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)

The difficulty in differentiating progressive supranuclear palsy (PSP, also called Steele-Richardson-Olszewski syndrome) from other related disorders was the incentive for a study to determine the clinical features that best distinguish PSP. Logistic regression and classification and regression tree analysis (CART) were used to analyse data obtained at the first visit from a sample of 83 patients with a clinical history of parkinsonism or dementia confirmed neuropathologically, including PSP (n = 24), corticobasal degeneration (n = 11), Parkinson's disease (PD, n = 11), diffuse Lewy body disease (n = 14). Pick's disease (n = 8) and multiple system atrophy (MSA, n = 15). Supranuclear vertical gaze palsy, moderate or severe postural instability and falls during the first year after onset of symptoms classified the sample with 9% error using logistic regression analysis. The CART identified similar features and was also helpful in identifying particular attributes that separate PSP from each of the other disorders. Unstable gait, absence of tremor-dominant disease and absence of a response to levodopa differentiated PSP from PD. Supranuclear vertical gaze palsy, gait instability and the absence of delusions distinguished PSP from diffuse Lewy body disease. Supranuclear vertical gaze palsy and increased age at symptom-onset distinguished PSP from MSA. Gait abnormality, severe upward gaze palsy, bilateral bradykinesia and absence of alien limb syndorme separated PSP from corticobasal degeneration. Postural instability successfully classified PSP from Pick's disease. The present study may help to minimize the difficulties neurologists experience when attempting to classify these disorders at early stages.
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PMID:Which clinical features differentiate progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) from related disorders? A clinicopathological study. 905 98

Dopaminergic psychosis frequently complicates the pharmacological treatment of Parkinson's disease. Dose reduction of dopaminomimetic therapy or treatment with conventional neuroleptics improves psychosis but worsens parkinsonism. In an open-label 12-month trial, the clinical antipsychotic efficacy of the atypical neuroleptic clozapine was investigated in 36 parkinsonian patients (age range 46-85 years) with symptoms of dopaminergic psychosis including delusions, vivid dreams, hallucinations, frank paranoid delirium, and hypersexuality. Clozapine, given orally at bedtime, was started at a dose of 6.25 mg and titrated upward to the minimal effective dose. In all patients, psychosis responded to very low clozapine doses (mean 10.59 +/- 6.48 mg/day). Clozapine doses correlated with the severity of psychosis. During clozapine treatment, parkinsonian disabilities and levodopa dosage remained statistically unchanged. During the 12-month study, no patient had clozapine-induced agranulocytosis or other severe side effects. These findings indicate that even at low doses, clozapine effectively controls dopaminergic psychosis in Parkinson's disease patients without compromising motor function.
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PMID:Low dose of clozapine in the treatment of dopaminergic psychosis in Parkinson's disease. 919 42

We evaluated 109 Chinese patients with Parkinson's disease (PD) in three ways: using a standardized psychiatric interview for depression and anxiety, using standardized neurological evaluation for motor disability, and using cognitive assessment for cognitive impairment. Six of the 109 patients who had dementia and another two afflicted with organic delusional disorder were excluded from further analysis. The remaining 101 PD patients were divided into the following three groups according to the DSM-III-R criteria: major depressive disorder (n = 18), other depressive disorders (n = 25) including dysthymic disorder and depressive disorder not otherwise specified, and no depression (n = 58). The frequency of major depressive disorder of the 109 PD patients was 16.5%, and the frequency of major and other depressive disorders, taken together, was 42.2%. Using the percentage points measured on the Schwab & England Activities of Daily Living Scale as the dependent variable to fit a multivariate regression model, we found the lower score significantly correlated with the diagnosis of depressive disorder and higher score of the Hamilton Depression Rating Scale, in addition to motor disability and disease severity of PD. Given the high frequency of depression and the significant correlation between depression and performance in daily functional activites, we believe that an evaluation of PD patients for coexisting depression is necessary for a better therapeutic outcome.
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PMID:The correlation of depression with functional activity in Parkinson's disease. 930 55

Electroconvulsive therapy is an important treatment of depressive states in late life. However in the Netherlands ECT is not often practiced and mostly indicated after a long period of fruitless clinical therapy. The primary aims of this literature study were to review the efficacy of ECT in late life depression, to identify predictors of good response, to discuss contraindications, side effects and finally modifications of technique. Eighteen studies were found addressing the topic of efficacy. Outcome ranged between 50%-100% clinically significant improvement. Positive predictors are melancholic features and delusional depression. Unlike in younger patients hypochondriacal symptoms and anxiety do not predict a negative outcome in older patients. ECT has been used successfully in depression complicated by dementia, cognitive decline and cerebrovascular disease. Depression in Parkinson's disease may be a special indication where ECT may have a positive effect on motor symptoms. There are no firm indications of long term cognitive decline associated with ECT. Guidelines for practicing ECT (unipolar, brief pulse and anaesthesia) are in line with the state of the art in the literature. It is concluded that, especially in severe depression associated with comorbidity, current Dutch practice in using ECT, often leads to unwarranted delay.
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PMID:[Electroconvulsive therapy in late life depression: a review]. 938 18

The delusional misidentification syndrome (DMS) has been associated with a range of neurological conditions. Three cases of DMS in patients with Parkinson's disease and dementia, treated with dopaminergic medications, are presented. It is postulated that DMS associated with parkinsonism results from a combination of dopaminergic psychosis and cognitive dysfunction involving the frontal lobe in particular. DMS in the setting of parkinsonism may be more frequent than commonly supposed.
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PMID:Delusional misidentification in association with parkinsonism. 960 8

The authors administered electroconvulsive therapy (ECT) to four patients with intractable Parkinson's disease who were free from depression or dementia. After an initial "acute" phase, subjects received bitemporal maintenance ECT every 3 to 4 weeks for up to 12 months. Serial measures of mood, cognition, and motor function were performed. One subject developed cognitive impairment after seven maintenance treatments, and another developed delusions during the acute phase of the study. The two subjects completing the 12-month maintenance phase noted significant reductions in "off" time without impairment of cognitive functioning.
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PMID:Maintenance electroconvulsive therapy for intractable Parkinson's disease. 965 59

The majority of patients with Parkinson's disease develop psychiatric symptoms. 40% of the patients suffer from symptoms of depression, severely affecting daily functioning, motor symptoms, cognition, and quality of life for both the patients and their spouses. Antidepressants may alleviate the depressive symptoms, but treatment is complicated by complex pharmacodynamic interactions. Hallucinations, with or without delusions, occur in 15-20% of patients, and are usually caused by dopaminergic treatment. Patients suffering from dementia and depression are, however at particular risk of developing psychosis. Treatment consists of lowering the dose of dopaminergic agents, but many patients require symptomatic treatment with atypical antipsychotic drugs. Most Parkinsonian patients develop impairment of memory and executive functions, and more than 25% of patients develop dementia. Dementia increases with the age at onset and the duration of Parkinson's disease. Subcortical dementia is the most commonly observed syndrome, but symptoms of cortical dementia are also observed. No treatment is available, although cholinergic agents may prove useful.
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PMID:[Emotional and cognitive disorders in Parkinson disease]. 983 Mar 42

We report sinus bradycardia induced by talipexole hydrochloride in a 65-year-old man with Parkinson disease. Approximately four hours after he had taken 0.8 mg of talipexole hydrochloride, he acutely developed sleepiness, delusion, akinesia, and faintness associated with hypotension and sinus bradycardia. Another similar episode occurred when he had taken talipexole hydrochloride 1.2 mg/day in combination with a daily dose of 200 mg of levodopa and 20 mg of carbidopa. These symptoms persisted for 12 hours and diminished gradually without any specific treatments. Talipexole hydrochloride, a stimulator of both the D2 and alpha 2 receptors probably induced bradycardia and hypotension in the present case.
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PMID:[Sinus bradycardia induced by talipexole hydrochloride in a patient with Parkinson disease]. 991 27

Behavioural disorders are a common feature in dementia, especially in the later stages of the disease. The most frequent disorders are agitation, aggression, paranoid delusions, hallucinations, sleep disorders, including nocturnal wandering, incontinence and (stereotyped) vocalisations or screaming. Behavioural disorders, rather than cognitive disorders, are the main reason why caregivers place patients with dementia in a nursing home. However, although behavioural disorders are important, there is still no international agreement with respect to the description and definition of symptoms and syndromes. This also holds true for the wide variety of scales for quantification and measurement of behavioural disorders. Drug therapy should be considered after possible underlying causes such as physical illness, drug adverse effects and environmental stressors have been ruled out, or specifically addressed, and a behavioural approach has also failed. This article briefly reviews the evidence for non-antipsychotic drug therapies, which include a variety of substances. However, antipsychotics are the group of drugs which have been most frequently studied for the treatment of behavioural syndromes in dementia. Drug responsive symptoms include anxiety, verbal and physical agitation, hallucinations, delusions, uncooperativeness and hostility, whereas wandering, hoarding, unsociability, poor self-care, screaming and other stereotyped behaviour seem to be unresponsive to all drugs. Although the use of classical antipsychotics is limited by extrapyramidal symptoms, anticholinergic adverse effects, sedation and postural hypotension, the newer antipsychotics offer the chance of a better risk:benefit ratio. This article reviews the small amount of data published on the use of the newer antipsychotics, and concludes that risperidone at low dosages (0.5 to 2 mg/day) seems to be especially useful for the treatment of behavioural symptoms in dementia because of its negligible anticholinergic adverse effects. The use of clozapine is limited by its anticholinergic activity, at least in dementia of the Alzheimer and Lewy body types. However, in patients with psychosis arising from Parkinson's disease it seems to be the drug of choice, and similar activity is likely for olanzapine. There are no published data on other newer drugs, such as sertindole, quetiapine or ziprasidone. Future studies should also address questions of dementia heterogeneity and should compare different drug treatments and treatment combinations.
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PMID:Behavioural problems associated with dementia: the role of newer antipsychotics. 1006 7

An autopsy case of myotonic dystrophy (MD) is reported. The patient was a 58-year-old male. He presented with muscular weakness and muscular atrophy at the age of 33 and was diagnosed as having MD from myotonic symptoms (i.e. percussion and grip myotonia) at 49 years old. Mental disorders including a delusional hallucinatory state, mental slowness, indifference, and lack of spontaneity as well as visual cognitive impairments were noted at the age of 55. He showed Parkinsonism and died of septic shock. T2-weighted magnetic resonance imaging demonstrated diffuse cortical atrophy with a marked frontal atrophy and high-intensity signals in the white matter. Single photon emission computed tomography demonstrated hypoperfusion in the frontal cortex. Neuropathologic observation revealed neuronal loss in the superficial layer of the frontal and parietal cortices and extensive neuronal loss in the occipital cortex, intracytoplasmic inclusion body in the nerve cell of the medial thalamic nuclei, neuronal loss and presence of Lewy bodies in the substantia nigra and locus ceruleus corresponding to the pathologic features of Parkinson's disease, as well as abnormalities of myelin in the white matter. The present case suggests that in MD brain, various neuropathologic changes may occur and they contribute to the mental disorders.
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PMID:An autopsy case of myotonic dystrophy with mental disorders and various neuropathologic features. 1020 Dec 84


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