Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Patients affected by Parkinson's disease (PD) often complain of disturbed sleep resulting from nighttime motor disabilities such as nocturnal akinesia, tremor and rigidity, motor behaviour during REM sleep or periodic leg movements (PLM) during sleep. Sleep may also be affected by dopaminergic and anticholinergic drugs or coexisting depressive syndrome. Deep brain stimulation (DBS) of subthalamic nucleus (STN) effectively reduces PD motor disability. The aim of this study is to evaluate the sleep architecture modifications after STN DBS. We assessed five patients (two men and three women, mean age 63.8+/-3.3 years, with a mean history of PD of 13.8+/-4.9 years) who underwent STN DBS. The mean levodopa equivalent dosage (LED) was 1010+/-318 mg before surgery and 116+/-93 mg 3 months after surgery. Polysomnography (PSG) with audiovisual recordings was performed on two separate nights, the first assessment in the week before surgery and the second 3 months after surgery. Three months after surgery, PSG showed an increase in total sleep time, in the longest period of uninterrupted sleep, and in the percentage of stage 3-4 NREM sleep, while there was a reduction of wakefulness after sleep onset. PLM, apnea-hyopnea index and REM sleep behaviour disorder were unaffected by STN DBS. STN DBS seems to be an effective therapeutic option for the treatment of advanced Parkinson's disease because it improves the cardinal symptoms and also seems to improve sleep architecture.
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PMID:Effects of deep brain stimulation of the subthalamic nucleus on sleep architecture in parkinsonian patients. 1503 45

Parkinson's disease is a progressive disorder of the central nervous system. Degeneration of the dopaminergic neurons is the main cause of the disease. The basic symptoms of Parkinson's disease are bradykinesia, rigidity and resting tremor. Disturbances of the autonomous nervous system, depression, dementia and sleep disorders are common, too. People with Parkinson's disease suffer from insomnia, excessive daytime sleepiness, "sleep attacks", nightmares, REM sleep behaviour disorder, periodic limb movement in sleep, restless legs syndrome and sleep apnea syndrome. The main cause of sleep disorders in Parkinson's disease are age-connected changes in sleep architecture, disturbances of neurotransmission, movement disturbances in sleep, medications and concomitant diseases. The authors present the current state of knowledge on sleep disorders in Parkinson's disease, especially, the role of dopaminergic therapy, methods of diagnostics and treatment as well as the influence of sleep disturbances on patient's quality of life.
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PMID:[Sleep disturbances in Parkinson's disease]. 1627 62

Although normal subjects do not move during REM sleep, patients with Parkinson's disease may experience REM sleep behaviour disorder (RBD). The characteristics of the abnormal REM sleep movements in RBD have, however, not been studied. We interviewed one hundred consecutive non-demented patients with Parkinson's disease and their bed partners using a structured questionnaire assessing the presence of RBD. They rated the quality of movements, voice and facial expression during RBD as being better, equal or worse than in awake ON levodopa condition. Night-time sleep and movements were video-monitored during polysomnography in 51 patients to evaluate the presence of bradykinesia, tremor and hypophonia during REM sleep. Fifty-nine patients had clinical RBD with 53/59 bed partners able to evaluate them. All 53 (100%) reported an improvement of at least one component of motor control during RBD. By history, movements were improved in 87% patients (faster, 87%; stronger, 87%; smoother, 51%), speech was better in 77% patients (more intelligible, 77%; louder, 38%; better articulated, 57%) and facial expression was normalized in 47% patients. Thirty-eight per cent of bed partners reported that movements were 'much better', even in the most disabled patients. The video-monitored purposeful movements in REM sleep were also surprisingly fast, ample, coordinated and symmetrical, without obvious sign of parkinsonism. The movements were, however, jerky, violent and often repetitive. While all patients had asymmetrical parkinsonism when awake, most of the time they used the more disabled arm, hand and leg during the RBD (P = 0.04). Movements involved six times as often the upper limbs and the face as the lower limbs (OR: 5.9, P = 0.004). The percentage of time containing tremor EMG activity decreased with sleep stages from 34.9 +/- 15.5% during wakefulness, to 3.6 +/- 5.7% during non-REM sleep stages 1-2, 1.4 +/- 3.0% during non-REM sleep stages 3-4, and 0.06 +/- 0.2% during REM sleep (in this last case, it was subclinical tremor). The restored motor control during REM sleep suggests a transient 'levodopa-like' reestablishment of the basal ganglia loop. Alternatively, parkinsonism may disappear by REM sleep-related disjunction between pyramidal and extrapyramidal systems. We suggest the following model: the movements during the RBD would be generated by the motor cortex and would follow the pyramidal tract bypassing the extrapyramidal system. These movements would eventually be transmitted to lower motor neurons because of brainstem lesions interrupting the pontomedullary pathways which mediate the REM sleep atonia.
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PMID:Restoration of normal motor control in Parkinson's disease during REM sleep. 1723 26

The International Classification of Sleep Disorders (ICSD-2) has separated sleep-related movement disorders into simple, repetitive movement disorders (such as periodic limb movements in sleep [PLMS], sleep bruxism, and rhythmic movement disorder) and parasomnias (such as REM sleep behavior disorder and disorders of partial arousal, e.g., sleep walking, confusional arousals, night terrors). Many of the parasomnias are characterized by complex behaviors in sleep that appear purposeful, goal directed and voluntary but are outside the conscious awareness of the individual and therefore inappropriate. All of the sleep-related movement disorders described here have specific polysomnographic findings. For the purposes of developing and/or revising specifications and polysomnographic scoring rules, the AASM Scoring Manual Task Force on Movements in Sleep reviewed background literature and executed evidence grading of 81 relevant articles obtained by a literature search of published articles between 1966 and 2004. Subsequent evidence grading identified limited evidence for reliability and/or validity for polysomnographic scoring criteria for periodic limb movements in sleep, REM sleep behavior disorder, and sleep bruxism. Published scoring criteria for rhythmic movement disorder, excessive fragmentary myoclonus, and hypnagogic foot tremor/alternating leg muscle activation were empirical and based on descriptive studies. The literature review disclosed no published evidence defining clinical consequences of excessive fragmentary myoclonus or hypnagogic foot tremor/alternating leg muscle activation. Because of limited or absent evidence for reliability and/or validity, a standardized RAND/UCLA consensus process was employed for recommendation of specific rules for the scoring of sleep-associated movements.
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PMID:The scoring of movements in sleep. 1755 25

On the French West Indian island of Guadeloupe, atypical parkinsonian patients represent two-thirds of all cases of parkinsonism, which is exceptionally frequent compared to epidemiological data from European countries where atypical parkinsonism accounts for only approximately 5% of all cases. The clinical entity was a unique combination of levodopa-resistant parkinsonism, tremor, myoclonus, hallucinations, REM sleep behavior disorder and fronto-subcortical dementia. Based on the presence or the absence of supranuclear gaze palsy, two subgroups of patients were distinguished. In patients with oculomotor signs that came to autopsy, neuronal loss was found to predominate in the substantia nigra and the striatum but other brain areas were also affected, including the frontal cortex. In addition, tau-containing lesions were detected throughout the brain. Epidemiological data suggested a close association of the disease with the regular consumption of soursop, a tropical annonaceous plant. Experimental studies performed in midbrain cell cultures identified annonacin, a selective mitochondrial complex I inhibitor contained in the fruit and leaves of soursop, as a probable etiological factor. Consistent with this view, chronic administration of annonacin to rats through Alzet osmotic minipumps showed that annonacin was able to reproduce the brain lesions characteristic of the human disease.
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PMID:Atypical parkinsonism in the Caribbean island of Guadeloupe: etiological role of the mitochondrial complex I inhibitor annonacin. 1881 93

Rapid eye movement sleep behavior disorder (RBD) is commonly accompanied in Parkinson disease (PD). However, the underlying mechanism linking RBD to PD remains unclear. We interviewed and examined 447 consecutive patients with PD to investigate factors associated with the presence of RBD in PD patients. Using the minimal diagnostic criteria for parasomnias provided in the International Classification of Sleep Disorders-Revised (ICSD-R), 164 patients (36.5%) were diagnosed with clinically probable RBD (cpRBD). PD patients with cpRBD were older, had a longer duration of PD, a more severe level of disability, a longer duration of antiparkinsonian medication, and a lower proportion of their Unified Parkinson Disease Rating Scale (UPDRS) scores accounted for by tremor than those without RBD. Multivariate and univariate logistic regression analyses revealed that patient age, PD symptom duration (and, accordingly, more severe motor disability), tremor score, and proportion of the UPDRS score accounted for by tremor were significant factors associated with the presence of RBD in PD patients. The results of the present study support previous observations that PD with RBD may result from a different underlying pattern of neurodegeneration than PD without RBD.
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PMID:Factors related to clinically probable REM sleep behavior disorder in Parkinson disease. 1971 33

Parkinson's disease is the second most common neurodegenerative disorder, after Alzheimer's disease. It predominantly affects the elderly. Age is the most clearly established risk factor and there is a male:female ratio of 1.5:1. Current incidence in the general population is 8.4-19 per 100,000 population per year with an approximate prevalence of 120 per 100,000 population. NICE recommends that patients with suspected Parkinson's disease should be referred untreated to a specialist with expertise in parkinsonian disorders. The diagnosis is primarily clinical. Parkinson's disease should be suspected in all patients presenting with bradykinesia (which is essential for the diagnosis of any form of parkinsonism, including Parkinson's disease), muscular rigidity, resting tremor (4-6 Hz) and postural instability not caused by a primary visual, vestibular, cerebellar, or proprioceptive dysfunction. At present, there are no specific biochemical, imaging or genetic tests to assist in the diagnosis of Parkinson's disease. Structural brain imaging (MRI or CT) has no role in the diagnosis of Parkinson's disease but may be useful to exclude cerebrovascular disease, hydrocephalus and Wilson's disease in selected cases. Parkinson's disease is a condition that results in both motor and non-motor symptoms. Morbidity associated with non-motor symptoms in Parkinson's disease is becoming increasingly recognised and some non-motor symptoms such as hyposmia, apathy, depression and REM sleep behaviour disorder may precede the onset of motor symptoms.
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PMID:Non-motor symptoms may herald Parkinson's disease. 1987 55

Autonomic dysfunction is common in Lewy body disorders (Parkinson's disease, Dementia with Lewy Bodies, Pure Autonomic Failure, and REM sleep disorder). The loss of post-ganglionic myocardial sympathetic nerve fibers is a prominent feature of autonomic dysfunction in such disorders. (123)I-metaiodobenzylguanidine (MIBG) scintigraphy that visualizes catecholaminergic terminals in vivo is a biomarker used to detect cardiac sympathetic degeneration. Abnormal MIBG uptake has been consistently reported in Lewy body disorders. Some studies agree in the notion that increasing bradykinesia is related with an incremental cardiac sympathetic denervation, whereas tremor is not closely linked to cardiac denervation. "Atypical" parkinsonian syndromes, including Multiple System Atrophy, Progressive Supranuclear Palsy, and others, show modest reductions of cardial MIBG uptake. MIBG scintigraphy is moderately sensitive and specific in differentiating Parkinson's disease from such syndromes. Conversely, its sensitivity and specificity might be better in cognitively impaired patients, helping differential diagnosis between Dementia with Lewy Bodies, and Alzheimer disease. Confounding factors (comorbidities, comedications) should be carefully controlled before analyzing MIBG scintigraphy.
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PMID:123I-metaiodobenzylguanidine scintigraphy in Parkinson's disease and related disorders. 1987 2

Parkinson's disease (PD) is the second most common neurodegenerative disease and primarily considered as a movement disorder defined by the presence of motor symptoms, such as bradykinesia, tremor and rigidity. However, it is nowadays widely recognized that in addition there is impairment of cognitive function, mood and the autonomic nervous system in a high percentage of PD patients, which is sometimes even more harming quality of life. These symptoms not only occur during the course of the disease but may even precede the onset of motor symptoms. Typical examples of non-motor features of PD are depression, constipation, REM sleep behaviour disorder, and hyposmia.
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PMID:Non-motor features of Parkinson's disease: depression and dementia. 2008 17


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