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)

Animal data indicate that serotonin (5-HT) is a major neurotransmitter involved in the control of numerous central nervous system functions including mood, aggression, pain, anxiety, sleep, memory, eating behavior, addictive behavior, temperature control, endocrine regulation, and motor behavior. Moreover, there is evidence that abnormalities of 5-HT functions are related to the pathophysiology of diverse neurological conditions including Parkinson's disease, tardive dyskinesia, akathisia, dystonia, Huntington's disease, familial tremor, restless legs syndrome, myoclonus, Gilles de la Tourette's syndrome, multiple sclerosis, sleep disorders, and dementia. The psychiatric disorders of schizophrenia, mania, depression, aggressive and self-injurious behavior, obsessive compulsive disorder, seasonal affective disorder, substance abuse, hypersexuality, anxiety disorders, bulimia, childhood hyperactivity, and behavioral disorders in geriatric patients have been linked to impaired central 5-HT functions. Tryptophan, the natural amino acid precursor in 5-HT biosynthesis, increases 5-HT synthesis in the brain and, therefore, may stimulate 5-HT release and function. Since it is a natural constituent of the diet, tryptophan should have low toxicity and produce few side effects. Based on these advantages, dietary tryptophan supplementation has been used in the management of neuropsychiatric disorders with variable success. This review summarizes current clinical use of tryptophan supplementation in neuropsychiatric disorders.
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PMID:L-tryptophan in neuropsychiatric disorders: a review. 130 30

Akathisia is a common and distressing side effect of antipsychotic and some other psychotropic medications. This paper reviews the current state of knowledge of its clinical features, pathophysiology, and treatment. Restless legs syndrome and akathisia associated with Parkinson's disease are discussed in so far as they help understand drug-induced akathisia. The complexity of the disorder, and the difficulty in characterizing and quantifying it, may explain why researchers have relatively neglected akathisia for so long. The recent upsurge of research interest promises the hope of a better understanding of its pathophysiology so that effective therapy may result.
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PMID:The present status of akathisia. 135 Mar 4

Muscle activity during sleep is a new area of interest in sleep research. No precise brain structures are known to be involved in sleep movement. The etiology of periodic movements during sleep is unknown. The present study was dedicated to evaluate involvement of basal ganglia in periodic movements of the legs during sleep (PMS) in Parkinson's diseased patients. Sleep was monitored in 3 patients suffering from Parkinson's disease and PMS (PMS/PD) and in 3 patients suffering from restless legs syndrome and PMS (PMS/non PD). Following treatment, the six patients were monitored again during sleep. It was found that only the PMS/PD group of patients had improved significantly with appropriate treatment. Improved motor function in PD patients is associated with decreased PMS, regardless of wether the patients are treated with dopaminergic or anticholinergic agents. This is consistent with our previous data. It may be suggested that the striopallidal system is involved in periodic sleep movements of Parkinson's diseased patients.
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PMID:Are periodic movements in sleep a basal ganglia dysfunction? 368 Dec 89

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

Restless leg syndrome (RLS) is usually idiopathic but may occur in patients with Parkinson's disease (PD). Both respond to dopaminergic medications. Whether these disorders share a common pathophysiology is unclear. Because PD is associated with a loss of olfactory function, we compared the olfactory function of patients with RLS with control and PD patients. Using the University of Pennsylvania Smell Identification Test (UPSIT), olfactory function was found to be normal in patients with idiopathic RLS and significantly reduced in patients with PD. This suggests that the pathophysiology of RLS differs from PD, and that RLS likely is not a "forme fruste" or a preclinical sign of PD.
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PMID:Olfactory function in restless legs syndrome. 961 55

The authors investigated nine drug-naive patients with periodic limb movement disorder and restless legs syndrome (PLMD-RLS) and 27 healthy controls with PET using 6-[18F]fluoro-L-dopa (FDOPA). In the patients, the FDOPA uptake (Ki(occ)) in the caudate nucleus was 88% and in the putamen 89% of the control mean values. This equal affection of the caudate and the putamen differs, for example, from the dopaminergic dysfunction in Parkinson's disease, which affects the putamen earlier and more severely than the caudate. The current results indicate mild nigrostriatal presynaptic dopaminergic hypofunction in PLMD-RLS.
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PMID:An FDOPA PET study in patients with periodic limb movement disorder and restless legs syndrome. 1066 25

Restless legs syndrome (RLS) is a perplexing, debilitating, and fairly common condition that can be challenging to manage. Hallmark symptoms include an increase in the severity of sensations during rest and an irresistible urge to move the affected limbs. RLS often occurs concomitantly with periodic limb movement disorder. There are no known causes of RLS, but likely triggers include heredity, iron and vitamin deficiencies, caffeine, and alcohol. Chronic conditions such as diabetes, peripheral neuropathy, and Parkinson's disease can worsen and prolong RLS symptoms. Symptom management begins by establishing proper nutrition intake and improved sleep hygiene. If these fail, conservative pharmacologic treatment is appropriate, with regimens chosen from dopaminergic agents, benzodiazepines, opioids, and anticonvulsants.
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PMID:Restless legs syndrome. How to provide symptom relief with drug and nondrug therapies. 1077 1

The frequency of sleep complaints in patients with Parkinson's disease (PD) is estimated to be between 60-90% and a variety of either disease-related or secondary mechanisms and the dopaminergic treatment itself contributes to the development of different sleep disturbances. These comprise slight, fragmented sleep with increased number of arousals and awakenings, and PD-specific motor phenomena such as nocturnal immobility, rest tremor, eye-blinking, dyskinesias, and other phenomena such as periodic and nonperiodic limb movements in sleep, restless legs syndrome, fragmentary myoclonus, and respiratory dysfunction in sleep. Depression and hallucinations/psychosis further complicate the picture. The incidence of REM sleep behavior disorder (RBD) with nightmares and violent behavior is increased in PD and may occur as a preclinical disease-related symptom. A careful sleep history of patients and their partners, polysomnograms when necessary, motor and psychiatric assessments should precede individual treatment strategies, which include adjusting dopaminergic daytime treatment, benzodiazepines for RBD, reduction of anticholinergic drugs, and, if necessary, clozapine for nocturnal psychosis.
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PMID:Sleep dysfunction in Parkinson's disease. 1078 36

We studied the neurological comorbidity of parkinsonism in 368 consecutive patients from the Lausanne Movement Disorders Registry. Only 6 patients had no neurological comorbidity. We found that 23p.100 of our patients had ischemic strokes, especially large vessel strokes, i.e three times more than in an age-matched control study performed in a recent survey in our country, which is a new finding in contradiction with previous reports mentioning that Parkinson's disease may be a protective factor against stroke. This finding opens new directions for further studies concerning some shared mechanisms in both diseases associated with age. Predominantly tremulous parkinsonism (46p.100) and progressive supranuclear palsy patients (PSP) (40p.100) had the highest prevalence of cerebrovascular disease of all subgroups of parkinsonism, especially lacunar infarcts, which is in accord with a higher frequency of hypertension in these subgroups according to a recent study of ours. Transient ischemic attacks or hemorrhages were not more frequent than in the general population. We did not find a higher frequency of head trauma except for Parkinson's disease, but a trend for a higher frequency of headache and migraine. Brain tumors were more frequent in Parkinson's disease and hydrocephalus and radiculopathies in parkinsonism in general when compared to age-matched populations from the literature. Polyneuropathies were more frequently observed in familial parkinsonism only, but myopathies and cranial neuropathies were not more frequent in our patients. Epilepsy was significantly less frequent in parkinsonism, especially in Parkinson's disease, infectious diseases of the nervous system were rarely encountered, and restless legs syndrome was surprisingly not more frequent than in a normal population. Dementia was associated in 20p.100, but multiple sclerosis is noticeably absent.
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PMID:[Neurological comorbidity in parkinsonism]. 1124 May 47

The pathogenesis of restless legs syndrome (RLS) is poorly understood. Previously we have shown that a reach-to-grasp task can be used to differentiate Parkinson's disease (PD) patients from healthy age-matched control subjects. The aim of this study was to determine if performance on this task could be used to differentiate between patients with RLS, PD patients, and healthy control subjects. Results indicated that RLS and control participants produced movement patterns that were nearly identical to one another, while movement patterns produced by the PD patients were significantly different from the other two groups. These results suggest RLS patients do not show any abnormalities in the performance of upper extremity prehension movements. Thus, these movements can be used to effectively differentiate between patients with Parkinson's Disease and Restless Legs Syndrome. While RLS patients respond favorably to dopaminergic therapies, this study suggests that PD and RLS may not share the same basal ganglia pathophysiology.
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PMID:Prehension patterns in restless legs syndrome patients. 1124 97


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