Parkinson Disease: Merims D

Merims D, Freedman M. · Division of Neurology and Rotman Research Institute, Baycrest, Toronto. · Int Rev Psychiatry. · Pubmed #18925485 No free full text.

Abstract: Although Parkinson's disease (PD) has been considered to primarily affect motor abilities, increasing emphasis is being placed on cognitive and behavioural impairment in this disorder. Depression, dementia, psychosis and impulse control disorders have a major impact on quality of life for both patients and families. This article reviews cognitive and behavioural disturbances in PD and their relation to affective and motor symptoms, treatment of dementia associated with PD, and treatment approaches to psychosis in PD. We also discuss similarities between the dementia of PD and dementia with Lewy bodies.

Merims D, Giladi N. · Movement Disorders Unit, Department of Neurology, Tel-Aviv Sourasky Medical Center, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel. · Parkinsonism Relat Disord. · Pubmed #17988927 No free full text.

Abstract: Degeneration of the dopaminergic system in Parkinson's disease and longstanding exposure to dopaminergic drugs may cause reward system malfunction. This may manifest as addiction to l-dopa and behavioral disturbances associated with the impulse control system. These disturbances include: gambling, excessive spending (shopping), hypersexuality and binge eating. We included one such patient's personal story to emphasize the devastating consequences of these potentially reversible phenomena: the patient describes in his own words how gambling induced by an exposure dopamine agonist therapy significantly worsened his disease-related difficulties.

Zoldan J, Merims D, Kuritzky A, Ziv I, Melamed E. · Dept. of Neurology, Rabin Medical Center, Petah Tikva. · Harefuah. · Pubmed #10959339 No free full text.

Abstract: After 3-5 years of continuous use of 1-dopa preparations for Parkinson's disease, 25%-50% of patients develop side-effects such as the "on-off" phenomenon and involuntary movements that markedly impair function. One cause of these manifestations is evidently a disturbance in the absorption of 1-dopa. We attempted to avoid this problem by using subcutaneous injections. Apomorphine is a rapid-acting dopamine agonist which causes a return from "off" to "on" within minutes. We present the results of a trial of subcutaneous injections of apomorphine in 22 Parkinsonian patients (12 males, 10 females) with severe motor fluctuations. During 5 days prior to the apomorphine all received Motilium (domperidone, 60 mg/d) to prevent nausea and vomiting. All were hospitalized initially to determine optimal dosage and to teach them the technique of self-injection. 2 to 4 mg of apomorphine were injected 1 to 3 times daily for 2 to 12 months. In 17 patients (80%) "off" periods were reduced without significant side-effects. Apomorphine seems to be effective, tolerable treatment for shortening 1-dopa induced "off" periods.

Merims D, Balas M, Peretz C, Shabtai H, Giladi N. · Movement Disorders Unit, National Parkinson Foundation Parkinson's Center, Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv University, Tel Aviv, Israel. · Clin Neuropharmacol. · Pubmed #17095896 No free full text.

Abstract: OBJECTIVE: To compare the safety and efficacy of quetiapine versus clozapine for the treatment of psychosis in patients with Parkinson's disease (PD). METHODS: Twenty-seven patients with PD and recent-onset psychosis were randomly allocated to 2 arms of 22 weeks' treatment with quetiapine or clozapine after 2 weeks of adjustment of antiparkinsonian medications. Assessment was done by a blinded neuropsychologist using the Clinical Global Impression of Change (CGIC) questionnaire and the Neuropsychiatric Inventory (NPI). Mixed-effect models were used to compare CGIC and Neuropsychological Inventory scores over time between the 2 groups. RESULTS: Both drugs were equally effective based on the CGIC. Clozapine had a trend over quetiapine in controlling the frequency of hallucinations (P = 0.097) and a significant advantage in reducing delusions (P = 0.011). However, one patient in the clozapine arm developed leukopenia. None of the drugs worsened parkinsonism. CONCLUSIONS: Clozapine and quetiapine are effective atypical neuroleptics for the treatment of psychotic symptoms in PD. Clozapine had greater efficacy in reducing hallucinations and delusions frequency, but its use is associated with an increased risk of leukopenia.

Merims D, Shabtai H, Korczyn AD, Peretz C, Weizman N, Giladi N. · Movement Disorders Unit, Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. · J Neural Transm. · Pubmed #15480845 No free full text.

Abstract: BACKGROUND: It was commonly assumed that psychotic phenomena in Parkinson's disease (PD) are mainly drug related. Accumulating evidence suggests the existence of other risk factors for psychosis in PD. Aims. To evaluate the contribution of the drug profile of patients with PD to emergence of hallucinations. METHODS: We compared patients with and without hallucinations, using Cox proportional hazards model, concerning drug profile at the time of hallucinations emergence. RESULTS: Of 422 consecutive patients, 113 had dementia, while 90 patients experienced hallucinations (46 had both dementia and hallucinations). The mean levodopa dose for the group of patients with hallucinations was 650 +/- 279 mg/day at the time of hallucinations onset, which was not significantly different from the levodopa dose at last visit for the group without hallucinations (621 +/- 326 mg/day). Supplementary treatment with amantadine, selegiline, dopamine agonists, entacapone and anticholinergics did not increase the risk for the development of hallucinations. CONCLUSIONS: We did not confirm drug treatment as a risk factor for hallucinations in PD. Our study suggests the existence of "endogenic" factors as substantial contributors in the genesis of PD hallucinations. The clinical implications may be earlier administration of antipsychotic treatment and not as traditionally accepted, dose reduction of antiparkinsonian drugs.

Merims D, Djaldetti R, Melamed E. · Department of Neurology, Rabin Medical Center, Beilinson Campus, Petah Tiqva 49100, Israel. · Clin Neuropharmacol. · Pubmed #12897640 No free full text.

Abstract: The authors compared the two portions of the OFF period in patients with Parkinson disease and response fluctuations: time to ON (the latency from levodopa intake to turning ON) and wearing off (time from termination of the beneficial dose effect until the time when the next dose was taken). Time to ON was more than twice the duration of wearing off. Although underrecognized, time to ON is the major component of total daily OFF.

Djaldetti R, Treves TA, Merims D, Sroka H, Melamed E. · Department of Neurology, Rabin Medical Center, Beilinson Campus, Petah Tiqva, Israel. · Clin Neuropharmacol. · Pubmed #12567161 No free full text.

Abstract: The time of initiation of levodopa therapy in patients with Parkinson's disease (PD) is still debatable, as is the hypothesis of levodopa toxicity Some researchers argue that late initiation of treatment will delay the appearance of response fluctuations. In the present study, 11 patients in whom treatment with low doses of levodopa was delayed for a mean of 7.9 +/- 3.1 years were followed for a mean of 15.7 +/- 3.3 years. Time of onset of response fluctuations and disease severity were compared with those in 17 patients with fluctuating PD who were treated with levodopa from disease onset. There was no significant change in time to onset of response fluctuations and dyskinesias once levodopa treatment was started, and late initiation of levodopa did not affect disease progression. The authors conclude that the decision of when to initiate levodopa treatment should be taken according to the patient's needs.

Merims D, Ziv I, Sherki Y, Djaldetti R, Melamed E. · Department of Neurology, Rabin Medical Center, Belinson Campus, Petah Tikva. · Neurol Neurochir Pol. · Pubmed #12001656 No free full text.

Abstract: Dyskinesias are the most frequent adverse effect of chronic levodopa therapy in patients with Parkinson's disease (PD). Current pharmacological treatment for this problem is unsatisfactory. Recently, there is evidence for the role of glutamate in the basal ganglia neuronal circuitry in the generation of dyskinesias. If indeed glutamatergic overactivity beyond the dopaminergic synapses plays a role in the pathogenesis of these involuntary movements, there is hope that its suppression may be beneficial without causing loss of levodopa efficacy and parkinsonian deterioration. Indeed, NMDA receptor antagonists such as amantadine and dextrometorphan can reduce such dyskinesias. We tested the efficacy of riluzole, an inhibitor of glutamatergic transmission in the inhibition of levodopa-induced dyskinesias.

Merims D, Galili-Mosberg R, Melamed E. · Department of Neurology, Rabin Medical Center-Belinson Campus, and the Sackler School of Medicine, Tel Aviv University, Petach Tiqva, Israel. · Mov Disord. · Pubmed #11009217 No free full text.

This publication has no abstract.

Djaldetti R, Mosberg-Galili R, Sroka H, Merims D, Melamed E. · Department of Neurology, Rabin Medical Center, Petah Tiqva, Israel. · Mov Disord. · Pubmed #10348467 No free full text.

Abstract: Camptocormia is characterized by severe forward flexion of the thoracolumbar spine which increases while walking and disappears in the recumbent position. We describe for the first time eight patients with presumed idiopathic Parkinson's disease (mean age 66+/-5 yrs; mean symptom duration 13.1+/-5.1 yrs) who developed camptocormia. This impressive abnormal posture emerged 4-14 years from disease onset, and in some patients stooped posture was the prominent symptom at diagnosis. There was no clear correlation between camptocormia and levodopa treatment. In some patients the camptocormic posture improved, and in others it was unchanged or even aggravated following levodopa administration. Three patients reported worsening of this symptom during "off" periods and also with fatigue. The pathogenesis of this phenomenon is unknown but might represent either a rare type of dystonia or an extreme form of rigidity.

Merims D, Ziv I, Djaldetti R, Melamed E. · No affiliation provided · Lancet. · Pubmed #10347995 No free full text.

This publication has no abstract.