01), TAS and depression (r = 0.568; p < 0.05), BIQ and blunted affect (r = 0.636; p < 0.02), BIQ and poverty of speech (r = 0.629; p < 0.02). These correlations were not significant in the deficit group of patients. Alexithymia in schizophrenic patients seems to be a trait characteristic in deficit patients, and a state related to many symptoms, such as flattening of affect, poverty of speech, depression and anxiety in nondeficit patients.
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PMID:[Alexithymia in negative symptom and non-negative symptom schizophrenia]. 945 28

Altered glutathione metabolism in association with increased oxidative stress has been implicated in the pathogenesis of many diseases. However, whether strategies aimed at restoring glutathione concentration and homeostasis are effective in ameliorating or modifying the natural history of these states is unknown. In this review we discuss the pathogenic role for altered glutathione metabolism in such diseases as protein energy malnutrition, seizures, Alzheimer's disease, Parkinson's disease, sickle cell anaemia, chronic diseases associated with ageing and the infected state. In addition, we discuss the efficacy of glutathione precursors in restoring glutathione homeostasis both in vitro and in vivo.
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PMID:Glutathione in disease. 1112 62


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