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)

Abnormal motor behaviors during sleep can be classified into four categories, ranging from myoclonic jerks to complex and integrated motor behaviors There have been recent developments in several of these conditions, in particular restless legs syndrome (RLS) and rapid-eye-movement sleep behavior disorder (RBD). RLS is one of the major causes of insomnia. Familial aggregation of RLS has been demonstrated by several groups, and molecular genetics studies have suggested the presence of susceptibility genes on chromosomes 12q and 14q. Pharmacologic and brain imaging studies suggest the involvement of dopaminergic mechanisms in RLS, but recent work has focused on brain iron metabolism. Studies indicate that RBD patients may eventually develop Parkinson's disease (PD). Conversely, RBD has been found in patients already diagnosed with PD. Single-photon emission computed tomography and positron emission tomography studies have shown a decrease in binding to presynaptic dopamine transporter in both idiopathic RBD and PD. Patients with RBD (associated or unassociated with PD) also have neuropsychological deficits. RBD may therefore represent the prodrome of a neurodegenerative disease leading to multiple system atrophy and Lewy body dementia. Understanding the underlying pathophysiology of abnormal sleep motor behaviors may prove useful in the management of insomnia.
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PMID:Abnormal motor behavior during sleep. 1530 95

Dementia with Lewy bodies results from the accumulation from Lewy-type pathology (Lewy bodies, Lewy neurites), secondary cellular injury, and apoptotic neurodegeneration. The severity of dementia correlates with the abundance of Lewy bodies in the cortex. Dementia with Lewy bodies co-occurs with 2 specific syndromes, one beginning with dementia complicated by visual hallucinations and parkinsonism; the other beginning with Parkinson's disease and progressing to a parkinsonian-dementia syndrome. Clinical syndromes associated with these 2 pathways to dementia share many clinical features including the type of cognitive impairment, fluctuating attentional disturbances, prominent visual hallucinations and psychosis, depression, and rapid eye movement sleep behavior disorder. Lewy pathology results from protein misfolding and the accumulation of alpha-synuclein in the cell cytoplasm. Dementia with Lewy bodies is one of many neurodegenerative disorders linked to protein misfolding. Identification of clinical symptoms indicative of the presence of a specific protein disturbance will assist in choosing therapies when protein-specific disease-modifying treatments are available. Classification systems based on symptom complexes related to the presence of protein misfolding will assist therapeutic decisions.
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PMID:Dementia with lewy bodies: molecular pathogenesis and implications for classification. 1531 74

Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia manifested by vivid, often frightening dreams associated with simple or complex motor behavior during REM sleep. Patients appear to "act out their dreams," in which the exhibited behaviors mirror the content of the dreams. Management of RBD involves counseling about safety measures in the sleep environment; in those at risk for injury, clonazepam and/or melatonin is usually effective. In this article, the authors present a detailed review of the clinical and polysomnographic features, differential diagnosis, diagnostic criteria, management strategies, and pathophysiologic mechanisms of RBD. They then review the literature and their institutional experience of RBD associated with neurodegenerative disease, particularly Parkinson's disease and dementia with Lewy bodies. The evolving data suggests that RBD may have clinical diagnostic and pathophysiologic significance in isolation and when associated with neurodegenerative disease.
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PMID:REM sleep behavior disorder in Parkinson's disease and dementia with Lewy bodies. 1531 78

Behavioral impairments in parkinsonian patients include agitation, hypersexuality, stereotypic movement, pathological gambling, abuse of antiparkinsonian drugs, REM sleep behavioral disorder, and restless legs syndrome. Dementia, psychoses, and emotional disorders, such as depression and anxiety/panic disorder, also impair behavior. Symptoms may be produced by dysfunction of the central nervous system, medication, and/or the psychosocial problems associated with Parkinson's disease. Treatment therefore should be based on the cause of the symptoms seen. In some cases, the reduction or change of antiparkinsonian drugs, or both, may be effective. Treatment of the motor symptoms of Parkinson's disease, including motor fluctuations, may reduce the risk of panic attacks being evoked in the 'off' period. Use of antidepressants, sedatives, and neuroleptics may often be effective. Physicians should identify the causes of the symptoms of behavioral impairment and select appropriate treatments.
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PMID:[Behavioral impairments in Parkinson's disease]. 1546 83

Nocturnal disturbances are common in Parkinson's disease (PD) patients, with almost 70% of these patients reporting nocturnal disturbances. The etiology of sleep disturbances in patients with PD is still controversial. They might be dependent on dopaminergic drugs, on disease progression, or on a combination of these two factors. Nocturnal disturbances can be categorized in four groups: 1) PD-related motor symptoms, including nocturnal akinesia, early-morning dystonia, painful cramps, tremor, and difficulty turning in bed; 2) treatment-related nocturnal disturbances; 3) psychiatric symptoms, including hallucinations, vivid dreams, depression, dementia, insomnia, psychosis, and panic attacks; 4) other sleep disorders, including insomnia, REM behavioral disorder (RBD), restless legs syndrome (RLS), periodic leg movements (PLMS), and excessive daytime sleepiness (EDS). Specific treatment options are supplied for every group. A global evaluation of nocturnal disturbances would provide clinicians with a valuable tool to establish an optimal regimen that could positively influence all nocturnal disturbance categories and thus improve PD management on. However, it is important to consider that management of some nocturnal disturbances in a group may worsen nocturnal symptoms of another group or may increase EDS. PD-related symptoms can be treated with long-acting DA agonists to obtain continuous DA receptor stimulation during the night. Both treatment-related nocturnal disturbances and psychiatric symptoms may be related to drug treatment, and therefore, in both cases, drug reduction or discontinuance should be considered. Some sleep disorders, such as RLS and PLMS, may be controlled by DA agents, and others, such as insomnia and EDS, may be improved by reducing dopaminergic stimulation.
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PMID:Treatment of nocturnal disturbances and excessive daytime sleepiness in Parkinson's disease. 1550 42

A large number of patients with Parkinson's disease (PD) experience nocturnal problems that impair their sleep quality. Among them, motor disorders such as tremor, rigidity, akinesia, akathisia, periodic leg movements, painful dystonia, dyskinesias, restless legs syndrome, and rapid eye movement sleep behavior disorder are common. This article reviews the clinical characteristics of some nocturnal motor problems that often induce sleep disruption in PD patients.
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PMID:Nocturnal problems occurring in Parkinson's disease. 1550 43

Parkinson's disease (PD) is a progressive disease that usually affects the motor system but is also associated with a non-motor symptom (NMS) complex that ranges from dribbling saliva, constipation, depression, sleep disorders, apathy, hallucinations, and dementia. These features contribute significantly to morbidity and institutionalization, more than quadrupling the cost of care. Furthermore, recent evidence suggests that NMS such as constipation, olfaction, rapid eye movement behavior disorder, fatigue, and depression may be markers of a preclinical stage of PD. PD-NMS are not well recognized in clinical practice and part of the reason is the lack of any instrument that aims to assess the complex range of NMS of PD in a unified and integrated manner. Recently, an international, multidisciplinary PD-NMS group has developed an integrated questionnaire and scale to assess NMS of PD in a comprehensive manner. This will help improve care and treatment of PD in the future.
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PMID:The non-motor symptom complex of Parkinson's disease: a comprehensive assessment is essential. 1598 11

Although the current guidelines for the clinical diagnosis of multiple system atrophy (MSA) do not require structural or functional brain imaging, investigations utilizing positron emission tomography (PET) have been helpful diagnostically in differentiating between MSA and primary autonomic failure; idiopathic Parkinson's disease; and sporadic olivopontocerebellar atrophy. These investigations have demonstrated different patterns of cerebral glucose utilization and of nigrostriatal projection abnormalities among these disorders and between the cerebellar and parkinsonian forms of MSA. Most of the studies have focused upon patients with well-established disease and none have examined the utility of PET imaging in early stage patients with follow-up of clinical course and autopsy verification to ensure accuracy of diagnosis and to determine the sensitivity and specificity of PET techniques for diagnosis. Recent PET studies have revealed denervation of myocardial post-ganglionic sympathetic neurons in some MSA patients, indicating that this disorder can affect the peripheral autonomic as well as the central nervous system. Investigations utilizing ligands to quantify central nervous system dopaminergic and cholinergic terminals have begun to provide insight into the neurochemical disorders that may underlie two of the sleep disturbances common in MSA, rapid eye movement sleep behavior disorder and obstructive sleep apnea.
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PMID:Functional imaging with positron emission tomography in multiple system atrophy. 1608 7

We characterize the clinical features of Parkinson's syndrome on Guadeloupe and describe possible environmental causes. Consecutive patients who were referred to the University Hospital at Pointe a Pitre with parkinsonism from September 1996 to May 2002 were included. All cases were examined in a standardized manner by a neurologist with a special interest in movement disorders and independently by 3 external movement disorders specialists, using standard operational clinical diagnostic criteria. The subjects were 265 patients with Parkinson's syndrome living on Guadeloupe, four fifths of whom had been referred by primary care physicians and one fifth by neurologists. The levodopa response was assessed after a minimum period of 1 month of continuous treatment. All patients had brain computed tomography or brain magnetic resonance imaging scans and detailed neuropsychological examinations. Of 265 patients, only 66 were classified as Parkinson's disease, whereas 58 fulfilled the National Institute of Neurological Disorders and Stroke (NINDS) and Society for Progressive Supranuclear Palsy (SPSP) criteria for progressive supranuclear palsy, 100 had unclassifiable parkinsonism, characterized by dopa-unresponsiveness, marked axial rigidity, relative symmetry of parkinsonian features, early dysarthria, and frontolimbic cognitive impairment. Within this group, early postural instability, dysarthria, a frontal behavior disorder, cortical or subcortical atrophy, pyramidal signs, axial rigidity, and family history of neurodegenerative disorders were associated with poorer prognosis. A very large number of unclassifiable cases of atypical parkinsonism that do not fulfill operational criteria for Parkinson's disease or other defined motor neurodegenerations has been observed on Guadeloupe. Most patients closely resemble descriptions of bodig from Guam. In both geographic isolates, an environmental cause has been discussed. Annonaceae fruits and herbal teas are consumed on both islands. These plants contain several neurotoxins, particularly acetogenins, which induce dopaminergic neuron loss in animals. Neuronal death involves cholinergic and dopaminergic cells of the substantia nigra and GABAergic neurons of the striatum, associated with microglial proliferation. The development of atypical parkinsonism in Guadeloupe and probably elsewhere, could result from synergistic toxicity, but acetogenins are probably the most potent neurotoxin, acting as mitochondrial complex I inhibitor.
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PMID:Atypical unclassifiable parkinsonism on Guadeloupe: an environmental toxic hypothesis. 1609

The neuropsychiatry of Parkinson's disease (PD) and its correlates are reviewed. Dementia occurs in up to 30% and can be treated with cholinesterase inhibitors. Cognitive impairments involve executive, visuospatial, attentional, and memory dysfunctions. Apathy may respond to dopamine agonists or cholines-terase inhibitors. Cognitive impairment, psychosis, and depression predict quality of life. Visual hallucinations and paranoia are common, and respond to low dose clozapine. Depression is common and predicts caregiver burden and depression. The best data suggest the efficacy of nortriptyline and the safety of SSRIs. Anxiety disorders occur in 40% of patients, especially off-period panic attacks and specific phobias. Bromazepam has proven useful for anxiety in PD, but buspirone has only diminished drug-induced dyskinesias to date. Sleep disorders occur in up to 94% of patients. Insomnia is common and is treated by dopaminergic agent dose reduction, nocturnal dosing, treatment of depression, or use of short half-lived hypnotics, depending on etiology. Parasomnias include REM behavior disorder and vivid dreams and nightmares. Excessive daytime somnolence occurs in at least 15% of patients. Sleep attacks are common and patients should be warned about driving when taking dopamine agonists. Sexual disorders occur in most patients. Paraphilias are associated with dopamine agonists, and clozapine may be useful in their treatment. Surgical therapies are associated with a wide variety of neuropsychiatric features, and vigilance for suicide attempts with subthalamic nucleus stimulation seems warranted. Neuropsychiatric disorders are important determinants of quality of life and caregiver burden in PD. More clinical research is needed to establish effective treatments.
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PMID:The neuropsychiatry of Parkinson's disease. 1617 59


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