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)

Depression, dementia, and physiologic changes contribute to the high prevalence of sleep disturbances in patients with Parkinson's disease (PD). Antiparkinsonian drugs also play a role in insomnia by increasing daytime sleepiness and affecting motor symptoms and depression. Common types of sleep disturbances in PD patients include nocturnal sleep disruption and excessive daytime sleepiness, restless legs syndrome, rapid eye movement sleep behavior disorder, sleep apnea, sleep walking and sleep talking, nightmares, sleep terrors, and panic attacks. A thorough assessment should include complete medical and psychiatric histories, sleep history, and a 1- to 2-week sleep diary or Epworth Sleepiness Scale evaluation. Polysomnography or actigraphy may also be indicated. Treatment should address underlying factors such as depression or anxiety. Hypnotic therapy for sleep disturbances in PD patients should be approached with care because of the risks of falling, agitation, drowsiness, and hypotension. Behavioral interventions may also be useful.
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PMID:Sleep disorders in Parkinson's disease. 1525 35

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

Restless legs syndrome (RLS) symptoms are often reported in Parkinson's disease (PD), but prevalence studies of RLS in PD are few and the results are inconsistent. In addition, clinical overlapping between RLS, "wearing-off"-related lower limb discomfort and restlessness, and akathisia complicate the clinical assessments of true RLS in PD. Underlying pathophysiology potentially shared by RLS and PD is mainly suggested by similarities in treatment response. Functional imaging studies in RLS are still inconclusive, although some authors have found subtle deficits in nigrostriatal terminal function. Long-term prospective studies of RLS cohorts will clarify whether or not RLS is associated with an increased risk for development of PD.
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PMID:Akathisia, restless legs and periodic limb movements in sleep in Parkinson's disease. 1550 35

A new mechanism has been recently proposed, whereby melatonin may participate in the ongoing process of neuronal degeneration in models of neurodegenerative disorders, such as Parkinson's disease (PD). Antagonism of the melatonin receptor in rats using constant light or pinealectomy induced recovery and reduced the mortality typically associated with dopamine (DA) degeneration. In additional studies, employing ML-23 in the 6-OHDA-treated rat, remission from experimental PD was achieved using this drug in a post 6-OHDA treatment regime. To permit the further assessment of ML-23 as a potential clinical candidate for the treatment of PD, the present study was undertaken to determine the efficacy of ML-23 in the 1-methyl-4-phenyl, 1,2,3,6 tetrahydropyridine (MPTP) model in the common marmoset. ML-23 was administered orally in a dose of 3 mg/kg twice daily to half of the animals, while the other half received vehicle only, in a blinded protocol, for 56 days. The effects of the treatment on positive and negative features of MPTP-induced PD were assessed, including horizontal and vertical movement, head checking, general behaviour and Parkinsonian condition, raisin board performance, the ability to remove a foot label, palatable and dry food intake, water consumption, bradykinaesia, and the positive symptoms of tremor, obstinate progression, and agitation. On all parameters, ML-23 produced a significant remission from MPTP-induced Parkinsonism, and this effect did not abate when ML-23 treatment was withdrawn. In a further pilot study involving a crossover of two animals, one animal treated previously with MPTP plus vehicle showed some remission of negative and positive features, although ML-23 treatment was not commenced until 8 weeks post-MPTP. Conversely, a recurrence of Parkinsonian signs was not observed when ML-23 treatment was withdrawn and substituted with oral vehicle. Dopamine transporter was severely impaired in all marmosets treated with ML-23 or vehicle for the duration of the study. These results suggest that a novel mechanism involving melatonin is involved in the primary aetiology of the chronic aspects of PD, and such a mechanism is not related to the antioxidative function of this hormone. From these preliminary results, it is concluded that ML-23 and other melatonin analogues have an important role to play in the treatment and clinical management of Parkinson's disease.
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PMID:Recovery from experimental Parkinson's disease in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride treated marmoset with the melatonin analogue ML-23. 1565 76

The frequency, phenomenology, and risk factors of hallucinations and delusions were investigated in 64 consecutive inpatients with Parkinson's disease. Fifty patients were admitted to our hospital with symptoms related to Parkinson's disease: psychiatric problems 27 (psychosis 22; anxiety 2; depression 2; mania 1): motor symptoms, 20 (wearing-off 5; akinesia 4; freezing 4; postural instability 4; dyskinesia 2; tremor 2; dystonia 1), and sensory symptoms, 3. Fourteen patients were admitted with other medical problems (pneumonia 4; cerebral infarction 3; bone fracture 3; lumbago 2; seizure 1; cat bite 1). Totally 49 patients had psychiatric problems. Psychosis was present in 43 patients, dementia in 10, depression in 8, mania in 1, anxiety in 10, agitation in 6, stereotypy in 2, and hypersexuality in 2. Of the 43 patients with psychoses, 40 presented with visual hallucinations, 18 with auditory hallucinations, and 23 with delusions. To determine what the clinical correlates with the severity of psychosis were, we divided the patients into 3 groups: the severe group, 22 patients admitted because of psychotic symptoms; the mild group, 21 patients admitted because of problems other than psychosis but presenting psychotic symptoms; and the control group, 21 patients who had no psychotic symptoms. Incidences of auditory hallucinations and delusions were higher in the severe group as compared to the mild group. Patients in the severe group had higher Hoehn-Yahr stages, lower Mini-Mental State Examination scores, decreased H/M ratios of cardiac 123I-MIBG uptake, and lower frequencies of background activity on electroencephalograms. There were no differences in age at admission, age at onset of Parkinson's disease, duration of illness, amounts of levodopa and dopamine agonists received, Hamilton's depression rating scores, and brain MR findings, including atrophy and ischemic changes. Emergence of psychotic symptoms in parkinsonian patients appears to be clearly associated with impaired cognitive function. Therefore, it may be associated with the disease process itself. Terms such as dopaminomimetic or levodopa-induced psychosis may not be appropriate when describing psychosis in Parkinson's disease.
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PMID:[Psychoses in patients with Parkinson's disease; their frequency, phenomenology, and clinical correlates]. 1571 92

This is a report on a case series of five patients with psychosis in Parkinson's disease who were treated successfully with an intramuscular injection of ziprasidone (10-20 mg) for acute agitation. No deterioration of motor function or other clinically relevant side effects were seen.
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PMID:Parenteral ziprasidone: a new atypical neuroleptic for emergency treatment of psychosis in Parkinson's disease? 1579 11

There are reports that melatonin secretion from the pineal gland gradually diminishes with advancing age. It has been suggested that various forms of neuropsychiatric disease, in particular, Parkinson's disease (PD), is consequentially related to this decrease by virtue of increased oxidative stress which enhances the process of dopamine (DA) degeneration. There is, however, considerable disagreement on this theme as very little is generally known about the role of the pineal gland in the aetiology and treatment of PD. To assess the role of the pineal gland in PD and in dopamine replacement therapy (DART), the effect of three anti-Parkinsonian drugs on motor and psychiatric function was assessed in normal, pinealectomized (PX) and DA deficient, PX rats. In the first study, rats underwent PX or sham operation and were then injected (IP) with Amantadine (30 or 50 mg/kg), Bromocriptine (5 or 10 mg/kg) or L-Dopa (30 or 60 mg/kg plus 50 mg/kg of R-044602) 3-8 weeks after surgery. Open field performance and motor reflex tests were assessed during the light and dark phases of the L/D cycle. In a second study, clinically effective doses of Bromocriptine (10 mg/kg) and L-Dopa (30 and 100 mg/kg with 50 mg/kg R-044602) were injected into depleted, PX or sham operated rats. In study I, sham operated and PX rats responded differently to Bromocriptine and L-Dopa, while Amantadine did not differentially effect motor performance in the two groups. In study II, 6-OHDA induced degeneration of the nigro-striatal system abolished the effects of Bromocriptine and dramatically altered the effects of L-Dopa seen in study I, in sham operated versus PX rats. DART significantly altered emotionality, as measured by escape attempts, agitation and rage in sham operated animals, compared to PX rats. DA deficiency abolished the tendency to escape in all groups except those treated with 100mg/kg of L-Dopa. Conversely, agitation and rage scores were greater after 100 mg/kg of L-Dopa, in rats with intact pineal function, than in PX rats. These results provide compelling evidence that altered pineal function plays a major role in the aetiology of PD, the therapeutic effect of anti-Parkinsonian drugs and in the psychiatric side effects of DART.
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PMID:The therapeutic effects of dopamine replacement therapy and its psychiatric side effects are mediated by pineal function. 1583 10

Psychotic symptoms are common in Parkinson's disease (PD) and occur in at least 20% of medication-treated patients. Benign visual hallucinations usually appear earlier, while malignant hallucinations, confusional states, delusions, paranoid beliefs, agitation, and delirium become more frequent with disease progression. Virtually all antiparkinsonian drugs may produce psychotic symptoms. Cognitive impairment, increased age, disease duration and severity, depression, and sleep disorders have been consistently identified as independent risk factors for their development. Although the precise pathoetiologic mechanisms remain unknown, we review evidence that links ventral dopaminergic pathway dysfunction (overactivity) together with the involvement of other neurotransmitter system imbalances as likely contributors. The clinical importance of the proposed mechanism is that successful management of psychotic symptoms in PD may rely on a multitarget approach to restore neurotransmitter imbalances rather than focusing exclusively on the dopaminergic dysfunction.
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PMID:Psychotic symptoms in Parkinson's disease. From description to etiology. 1599 34

Parkinson's disease is a neurodegenerative disorder causing not only motor dysfunction but also cognitive, psychiatric, autonomic and sensory disturbances. Symptoms of dementia and psychosis are common: longitudinal studies suggest that up to 75% of patients with Parkinson's disease may eventually develop dementia, and the prevalence of hallucinations ranges from 16-17% in population-based surveys to 30-40% in hospital-based series. These cognitive and behavioural features are important in terms of prognosis, nursing home placement and mortality. The pattern of cognitive deficits in Parkinson's disease is variable, but often includes executive impairment similar to that seen in patients with frontal lesions, as well as episodic memory impairment, visuospatial dysfunction and impaired verbal fluency. The most common manifestation of psychosis in Parkinson's disease is visual hallucinations, but delusions, paranoid beliefs, agitation and florid psychosis can also occur. An understanding of the pathophysiology underlying these symptoms is essential to the development of targeted therapeutic strategies. Post-mortem studies suggest an association between Lewy body deposition and dementia in Parkinson's disease, and indeed Parkinson's disease and dementia with Lewy bodies may form part of the same disease spectrum. Whether Lewy bodies actually play a causative role in cognitive dysfunction, however, is unknown. Deficits in neurotransmitter systems provide more obvious therapeutic targets and dysfunction of dopaminergic, cholinergic, noradrenergic and serotonergic systems have all been implicated; these may each underlie different features of Parkinson's disease dementia, perhaps explaining some of the heterogeneity of the syndrome. Psychosis has traditionally been considered as a dopaminergic drug-induced phenomenon, but factors intrinsic to the disease process itself also cause hallucinations and delusions. These factors may include Lewy body deposition in the limbic system, cholinergic deficits and impairments of primary visual processing. Therapeutic intervention for cognitive and behavioural symptoms in Parkinson's disease currently focuses on two main groups of drugs: cholinesterase inhibitors and atypical antipsychotics. A recent large, randomised, controlled trial suggests that cholinesterase inhibitors can produce a modest improvement in cognitive function, as well as psychotic symptoms, generally without an adverse effect on motor function. Certain atypical antipsychotics allow hallucinations, delusions and behavioural problems to be brought under control with minimal deleterious effects on motor function and cognition, but their safety in elderly patients has recently been called into question. Deep brain stimulation does not appear to be a useful treatment for cognitive and psychiatric dysfunction in patients with Parkinson's disease. Modafinil improves alertness in Parkinson's disease and warrants further investigation to establish its effects on cognitive performance.
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PMID:Cognitive deficits and psychosis in Parkinson's disease: a review of pathophysiology and therapeutic options. 1673 99

We report three cases of patients with Parkinson's disease without dementia, admitted to our hospital because of hallucinations. The anti-Parkinson medication was adapted and the patients started with rivastigmine. As a result, hallucinations no longer occurred. A 79 years old man also required short-term quetiapine because of agitation and anti-Parkinson doses were without side effects, as a result of which mobility improved. An 84 years old woman reported mild side effects of rivastigmine, without consequences, whereas her mobility appeared to be good. A 72 years old woman reported mild memory problems upon admission, which improved during admission, as did her mobility after increasing the anti-Parkinson medication doses. Treatment of rivastigmine can be useful in the therapeutic dilemma in the treatment of hallucinations in patients with Parkinson's disease (start anti-psychotic or reduce anti-Parkinson medication). In addition to adapting anti-Parkinson doses and sometimes short-term treating with an anti-psychotic, treatment with rivastigmine appears to be a quick improvement, without serious side effects. Also, mobility can improve, due to the possibility of increasing the anti-Parkinson doses, if necessary. Because of the many remaining questions, prospective randomised trials are needed.
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PMID:[Rivastigmine as adjunctive therapy in the therapeutic dilemma for the treatment of hallucinations due to Parkinson disease]. 1688 19


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