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)

Seven patients with idiopathic Parkinson's disease, aged 62 to 76 years, average duration of the disease approximately eleven years, suffering from severe hallucinosis and paranoid delusions of different degree, in whom conventional therapeutic strategies (administration of benzodiazepines and mild neuroleptics) had no antipsychotic effect, received clozapine, a non-classical highly potent neuroleptic, while blood count was strictly monitored. Paranoid ideas disappeared in all seven patients after a maximum of four days administration of 25-125 mg/day. No deterioration of parkinsonian symptoms, quantified according to UPDRS was seen. Given the protection of clozapine, we could increase the L-dopa dose in two cases, thereby improving the patients' motor function. Blood count showed no abnormalities in any of the patients during an average observation period of seventeen months. Our results support the assumption that clozapine has a potent antipsychotic effect in the treatment of psychotic decompensation in advanced Parkinson's disease in carefully selected patients. We saw no negative influence of the neuroleptic on extrapyramidal symptoms.
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PMID:Therapeutic effect of clozapine in psychotic decompensation in idiopathic Parkinson's disease. 833 9

Recently distorted chromatic contour perception has been demonstrated in Parkinson's disease (PD). The aim of our study is to determine the clinical factors which influence chromatic contour perception in PD. Chromatic and achromatic contour perception, colour discrimination and clinical data were evaluated in 73 patients with PD. We used a computer-aided method to determine the chromatic fusion time (CFT) which indicates the acuity of monochromatic contour perception. Chromatic CFT was generally shortened in patients as compared to controls (p < 0.01), whereas achromatic CFT was not significantly different. Variance analysis revealed the ability of colour discrimination and the risk of visual hallucinations as statistically significant (p < 0.05) variables influencing contour perception of certain stimuli. In contrast, disease stage, disease duration and disease severity have no relevant effect on chromatic contour perception in Parkinson's disease. On the basis of those properties one may suggest that distorted chromatic contour perception is due to an impairment at a central stage of visual processing in PD and an imbalance of the serotonergic system. Whether CFT is a reliable method to predict the individual risk of hallucinosis in PD has to be evaluated.
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PMID:Visual hallucinosis: the major clinical determinant of distorted chromatic contour perception in Parkinson's disease. 901 6

We could quantify the tetrahydroisoquinoline derivative salsolinol in urine of patients with Parkinson's disease and normal control subjects by means of high performance liquid chromatography and electrochemical detection. Urine levels of salsolinol were positively related to the homovanillic acid/3-O-methyl-dopa ratio in the cerebrospinal fluid that reflects dopamine metabolism. In the patient group with visual hallucinations, mean salsolinol level was significantly increased to almost the 3-fold of those found in patients without hallucinations. Since the daily L-dopa doses of both patient groups were nearly identical this result is not due to different L-dopa medications. Additionally, either high values of the main serotonin metabolite, 5-hydroxyindole acetic acid (HIAA) or the L-dopa/3-O-methyl-dopa ratio were found in cerebrospinal fluid of patients with hallucinations. The enhanced salsolinol levels in patients with visual hallucinations seem to be due to an overloaded dopaminergic pathway with an imbalance between dopaminergic and serotonergic systems. Thus, salsolinol appears as a predictor for hallucinosis in Parkinson's disease.
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PMID:Salsolinol, catecholamine metabolites, and visual hallucinations in L-dopa treated patients with Parkinson's disease. 961 86

Complex visual hallucinations may affect some normal individuals on going to sleep and are also seen in pathological states, often in association with a sleep disturbance. The content of these hallucinations is striking and relatively stereotyped, often involving animals and human figures in bright colours and dramatic settings. Conditions causing these hallucinations include narcolepsy-cataplexy syndrome, peduncular hallucinosis, treated idiopathic Parkinson's disease, Lewy body dementia without treatment, migraine coma, Charles Bonnet syndrome (visual hallucinations of the blind), schizophrenia, hallucinogen-induced states and epilepsy. We describe cases of hallucinosis due to several of these causes and expand on previous hypotheses to suggest three mechanisms underlying complex visual hallucinations. (i) Epileptic hallucinations are probably due to a direct irritative process acting on cortical centres integrating complex visual information. (ii) Visual pathway lesions cause defective visual input and may result in hallucinations from defective visual processing or an abnormal cortical release phenomenon. (iii) Brainstem lesions appear to affect ascending cholinergic and serotonergic pathways, and may also be implicated in Parkinson's disease. These brainstem abnormalities are often associated with disturbances of sleep. We discuss how these lesions, outside the primary visual system, may cause defective modulation of thalamocortical relationships leading to a release phenomenon. We suggest that perturbation of a distributed matrix may explain the production of similar, complex mental phenomena by relatively blunt insults at disparate sites.
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PMID:Complex visual hallucinations. Clinical and neurobiological insights. 979 40

The atypical antipsychotic drug olanzapine has been proposed for treatment of dopaminergic psychosis in Parkinson's disease (PD). We report on a 68-year-old patient who developed a severe akinetic-rigid extrapyramidal syndrome, accompanied by additional paranoid symptoms, following olanzapine treatment of optic hallucinosis in PD. Olanzapine may also induce clinically relevant extrapyramidal side effects in PD patients.
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PMID:Deterioration of parkinsonian symptoms following treatment of dopaminergic hallucinosis with olanzapine. 1057 71

Sialorrhea is a relatively common symptom in idiopathic Parkinson's disease and related conditions for which most of the accepted treatments are either highly invasive or may cause substantial systemic side effects. This study describes an open-label pilot study of sublingual atropine drops for the treatment of sialorrhea in 7 patients (6 with Parkinson's disease, 1 with progressive supranuclear palsy). Participants demonstrated statistically significant declines in saliva production, both objectively and subjectively. Self-reported drooling severity showed a significant decline between baseline and 180 minutes, t(6) = 3.240 P < 0.025 (eta(2) = 0.636), and between baseline and 1 week, t(6) = 4.583 P < 0.005 (eta(2) = 0.778). Objectively measured saliva production decreased significantly between baseline and the 1-week follow-up, t(6) = 2.711 P < 0.05 (eta(2) = 0.551). Delirium occurred in 1 patient (concurrent with a urinary tract infection), and 2 patients experienced worsening of hallucinations (active hallucinosis was concealed by both individuals to allow participation in the trial). The remaining trial participants did not experience any anticholinergic side effects. This trial shows that, in selected patient populations, sublingual atropine is a simple and inexpensive treatment for sialorrhea associated with parkinsonism.
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PMID:Sublingual atropine for sialorrhea secondary to parkinsonism: a pilot study. 1246 75

Five patients (4 women) with Parkinson's disease (PD) and primary major psychiatric disorder (PMPD) meeting DSM-IV criteria for the diagnosis of bipolar affective disorder (BAD) were studied. Four patients had early onset PD. Four developed a severe psychiatric disorder a few years after starting dopaminergic therapy in presence of a mild motor disability and a mild cognitive impairment, with no evidence of cerebral atrophy at CT or MRI. Two patients developed a clear manic episode; the other three presented a severe depressive episode (in one case featuring a Cotard syndrome). None showed previous signs of long term L-dopa treatment syndrome (LTS), hallucinosis or other minor psychiatric disorders. The two manic episodes occurred shortly after an increase of dopaminergic therapy and in one case rapid cyclic mood fluctuations were observed. At the onset of psychiatric symptoms, all patients had an unspecific diagnosis of chronic delusional hallucinatory psychosis (CDHP).
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PMID:Bipolar affective disorder and Parkinson's disease: a rare, insidious and often unrecognized association. 1254 47

Neuropsychiatric, perceptual and cognitive deficits are increasingly recognized as non-motor manifestations of Parkinson's Disease (PD).The premorbid personality profile of PD patients is characterized by a number of traits which figure prominently after the disease becomes manifest. In particular, less novelty seeking is one premorbid trait providing an understanding of later cognitive deficits. Anxiety and depression have been shown to precede in some patients motor manifestations and cannot be attributed to anti-parkinsonian therapy. Some neuropsychiatric manifestations and in particular hallucinosis are linked to select perceptual and cognitive changes. Cognitive deficits are common in PD, in particular in younger onset patients. Current animal studies link genetic differences in the dopamine transporter and dopamine catabolic enzyme system to select cognitive impairments attributed to frontal lobe dysfunction.Visuo-cognitive impairment is prevalent in PD. Retinal dopaminergic deficiency has been shown in patients and in the animal model of PD. Visuo-spatial deficits, however, are not simply passive reflections of retinal deficiency. In addition to vision, saccadic eye movements are affected in PD whether they contribute to visuo-spatial dysfunction is unknown. However, recent functional Magnetic Resonance Imaging (fMRI) and electroencephalogram (EEG) studies show an essential role of the occipital cortex in saccadic eye movements and positron emission tomography (PET) studies show occipital hypometabolism in PD. Visual and eye movement studies suggest that certain neuropsychiatric and cognitive deficits in PD are linked to the visual system. Synchrony of signals are essential for the co-operation of distributed neuronal network engaged in sensory-motor coordination. Local, dopaminergic neuronal groups in the retina, basal ganglia and frontal cortical memory system are affected in PD. These connections may not primarily rely on dopamine as a neurotransmitter. It is suggested that to understand visuocognitive changes we should consider pathology affecting neuronal connections, necessary for binding parallel distributed networks.
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PMID:Neuropsychological and perceptual defects in Parkinson's disease. 1291 72

Recent studies have suggested that initial dopamine agonist therapy with pramipexole or ropinirole may slow the progression of Parkinson's disease (PD) and also reduce the subsequent risk of levodopa motor complications. This presumed effect on PD progression, however, could be artifactual, resulting from the influence of chronic drug treatment on regulation of dopamine system proteins. With respect to levodopa motor complications, there is no dispute that pramipexole and ropinirole are effective in reducing levodopa dyskinesias and motor fluctuations; however, it is not clear that they must be started early, as opposed to initiation only after the levodopa complications develop. Levodopa therapy has numerous advantages that include greater efficacy, much lesser expense, simpler administration, and a lower frequency of hallucinosis and somnolence. Carbidopa/levodopa, pramipexole, and ropinirole are all appropriate first choices in the treatment of PD.
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PMID:Parkinson's disease: is the initial treatment established? 1293 Jun 98

The syndrome of dementia with Lewy bodies (DLB) is characterised by the clinical triad of fluctuating cognitive impairment, recurrent visual hallucinations and spontaneous motor features of Parkinsonism. In an attempt to define DLB as a distinct clinical syndrome separate from Alzheimer's disease (AD) and Parkinson's disease (PD) with dementia, a consensus workshop in 1995 established a new set of diagnostic criteria. Dementia that precedes or accompanies the onset of spontaneous (i.e., not neuroleptic-induced) Parkinsonism is termed DLB. In addition, fluctuations in alertness, cognition and function and visual hallucinations are emphasised and included as core features of DLB. The degree to which an individual patient exhibits cognitive impairment, behavioural problems and Parkinsonian features is variable. Therefore, treatment must be individualised. Although there are no officially approved drugs for DLB, limited experience from clinical trials, as well as past experience with the treatment of AD and PD patients, provide some basis for making drug choices. The cholinergic deficit seen in DLB makes cholinesterase inhibitor drugs the mainstay of treatment for cognitive impairment. This class of drugs has also shown therapeutic benefit in reducing hallucinations and other neuropsychiatric symptoms of the disease. Because of their relatively greater therapeutic window, cholinesterase inhibitors are also used as first-line therapy for the treatment of psychosis in DLB. Patients with DLB are extremely sensitive to the extrapyramidal side effects of neuroleptic medications. Thus, only atypical antipsychotic agents such as quetiapine, should be considered as alternative treatment for psychosis. Anxiety and depression are best treated with selective serotonin re-uptake inhibitors, whereas REM sleep behaviour disorder may be treated with low dose clonazepam. Parkinsonism responds to dopaminergic agents; however, precipitation or aggravation of hallucinosis may occur. Levodopa is preferred over dopamine agonists due to its lower propensity to cause hallucinations and somnolence. As the diagnostic criteria for DLB become more refined and validated by postmortem studies, it is hoped that rigorous, well-designed trials will be performed, aimed at alleviating the primary target symptoms of dementia, psychosis and Parkinsonism.
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PMID:Pharmacotherapy of dementia with Lewy bodies. 1459 56


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