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

To study the neurological sequelae in liver transplanted recipients, 25 patients were followed up between 5 and 30 months after transplantation and another 14 patients were seen before and after transplantation. Physical examination took special note of tremor and polyneuropathy; additionally, patients estimated concentration and memory, tremor, paraesthesias and sleep disturbances on a self-rating scale. Tremor was reported to be preexistent in 50% of the later FK 506 and cyclosporin group and only temporarily rose afterwards. Twenty-eight percent complained of tremor and 20% said that it interfered mildly with daily activity. Only 2 of 39 patients showed new signs of polyneuropathy. Concentration and memory improved significantly after transplantation. In the second group of patients, MRI, EEG, lumbar puncture and neuropsychological tests were done just before and routinely after transplantation, revealing numerous preexisting neurological deficits with only singular changes afterwards.
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PMID:Neurological examinations after liver transplantation concerning patients under corticosteroid immunosuppression and either FK 506 or cyclosporin. 1127 Dec 73

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

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 significant number of patients with terminal cancer experience terminal restlessness or an agitated delirium in the final days of life. Multifactorial etiologies may contribute to agitation and restlessness for any one patient; alcohol withdrawal may be underrated as a contributing factor. The symptoms and signs of alcohol withdrawal--autonomic dysfunction, tremor, anxiety, sleep disturbances, insomnia, and abnormal vital signs--may continue for 6 to 12 months after the cessation of alcohol. We report four patients with terminal restlessness in whom we believe alcohol withdrawal to be a significant causal factor and a fifth patient who subsequently benefited from our team's increased awareness of this clinical problem. Formal assessment of alcohol withdrawal may be of more value in the palliative setting than using the currently accepted assessment instruments. Many of the medications utilized for the treatment of agitated delirium and terminal restlessness in the palliative care setting are effective therapies for alcohol withdrawal.
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PMID:Alcohol withdrawal as an underrated cause of agitated delirium and terminal restlessness in patients with advanced malignancy. 1565 44

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

Atypical antipsychotics may be useful in chronic pain treatment. The objective of the present study was to assess the effect of ziprasidone in fibromyalgia management. Ziprasidone was administered to 32 fibromyalgia patients at a dose of 20 mg/day, subsequently adjusted according to clinical response and tolerability. Fibromyalgia Impact Questionnaire (FIQ), Pittsburgh Sleep Quality Index (PSQI), a Clinical Global Impression improvement scale (CGIi), and a scale evaluating the severity of fibromyalgia symptoms were administered at 4 week intervals for 12 weeks. Drug adverse reactions were recorded. Ten patients withdrew from the study. The CGIi showed 32% of responders. FIQ and PSQI scores showed a non-statistically significant decrease. The conditions of stiffness, anxiety and sadness improved significantly. Most frequent side effects included sleep disturbances, headache, tremor, and rigidity. Although ziprasidone does not seem an especially useful adjunct drug in fibromyalgia, it could be tried on patients who are markedly anxious and/or depressed.
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PMID:Use of ziprasidone in patients with fibromyalgia: a case series. 1703 63

We report on three patients with MeCP2 mutation and male Rett phenotypes. Two brothers with T158M mutations and normal karyotype had a severe early onset encephalopathy, progressive microcephaly, severe feeding problems, breathing and sleep disturbances. They died at the ages of 1 year and 8 months, and 3 years and 1 month. This mutation has previously been reported in three males. The phenotypes show a strong resemblance, and might in fact represent a clinical-genetic entity of the T158M mutation within the complex of congenital encephalopathies in males with MeCP2 mutations. We also report a 3-year-old boy with a R294X mutation, normal karyotype, and a more protracted course. He was inactive and sucked poorly from start. The head growth decelerated from the age of 6 months and the feeding problems increased requiring gastrostomy. He had a rapid deterioration period at 2 years and lost sitting and hand grasping functions. He had prolonged periods with tremor and epileptic myoclonus, shifting tonus, and dystonic extension of the trunk and legs, bruxism, and irregular breathing. He was clinically stable with preserved visual and emotional contact function by the age of four years. None of the boys had dysmorphic features.
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PMID:Male Rett phenotypes in T158M and R294X MeCP2-mutations. 1723 9

In the field of neurology, Parkinson's disease (PD) is commonly perceived to be a disorder affecting only the (extrapyramidal) motor system, characteristically manifesting as bradykinesia, rigidity, tremor and postural instability. Although non-motor symptoms such as behavioural abnormalities, dysautonomia, sleep disturbances and sensory dysfunctions are also common and quite disabling manifestations of the disease, they are often not formally assessed and thus are frequently misdiagnosed and/or under diagnosed. For this reason, in this review we have concentrated on the pathophysiological and clinical basis of non-motor involvement such as olfactory dysfunction, depression, dementia, dysautonomia and sleep disorders in PD. The early recognition of these symptoms may well perhaps lead to an earlier diagnosis of PD, but in any case should lead to more prompt and effective treatment of the relatively unrecognized non-motor problems associated with PD.
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PMID:Non-motor dysfunction in Parkinson's disease. 1734 13

Several observations suggest a beneficial effect of melatonin antagonism for Parkinson's disease (PD). Although bright light therapy (BLT) suppresses melatonin release and is an established treatment for depression and sleep disturbances, it has not been evaluated in PD. We examined effects of BLT on motor symptoms, depression, and sleep in PD in a randomized placebo-controlled double-blind study in 36 PD patients, using Parkinson's Disease Rating Scale (UPDRS) I-IV, Beck's Depression Inventory, and Epworth Sleepiness Scale. All patients received BLT for 15 days in the morning, 30 min daily. Illuminance was 7.500 lux in the active treatment group and 950 lux in the placebo group. Although group differences were small, BLT led to significant improvement of tremor, UPDRS I, II, and IV, and depression in the active treatment group but not in the placebo group. It was very well tolerated. Follow up studies in more advanced patient populations employing longer treatment durations are warranted.
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PMID:Bright light therapy in Parkinson's disease: a pilot study. 1751 92


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