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)

Comprehensive treatment of patients with parkinson's disease demands that not only motoric dysfunctions but also psychosocial aspects have to be considered. The scope of this review is to cover not only the frequent dementia and depressive states associated with this disease, but also the drug-induced behavioral abnormalities, insomnia, conflicts with those providing care and implications for professional activities. The fundamental pathophysiological and psychopathological mechanisms are explained and illustrated by examples.
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PMID:[Mental suffering IN patients with parkinsonism]. 793 73

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

The incidence of complications associated with disease and treatment was compared in younger versus elderly patients with Parkinson's disease (PD). One hundred sixty-five patient records were divided according to patient age into two groups ("younger," 41 to 64, and "elderly," > or = 65 years) and reviewed for the incidence of dyskinesias, fluctuations, freezing, psychosis, dementia, depression, and insomnia. Younger patients had a greater incidence of chorea (75.8 percent vs 49.5 percent), dystonia (82.3 percent vs 49.0 percent), fluctuations (90.1 percent vs 68.1 percent), depression (73.2 percent vs 36.8 percent), and insomnia (57.9 percent vs 18.1 percent). There were no significant differences in the incidence of freezing, dementia, or psychosis. At the time of the first adverse event, there was no difference in patient characteristics such as gender, lag time from disease diagnosis to levodopa initiation, disease symptoms at the time of diagnosis, levodopa dose, or concomitant drug use despite the fact that the older group had a longer duration of disease, higher Hoehn and Yahr stage, an older age at onset of PD, and longer duration of levodopa use. Younger patients with PD experience a greater incidence of adverse effects than do elderly PD patients. The spectrum of adverse effects is comparable to those of young-onset (< or = 40 years) patients.
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PMID:Complications of disease and therapy: a comparison of younger and older patients with Parkinson's disease. 887 56

This article summarizes sleep disturbances in a variety of neuro-degenerative diseases, including Parkinson's disease, multiple system atrophy, and amyotrophic lateral sclerosis. Sleep complaints in these conditions include insomnia, hypersomnia, abnormal motor activity and behavior during sleep, sleep-related breathing problems, and circadian rhythm sleep disturbances. Clinical examination followed in selected cases by polysomnographic, multiple sleep latency, and other laboratory tests is essential for correct diagnosis and treatment of these sleep disturbances.
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PMID:Sleep and degenerative neurologic disorders. 892 96

In Parkinson's disease, resting tremor is often the initial symptom. This report focuses on the mechanism underlying tremor in Parkinson's disease and quantitative assessment of tremor. Central factors including Vim (nucleus ventralis intermedius) in the thalamus, and peripheral factors, such as acceleration of input pathways from muscle spindles via muscle tonus, are important aspects of the tremor mechanism in Parkinson's disease. It has also been suggested that tremor in Parkinson's disease is associated with parasympathetic and sympathetic dysfunctions. Objective assessments of tremor, such as the application of surface electromyography, are useful in the diagnosis and treatment of Parkinson's disease. Actigraph, as introduced herein, is a three dimensional motor sensing apparatus. Therefore, motor counts over 0.01 G can be detected by actigraphy. To date, this device has been used for evaluating akinesia in Parkinson's disease and insomnia. In this study, actigraphy was used in Parkinson patients with tremor, and it reflected motor activity in the wrist and was associated with the severity of hand tremor. Activities of daily living (ADL) are disturbed by hyperkinesia of the hand for Parkinson patients with hand tremor. We demonstrated that actigraphy is a simple and quantitative method of assessing motor activity in Parkinson patients with tremor.
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PMID:[Clinicophysiological study of tremor in Parkinson's disease: quantitative tremor-based assessment of motor count using actigraphy]. 901 42

Different medications can have significant effects on sleep quality and/or quantity. When prescribing medications it is important to be aware of these possible adverse effects of drugs. Disturbances of the sleep/wake cycle caused by medications can vary and include insomnia, daytime sleepiness, nightmares and changes in the sleep architecture. Psychotropic drugs are well known to have an effect on the sleep/wake cycle, but there is only limited information about the sleep effects of nonpsychotropic medications. Cardiovascular drugs, especially beta-blockers, which are widely used drugs, often change the sleep architecture and cause nightmares and insomnia. Both of these effects can be a potential source of noncompliance. Because of the complicated relationship between sleep, nocturnal asthma and antiasthmatic agents, the appropriate dosage and timing of medications should always be considered. Patients with Parkinson's disease often experience disrupted sleep due to their disorder and the adverse effects of anti-parkinsonian medications.
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PMID:Drug-induced sleep disturbances. Focus on nonpsychotropic medications. 906 24

Diagnosis of Parkinsonism is made in two steps: 1. identification of the Parkinson syndrome, a combination of rest tremor, hypertonia, akinesia and postural disturbances; 2. then essentially on the basis of clinical observations, relation to Parkinson's disease. The main risks during the course with L-dopa treatment are, on the one hand, the appearance of akinetic changes and movement disorders, more common in the younger affected patients, and on the other hand, disorders that do not respond to L-dopa, especially postural and cognitive, that are favoured by old age. Anxiety, depression pain, autonomic disorders and insomnia increase the repercussions of the disease and complicate its management.
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PMID:[Diagnosis and course (under treatment) of Parkinson disease]. 920 68

A total of 335 patients with early Parkinson's disease (PD) were enrolled in a multicenter, randomized, double-blind trial designed to assess the efficacy and safety of pramipexole. Entry was restricted to patients with idiopathic PD who were not receiving levodopa. Pramipexole was administered according to an ascending dose schedule up to 4.5 mg/d. During the 7-week dose-escalation phase, each subject was titrated to his or her maximally tolerated dose of study medication. This was followed by a 24-week period of maintenance therapy. The mean daily dose during the maintenance period was 3.8 mg. Pramipexole significantly reduced the severity of PD symptoms and signs compared with placebo, as measured by decreases in parts II (Activities of Daily Living) and III (Motor Examination) of the Unified Parkinson's Disease Rating Scale at week 24 compared with baseline (p < or = 0.0001). Differences between the active drug and placebo groups emerged at week 3 (1.5 mg/d) in the ascending-dose interval and persisted throughout the maintenance phase (p < or = 0.0001). The majority of patients completed the study (pramipexole 83%, placebo 80%). In the assessment of adverse events, nausea, insomnia, constipation, somnolence, and visual hallucinations occurred more frequently in the pramipexole treatment group compared with placebo patients. No clinically significant changes were noted in blood pressure or pulse rate. Overall, these results indicate that pramipexole is safe and effective in the treatment of early PD.
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PMID:Efficacy of pramipexole, a novel dopamine agonist, as monotherapy in mild to moderate Parkinson's disease. The Pramipexole Study Group. 930 31

A clinically relevant sleep-wake disturbance is found in up to half the patients with dementia, and the sundowning agitation is a common cause of institutionalisation of demented geriatric patients. The circadian rhythm of demented patients is levelled off with increased daytime sleep and disrupted night sleep. Particularly in vascular dementia, Korsakow syndrome, Parkinson's disease, and depression the alteration of sleep architecture may be pronounced, whereas in Alzheimer's disease prominent hypersomnolence or insomnia is typically only found in later stages of the diseases. Greatly increased daytime sleepiness or striking insomnia at the very beginning of suspected dementia should thus prompt the search for other, possibly treatable causes of dementia. Neuropathological and neurophysiological studies support the hypothesis of a deteriorated hypothalamic suprachiasmatic nucleus (harbouring the biological clock) as a cause for the deranged circadian sleep-wake system in dementia. Management of sundowning behaviour includes restriction of daytime sleep, exposure to bright lights, and social interaction schedules during the day. The benzodiazepines and analogues usually not being sufficiently effectual, low doses of mild neuroleptics are often needed. Whether recent reports on efficacy of melatonin in elderly insomniacs also apply to demented patients is yet uncertain. The careful search and treatment of possible extracerebral physiologic factors causing reversible hypersomnia or insomnia is an important requisite. Polysomnographic studies are needed to recognise treatable sleep disturbance which could deteriorate or mimic dementia and sundowning. Particularly, a sleep-apnea-hypopnea syndrome must be searched for at the beginning of a suspected dementia, when successful treatment is still possible. Sleep studies should also identify periodic leg movements of sleep with restless legs and/or increased daytime sleepiness, and hyperkinetic parasomnias such as REM sleep behaviour disorder which may complicate or imitate sundowning.
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PMID:[Sleep disorders and dementia]. 938 Oct 26

A leading hypothesis of the pathogenesis of neuronal degeneration of the substantia nigra dopamine-containing cells in Parkinson's disease (PD) is excessive oxidative stress. In part, this oxidative stress is the result of the oxidation of dopamine by the action of monoamine oxidases (MAO) A and B to generate hydrogen peroxide and subsequent oxygen free radicals. Because of this hypothesis we have treated patients with early PD, not yet requiring any symptomatic treatment, with tranylcypromine, a drug that inhibits both MAO's. These patients were required to observe a tyramine-restricted diet. Thirty-seven patients on tranylcypromine have been followed by us for up to 33 months. Four patients discontinued the drug because of pending surgery. Of the remaining 33, six had adverse effects that lead to discontinuation of the drug, mainly impotency in men. Another common adverse effect encountered was insomnia, but this problem was not a cause of stopping the drug. Depression lifted in all five patients who had this problem at the time tranylcypromine was initiated. Only two patients have so far required treatment with levodopa or a dopamine agonist, and this need occurred within the first 6 months of treatment. The evaluation of all 37 patients revealed that parkinsonian symptoms improved slightly on introduction of tranylcypromine as measured by the United Parkinson's Disease Rating Scale, the Hoehn & Yahr Staging Scale, and the Schwab & England Activities of Daily Living Scale. Follow-up evaluations for a minimum of 6 months between the first post-tranylcypromine visit and the most recent visit revealed only slight worsening of parkinsonian signs and symptoms, with a mean interval of almost 1.5 years. A longer period of follow-up is needed to determine how long the severity of PD will remain mild in this group of patients.
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PMID:Experience with tranylcypromine in early Parkinson's disease. 956 7


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