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)

Sleep problems are an under-emphasised cause of disability in Parkinson's disease (PD) and may be seen independently of PD, associated with primary PD pathology, or as a result of antiparkinsonian medications. Common sleep disorders include excessive daytime sleepiness, rapid eye movement (REM) sleep behaviour disorder, night-time wakefulness and restless legs syndrome. A number of strategies may be used to improve sleep cycle disturbances, and often these interventions do not require pharmacological manipulation. Restoring traditional mealtimes and scheduling activities during predicted periods of sleepiness may help alleviate daytime somnolence; the use of controlled-release levodopa preparations or administration of a catechol-O-methyl transferase (COMT) inhibitor with levodopa at bedtime may reduce periods of night-time wakefulness. Administration of clonazepam at bedtime may assist with REM sleep behaviour disorder but, because this agent can result in daytime somnolence, experimentation with dosage times is recommended. Sleep attacks are described as a sudden, unavoidable transition from wakefulness to sleep and, although rare, have been described with pramipexole, ropinirole and other dopamine agonists. Although the condition has yet to be recognised by the International Association of Sleep Disorders, patients with PD who report rapid sleep onset should be evaluated for the possibility of sleep attacks. If sleep attacks are suspected, it is reasonable to strongly caution patients regarding potentially risk-associated activities such as driving, and to consider careful withdrawal of dopaminergic therapy.
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PMID:Sleep disorders in Parkinson's disease: epidemiology and management. 1239 50

While optimal treatment strategies are widely established for daytime treatment of Parkinson's disease (PD), nighttime problems of PD are often not adequately addressed in clinical practice. Nocturnal/sleep disturbance is common in PD and occurs due to a combination of the disease process and effect of dopaminergic and other treatments. The role of dopamine and other neuropeptides such as hypocretin is being investigated in the causation of sleep problems in PD. The impact of sleep dysfunction in PD on daytime fatigue and sleepiness is also being explored as such issues have important implications. The recently described Parkinson's disease sleep scale aims to measure the causes of sleep dysfunction in PD in a semi-quantitative manner and using this scale we have shown that sustained dopaminergic stimulation initiated at bedtime may help with improving motor symptoms at night and secondarily improve sleep and daytime functioning in PD.
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PMID:The basis for day and night-time control of symptoms of Parkinson's disease. 1246 20

We assessed the prevalence and risk factors for irresistible daytime sleepiness (IDS) in a cohort of patients with Parkinson's disease (PD) treated with dopamine agonists. Seventy consecutive PD patients on dopamine agonists were interviewed. IDS was experienced by 24 patients (34.3%). Fifty percent of the pramipexole patients, 15.4% of the pergolide patients, 23.1% of the ropinirole patients and the 2 patients on bromocriptine experienced IDS. Patients who experienced IDS were younger (p = 0.009). Nineteen patients had IDS while driving, 3 sustained a motor vehicle crash. Daytime somnolence (p = 0.05) and early arousals (p = 0.001) were risk factors and daytime napping (p = 0.007) and benzodiazepines (p = 0.006) were protective. Improvement was achieved by changing the dosing schedule, the amount of agonist per dose, discontinuing the agonist or accommodating the sleepiness. We conclude that dopamine agonists are commonly implicated in IDS.
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PMID:Dopamine agonists induce episodes of irresistible daytime sleepiness. 1246 15

Continuous subcutaneous infusion of apomorphine is now increasingly recognized as an effective treatment for refractory off periods and peak-dose dyskinesias in Parkinson's disease. We have reviewed our experience with apomorphine infusions, after a strategy decision in 1995 based on emerging preclinical data, to treat all patients with steady-state plasma levels of apomorphine throughout the waking day, minimizing additional pulsatile stimulation either by oral dopaminergic medication or bolus parenteral injections of apomorphine. Sixty-four patients have been treated with apomorphine pumps and 45 of these successfully converted to monotherapy, managing to discontinue all other forms of dopaminergic stimulation during the daytime treatment period with apomorphine. Patients were followed up for a mean of 33.8 months (range, 4-108 months) and clinical data analyzed retrospectively. The mean maintenance dose of apomorphine was 98 mg per 24 hours (monotherapy group: 103 mg/24 hours; polytherapy group: 93 mg/24 hours), which did not significantly increase at final follow-up. There was a mean maximum dyskinesia reduction of 64% (S.D. = 20) in the monotherapy group, compared to 30% (S.D. = 33) in those continuing on polytherapy (P < 0.001), despite a maintained increase in on time (monotherapy group: 55%, P < 0.005; polytherapy group: 50%, P = 0.05). Fifteen patients failed to successfully convert to monotherapy but benefited nonetheless, and only 3 failed apomorphine infusional therapy altogether. Reasons for failure were mixed, including difficulty with compliance and adverse effects such as daytime somnolence, skin complications, and painful dystonias. There was a significantly higher success rate in patients able to manage the treatment either independently or with the help of their caregiver. These results confirm that subcutaneous apomorphine monotherapy can reset peak-dose dyskinesia threshold in levodopa-treated patients and further reduce off-period disability after all available forms of oral medication, including long-acting dopamine agonists, have been tried.
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PMID:Apomorphine monotherapy in the treatment of refractory motor complications of Parkinson's disease: long-term follow-up study of 64 patients. 1246 62

YAWNING IS A COMMON PHYSIOLOGICAL EVENT THAT CAN BE DIVIDED INTO THREE DISTINCT PHASES: a long inspiratory phase, a brief acme and a rapid expiration. The aim of yawning is not yet well defined. However this semi-voluntary event increases vigilance and aims to alert when drowsiness occurs. Yawning probably has an important role for social communication as well. Yawning can be responsible for pain, luxation or even transient ischaemic attack. Abnormal yawning is present in various pathologies: migraine, Parkinson's disease, tumours, psychiatric diseases, infections or iatrogenic pathologies. The neuro-pharmacology of yawning is complex and knowledge of its mechanisms is incomplete. While under the control of several neurotransmitters, yawning is largely affected by dopamine. Dopamine may activate oxytocin production in the paraventricular nucleus of the hypothalamus. Oxytocin may then activate cholinergic transmission in the hippocampus and, finally, acetylcholine might induce yawning via the muscarinic receptors of the effectors. This is an over-simplification; many other molecules can modulate yawning, such as nitric oxide, glutamate, GABA, serotonin, ACTH, MSH, sexual hormones and opium derivate peptides. Dopamine involvement in yawning could have practical applications in the study of new drugs or the exploration of neurological diseases such as migraine or psychosis. 2001 Harcourt Publishers Ltd
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PMID:Yawning. 1253 Sep 94

Total sleep deprivation (TSD) for one whole night improves depressive symptoms in 40-60% of treatments. The degree of clinical change spans a continuum from complete remission to worsening (in 2-7%). Other side effects are sleepiness and (hypo-) mania. Sleep deprivation (SD) response shows up in the SD night or on the following day. Ten to 15% of patients respond after recovery sleep only. After recovery sleep 50-80% of day 1 responders suffer a complete or partial relapse; but improvement can last for weeks. Sleep seems to lead to relapse although this is not necessarily the case. Treatment effects may be stabilised by antidepressant drugs, lithium, shifting of sleep time or light therapy. The best predictor of a therapeutic effect is a large variability of mood. Current opinion is that partial sleep deprivation (PSD) in the second half of the night is equally effective as TSD. There are, however, indications that TSD is superior. Early PSD (i.e. sleeping between 3:00 and 6:00) has the same effect as late PSD given equal sleep duration. New data cast doubt on the time-honoured conviction that REM sleep deprivation is more effective than non-REM SD. Both may work by reducing total sleep time. SD is an unspecific therapy. The main indication is the depressive syndrome. Some studies show positive effects in Parkinson's disease. It is still unknown how sleep deprivation works.
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PMID:Therapeutic use of sleep deprivation in depression. 1253 Nov 27

The objective of this study was to monitor the long-term effect of clozapine administered to Parkinson's disease (PD) patients with psychosis. Confusion, visual hallucinations, and psychosis are major dose-limiting factors for long-term dopaminergic management of PD. Classic neuroleptic agents exacerbate the motor symptoms of the disease. For this reason, the introduction of atypical antipsychotic drugs has been a major advancement for the management of psychosis in patients with PD. Of them, clozapine is one of the most effective. Thirty-two patients (mean age, 73 years; mean disease duration, 12.2 years) with PD and psychosis (DSM-IV), 14 of them with dementia (DSM-IV), were followed for 5 years with periodic clinical evaluation, Mini Mental State Examination (MMSE), and Parkinsonian Psychosis Rating Scale (PPRS) administered before and following the study (at least once in 6 months). Periodic blood count was performed for tracking neutropenia. Nineteen patients (8 with dementia) have continued to receive clozapine (mean daily dose, 50 mg). Thirteen patients stopped medication: 9 because symptoms improved and did not return after weaning off clozapine; 3 patients because of somnolence; and 1 because of personal reasons. The average duration of treatment in those in whom medication was stopped was 8.5 months (range, 1-24 months). No correlation was found between age, sex, duration, and severity of disease (Yahr scoring), the presence of dementia, and the response to clozapine. Also, the PPRS scoring did not influence clozapine response. No case of neutropenia was found. According to the experience accumulated and the results of the present study, the authors believe clozapine is the best therapeutic choice currently available for the management of psychosis in patients with PD.
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PMID:Clozapine in Parkinson's disease psychosis: 5-year follow-up review. 1256 58

Disorders of sleep and daytime alertness are frequent in Parkinson's disease patients and arise from a number of diverse factors. The most common complaint of night-time sleep disturbance in Parkinson's disease is sleep fragmentation. Sleep fragmentation can be associated with recurrent parkinsonian symptoms, the effect of medications, concomitant medical disorders such as nocturia, or psychiatric disorders such as depression or anxiety. Likewise, nocturnal sleep disturbance may arise from sleep apnea, periodic limb movements of sleep, or rapid eye movement (REM) sleep behavior disorder. Nocturnal sleep deprivation may lead to excessive daytime sleepiness. Other potential sources of daytime sleepiness include the effects of medications or disruption of central sleep mechanisms due to the pathologic processes of Parkinson's disease itself. Diagnosis of sleep disturbances and daytime sleepiness requires a direct interview of the patient and the caregiver, and may involve consultation with the sleep specialist or medical physician. Treatment is aimed toward improving night-time sleep and daytime drowsiness by addressing the causative factors.
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PMID:Sleep disturbances in Parkinson's disease. 1258 48

Three patients with advanced Parkinson's disease, all of whom developed excessive daytime sleepiness and 'sleep attacks' after the administration of entacapone, are described. This is another demonstration that inappropriate daytime sleep episodes are not exclusive to dopamine agonists.
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PMID:Excessive daytime sleepiness and 'sleep attacks' induced by entacapone. 1258 37

The present article is meant to suggest an approach to the guidelines for the therapy of sleep disturbances in Parkinson's Disease (PD) patients.The factors affecting the quality of life in PD patients are depression, sleep disturbances and dependence. A large review of the literature on sleep disturbances in PD patients, provided the basis for the following classification of the sleep-arousal disturbances in PD patients. We suggest a model based on 3 steps in the treatment of sleep disturbances in PD patients. This model allowing the patient, the spouse or the caregiver a quiet sleep at night, may postpone the retirement and the institutionalization of the PD patient. I. Correct diagnosis of sleep disorders based on detailed anamnesis of the patient and of the spouse or of the caregiver. One week recording on a symptom diary (log) by the patient or the caregiver. Correct diagnosis of sleep disorders co morbidities. Selection of the most appropriate sleep test among: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), Epworth Sleepiness Scale, actigraphy or video-PSG. II. The nonspecific therapeutic approach consists in: a) Checking the sleep effect on motor performance, is it beneficial, worse or neutral. b) Psycho-physical assistance. c) Dopaminergic adjustment is necessary owing to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals, which alter the normal modulator mechanisms of the motor centers in PD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and NonREM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates PD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. The permanent adjustment according to the progression of the degenerative process of the disease will diminishe aggravation. The following types of sleep-arousal disturbances have to be considered in PD patients: - Sleep Disturbances, Light Fragmented Sleep (LFS), Abnormal Motor Activity During Sleep (AMADS), REM Behavior Disorders (RBD), Sleep Related Breathing Disorders (SRBD), Sleep Related Hallucinations (SRH), Sleep Related Psychotic Behavior (SRPB). - Arousal Disturbances, Sleep Attacks (SA), Excessive Daytime Sleepiness (EDS), Each syndrome has to receive a score according to its severity. III. The specific therapy consists in: LFS: Benzodiazepines & Nondiazepines. AMADS: Clonazepam, Opioid, Apomorphine infusion; RBD: Clonazepam and dopaminergic agonists; SRBD: CPAP, UPPP, nasal interventions, losing weight; SRH: Clozapine, Risperidone; SRPD: Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual PD patient.
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PMID:Sleep disturbances in Parkinsonism. 1258 74


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