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 article summarizes the prevention and treatment of malignant syndrome (MS) in Parkinson's disease. MS is often induced by sudden withdrawal of levodopa. However, many other events can be responsible for the induction of MS, including concomitant infections, dehydration, hot weather, discontinuation of other antiparkinsonian drugs, and 'wearing off' phenomenon. MS should be suspected when the body temperature rises above 38 degrees C without an apparent cause. The early detection and its prompt commencement of treatment are essential for improving the prognosis of the disease. The treatment consists of ample intravenous fluid, cooling the body, antiparkinsonian drugs (particularly, levodopa and bromocriptine), dantrolene sodium, and antibiotics if infection is present.
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PMID:[Prevention and treatment of malignant syndrome in patients with Parkinson's disease]. 1546 91

In an effort to gain deeper insight into the molecular processes underlying neurodegeneration in Parkinson's disease, we performed gene expression profiling at several early time points after MPTP-injection into old (1-year) mice. We used a PCR-based gene expression profiling method, digital expression pattern display (DEPD), a method of very high sensitivity and reproducibility, which displays almost all transcripts of a tissue. To identify cell death-associated genes, we defined clusters of differentially expressed transcripts with expression behaviour that correlated with the temporal profile of cell death progression and characterized one of these cell death clusters further. We selected one of the strongest regulated genes, the serum and glucocorticoid-regulated kinase 1 (sgk1), and validated its differential expression by Northern blot analysis, semiquantitative PCR and in situ hybridization. Up-regulation of sgk1 (i) coincides with the onset of dopaminergic cell death in both the 8-week acute and 1-year subacute MPTP models, (ii) spans the entire brain, (iii) is attenuated by the l-deprenyl-mediated inhibition of the MPTP conversion to its active metabolite MPP+ and (iv) is not induced by dehydration. This study demonstrated that the combination of the DEPD technology, clustering analysis and a detailed histopathology is a useful tool for elucidating molecular pathways in neurodegenerative diseases.
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PMID:sgk1, a member of an RNA cluster associated with cell death in a model of Parkinson's disease. 1567 31

The Dutch Association of Psychiatry, together with the Dutch Association of Clinical Geriatrics and with methodological support from the Dutch Institute for Healthcare Improvement (CBO) has developed a guideline for the optimal diagnosis, treatment and prevention of delirium. Delirium is caused by somatic illness or the use of medication, drugs or alcohol. Delirium is common among the somatically ill admitted to a general hospital and is associated with increased morbidity and mortality. Important predisposing factors for delirium are: age > or =70 years, cognitive disturbances, sensory impairments, problems in daily activities, and the use of alcohol and opiates. Precipitating factors that may provoke delirium are: infection, fever, dehydration, serum electrolyte imbalance, polypharmacy, and the use of psychotropic medication, particularly anticholinergic drugs. Detection, diagnosis, and assessment of the severity of delirium are based on clinical examination, case history, observation, mental status examination including tests of cognitive function, and diagnosis of underlying somatic diseases. For daily practice, measurement tools are not necessary, nor are laboratory or imaging tests, such as electroencephalography. Haloperidol is the treatment of first choice for delirium due to somatic illness, except in patients with delirium due to drug use or medication, Parkinson's disease or Lewy body dementia. In cases of concurrent alcohol withdrawal syndrome, delirium may be treated with haloperidol and a benzodiazepine and B-vitamins. Medical and environmental interventions have been shown to reduce the incidence and duration of delirium.
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PMID:[Guideline 'Delirium']. 1590 90

An 85-year-old woman with Parkinson's disease was admitted to our hospital to conduct a further work-up for progressive gait disturbance. She had been on medications for the disease for more than a decade prior to admission. In order to improve her condition, she was newly administered pramipexole, a dopamine agonist, from day 3 in addition to the preceding anti-Parkinson's therapy. However, on day 10, her consciousness level was rapidly deteriorated into delirium(JCS II-10), which was not accompanied by neurological signs and symptoms. Laboratory tests showed severe hyponatoremia with relatively increased urinary sodium excretion, and severe low serum osmolarity with an increased urinary osmolarity. Brain CT and brain MRI showed no specific abnormalities except for those related to aging. Blood concentration of ADH measured at the onset was substantially higher(39.5 pg/ml) than normal (0.3-3.5 pg/ml under normal osmolarity). Diseases causing hyponatremia, such as liver cirrhosis, congestive heart failure, hypotonic dehydration, and malignancy-associated inappropriate ADH secretion (SIADH), were all excluded. Under the suspicion of SIADH due to pramipexole, the drug was discontinued and as a result, her consciousness level improved rapidly together with a prompt reduction in ADH level (9.2 pg/ml). To the best of our knowledge, the present case is the first that demonstrates pramipexole-induced SIADH. Since pramipexole is classified as a dopaminergic receptor agonist, this case may provide new insight into a link between ADH and the dopaminergic receptor in the central nervous system.
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PMID:[Syndrome of inappropriate ADH secretion (SIADH) induced by pramipexole in a patient with Parkinson's disease]. 1613 Apr 8

In this 12-wk, multi-center, randomized, open-label, rater-blinded study, efficacy and tolerability of Entacapone (ENT) or Cabergoline (CBG) in conjunction with levodopa were compared in 161 older Parkinson's disease patients with wearing-off. Patients received either ENT, 3 to 5 times daily, or CBG, titrated according to requirements to a maximum of 6 mg/d. A significant decrease of nearly 2 hours in the daily OFF-time (primary efficacy variable) was recorded in both treatment groups. The non-inferiority test failed despite a trend in favor of ENT. Reduction in OFF-time occurred faster in the ENT compared to the CBG treated patients. A decrease of approximately 20% was detected in parts II and III of the UPDRS, with no differences between the groups. Forty-three percent of the patients in the ENT group reported dyskinesias at baseline, and 35% at the final visit. The corresponding figures in the CBG group were 46% and 43%. Quality of life, measured by PDQ-39, increased substantially with both ENT and CBG. The mean daily dosage at the final visit was 698 mg for ENT (plus 447 mg levodopa) and 3.45 mg for CBG (plus 475 mg levodopa). Adverse events (AE), leading to discontinuation, were reported in 8.5% of the ENT and 13.9% of the CBG treated patients. Nausea was the most common AE in each group, corresponding figures being 7.3% with ENT and 25.3% with CBG (P=0.0024). A probable or possible causal relationship with ENT was reported in 41% and with CBG in 64% of the AE. Among these, only one serious AE (dehydration) was recorded with each treatment group. ENT and CBG reduced the patient's motor complications effectively and to a similar degree. The clinical benefit was more quickly apparent with ENT, which also showed a more favorable AE profile than CBG.
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PMID:Efficacy and tolerability of Entacapone versus Cabergoline in parkinsonian patients suffering from wearing-off. 1751 84

A 79-year old woman was admitted with disturbed consciousness (JCS II-30). She had been given a diagnosis of type 2 diabetes 7 years previously, and was being treated with oral hypoglycemic agents. She also suffered Alzheimer's disease and Parkinson's disease. Plasma glucose and HbA1c upon admission was 676mg/dl and 9.7%, respectively. Serum Na was 153mEq/l. Urine ketone body test was negative and metabolic acidosis was not observed. Hyperglycemic hyperosmolar non-ketotic coma (HHNC) was diagnosed, and treatment was started immediately with normal saline infusion. Continuous infusion of regular insulin was needed to lower blood glucose. Disturbed consciousness and dehydration improved by the third hospital day. However, she became bedridden afterwards and received tube feeding. Up to 46 units of insulin was needed daily to control blood glucose. Urine C-peptide secretion was very low (10microg/day), suggesting that insulin therapy was essential for glycemic control long before admission. It is thought that a number of elderly diabetic patients who need insulin therapy do not receive or continue it for various reasons. Discussion is necessary to grasp the actual situation and defensive actions that can be taken.
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PMID:[An elderly case of hyperglycemic hyperosmolar non-ketotic coma (HHNC)]. 1819 60

Visual hallucinations are a typical feature of Lewy body parkinsonism and occur in some 40% of patients with Parkinson's disease. Age and cognitive decline are the most important intrinsic risk factors, but hallucinosis is often triggered by comorbid conditions such as infection and dehydration. The single most important trigger, however, is exposure to CNS drugs, in particular antiparkinsonian agents. While hallucinosis and psychosis can be triggered by amantadine and anticholinergics, they are more commonly experienced after changes in dopaminergic medication. Dopamine agonists have greater potential to induce hallucinosis compared with L-dopa. Attempting to reduce antiparkinsonian drugs is an important part in the management of these patients, but atypical neuroleptics like clozapine or quetiapine are frequently necessary. Visual hallucinations in Parkinson's disease patients with dementia can also be improved by treatment with the cholinesterase inhibitor rivastigmine.
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PMID:When a Parkinson's disease patient starts to hallucinate. 1864 10

Impairment of attention and memory in patients with Alzheimer's disease (AD) is associated with significantly lower levels of acetylcholine. Inhibition of the breakdown of acetylcholine by blocking the enzymes acetylcholinesterase and butyrylcholinesterase with rivastigmine improves this cholinergic depletion. Thus rivastigmine administration provides established, effective, long-term symptomatic treatment in AD and Parkinson's disease (PD) patients with dementia. A sustained treatment with cholinesterase inhibitors in general may also induce a certain deterioration of fine motor behavior, which may play a crucial role in the treatment of PD patients with dementia. Recent studies show that this altered balance between dopamine and acetylcholine due to cholinesterase inhibition, with its possible negative impact on motion behaviour, does not present a major problem in clinical practice in AD patients and may be compensated for by modification of dopaminergic substitution in PD patients with dementia. However, progression of neurodegeneration increases the vulnerability for psychosis in AD and PD patients with dementia in combination with dehydration and often requires additional application of neuroleptics. Since classical neuroleptics increase extrapyramidal symptoms, atypical neuroleptics are used. Out of these, quetiapine shows a distinct lower anticholinergic (muscarinergic) potency with beneficial effects on cognition. This favors its use in combination with rivastigmine.
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PMID:Rivastigmine in the treatment of patients with Alzheimer's disease. 1930 May 54

Persistent hiccups may have a considerable impact on general health through disturbance of diet, sleep, and mood. They can cause exhaustion, malnutrition, dehydration, wound dehiscence, and even death in extreme cases. We report a complex clinical case of intractable hiccups in a patient with cancer of the pancreas and Parkinson's disease and some of the problems encountered when attempting symptom control. We also discuss a potential therapeutic response to a novel agent, amantadine, unlicensed in the treatment of hiccups.
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PMID:Novel use of amantadine: to treat hiccups. 1973 5

Dysarthria and dysphagia occur frequently in Parkinson's disease (PD). Reduced speech intelligibility is a significant functional limitation of dysarthria, and in the case of PD is likely related articulatory and phonatory impairment. Prosodically-based treatments show the most promise for addressing these deficits as well as for maximizing speech intelligibility. Communication-oriented strategies also may help to enhance mutual understanding between a speaker and listener. Dysphagia in PD can result in serious health issues, including aspiration pneumonia, malnutrition, and dehydration. Early identification of swallowing abnormalities is critical so as to minimize the impact of dysphagia on health status and quality of life. Feeding modifications, compensatory strategies, and therapeutic swallowing techniques all have a role in the management of dysphagia in PD.
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PMID:Speech and Swallowing in Parkinson's Disease. 1994 86


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