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Journal articles on the topic 'Pramipexolo'

Author: Grafiati

Published: 9 March 2023

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1

Mihaylova, Anita S., Ilia D. Kostadinov, Nina D. Doncheva, Hristina I. Zlatanova, and Delian P. Delev. "Effects of Pramipexole on Learning and Memory Processes in Naïve and Haloperidol-challenged Rats in Active Avoidance Test." Folia Medica 61, no. 2 (June 1, 2019): 258–65. http://dx.doi.org/10.2478/folmed-2018-0063.

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Abstract Background: Parkinson’s disease (PD) is the second most common neurode-generative disease, usually detected by its motor symptoms. The non-motor symptoms, including cognitive deficits, have been of great interest to researchers in the last few decades. Aim: To assess the effect of pramipexole on learning and memory in naïve and haloperidol-challenged rats. Materials and methods: Male Wistar rats divided into 9 groups (n=8): naïve - saline, pramipexole 0.5; 1 and 3 mg/kg bw; Haloperidol groups - saline, haloperidol, haloperidol + pramipexole 0.5; 1 and 3 mg/kg bw. Two-way active avoidance test (TWAA) and activity cage were performed. The studied parameters were: number of conditioned and unconditioned responses, vertical and horizontal movements. Statistical analysis was done using SPSS 19. Results: The naïve experimental groups significantly increased the number of conditioned responses during the tests for short- and long-term memory, compared with the saline groups (p<0.05). During the short-memory test only the animals with the lowest dose of PMX significantly increased the number of unconditioned responses whereas during the long-term memory test all experimental groups increased the number of escapes in comparison with the saline groups (p<0.05). Challenge dose of haloperidol attenuates learning and memory in pramipexol treated rats. Only the highest dose of pramipexol showed significant increase in conditioned and unconditioned responses compared with the haloperidol group (p<0.05). Conclusion: Pramipexole improves learning and memory in naïve rats by enhancing dopaminergic neurotransmission. This is probably not the only mechanism involved. This is confirmed by the decrease in learning and memory ability in rats with haloperidol-challenge.

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Chomaničová, Kamila, Štefan Husár, Miroslava Sýkorová, Katarína Birošíková, and Beáta Vladovičová. "Development of Pramipexole Prolonged-Release Matrix Tablets." Chemické listy 117, no. 1 (January 15, 2023): 17–22. http://dx.doi.org/10.54779/chl20230017.

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The present work deals with the development of a prolonged release matrix tablet of the readily soluble drug pramipexole. The new excipient Kollidon SR (a mixture of 80% polyvinyl acetate and 20% polyvinylpyrrolidone) and hypromellose K15M were used as polymers to control drug release from selected prototypes. Various polymer concentrations were tested to achieve a stable and pH independent release of pramipexole of 0.26 mg over 24 hours; samples were prepared by wet granulation and compression of matrix tablets. Drug release was monitored in dissolution media with pH values from 1.2 to 6.8 and compared with a reference product based on a hydrophilic matrix with a combination of three different polymers. The required release profile of the low-dose drug formulation was achieved using 60.0% (w/w) of Kollidon SR in all dissolution media and the selected formulation F2 demonstrated a sufficient alcohol resistance up to the ethanol concentration of 40% (v/v). Predložená práca sa zaoberá vývojom matricovej tablety s predĺženým uvoľňovaním ľahko rozpustného liečiva pramipexolu. Ako polymér riadiaci uvoľňovanie liečiva z vybraných prototypov bol použitý nový excipient Kollidon SR (zmes 80 % polyvinylacetátu a 20 % polyvinylpyrolidónu) a hypromelóza K15M. Testovali sa rôzne koncentrácie polymérov s cieľom dosiahnúť stabilné a pH nezávislé uvoľňovanie pramipexolu 0,26 mg po dobu 24 hodín, vzorky boli pripravené vlhkou granuláciou a lisovaním matricových tabliet. Uvoľňovanie liečiva bolo sledované v disolučných médiách s hodnotami pH od 1,2 až po 6,8 a porovnávané s referenčným prípravkom na báze hydrofilnej matrice s kombináciu troch rôznych polymérov. Požadovaný liberačný profil nízkodávkového liečiva bol dosiahnutý použitím 60,0 hm.% Kollidonu SR vo všetkých médiách a vybraná formulácia F2 vykazovala dostatočnú odolnosť aj voči pôsobeniu etanolu až do koncentrácie 40 obj.%.

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Sun, Yongqi, Baohong Cui, Lin Ye, Yunxin Hu, and Yujun Pan. "Pramipexole Inhibits Neuronal Apoptosis in Rats with Parkinson’s Disease." Journal of Healthcare Engineering 2022 (April 13, 2022): 1–5. http://dx.doi.org/10.1155/2022/7002630.

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To explore the inhibition of pramipexole on the neuronal apoptosis and its influences on the expressions of brain tissue brain-derived neurotrophic factor (BDNF), and serum miR-103a and miR-30b and inflammatory factors in rats with Parkinson’s disease. A total of 36 Sprague-Dawley rats were randomly divided into normal group (n = 12), model group (n = 12) and pramipexole group (n = 12). Compared with that in normal group, the positive expression of BDNF was substantially increased in model group and pramipexole group, and its positive expression in pramipexole group was notably higher than that in model group. The WB results revealed that compared with those in normal group, the relative protein expression levels of Bax and Bcl-2 were markedly increased and decreased, respectively, in the other two groups, and that pramipexole group exhibited a remarkable decline in the relative protein expression level of Bax and a considerable increase in that of Bcl-2, compared with model group. The relative expression levels of miR-103a and miR-30b in model and pramipexole groups were markedly higher than those in normal group, and pramipexole group had remarkably higher relative expression levels of miR-103a and miR-30b than model group. It was found through ELISA that model and pramipexole groups had markedly raised IL-1β and IL-18 content compared with normal group, and their content in pramipexole group was remarkably lower than that in model group. Based on the TUNEL results, compared with that in normal group, the apoptosis rate of cells rose substantially in the other two groups, and the apoptosis rate in pramipexole group was notably lower than that in model group. Pramipexole may up-regulate the expressions of BDNF, miR-103a and miR-30b to inhibit the apoptosis and inflammation in Parkinson’s disease model rats.

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4

Martens, Marieke Annie Gerdine, Alexander Kaltenboeck, Don Chamith Halahakoon, Michael Browning, Philip J. Cowen, and Catherine J. Harmer. "An Experimental Medicine Investigation of the Effects of Subacute Pramipexole Treatment on Emotional Information Processing in Healthy Volunteers." Pharmaceuticals 14, no. 8 (August 14, 2021): 800. http://dx.doi.org/10.3390/ph14080800.

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Treatment with the dopamine D2/D3 receptor agonist pramipexole has demonstrated promising clinical effects in patients with depression. However, the mechanisms through which pramipexole might alleviate depressive symptoms are currently not well understood. Conventional antidepressant drugs are thought to work by biasing the processing of emotional information in favour of positive relative to negative appraisal. In this study, we used an established experimental medicine assay to explore whether pramipexole treatment might have a similar effect. Employing a double-blind, parallel-group design, 40 healthy volunteers (aged 18 to 43 years, 50% female) were randomly allocated to 12 to 15 days of treatment with either pramipexole (at a peak daily dose of 1.0 mg pramipexole salt) or placebo. After treatment was established, emotional information processing was assessed on the neural level by measuring amygdala activity in response to positive and negative facial emotional expressions, using functional magnetic resonance imaging (MRI). In addition, behavioural measures of emotional information processing were collected at baseline and on drug, using an established computerized task battery, tapping into different cognitive domains. As predicted, pramipexole-treated participants, compared to those receiving placebo, showed decreased neural activity in response to negative (fearful) vs. positive (happy) facial expressions in bilateral amygdala. Contrary to our predictions, however, pramipexole treatment had no significant antidepressant-like effect on behavioural measures of emotional processing. This study provides the first experimental evidence that subacute pramipexole treatment in healthy volunteers modifies neural responses to emotional information in a manner that resembles the effects of conventional antidepressant drugs.

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Eisenreich, Wolfram, Bernd Sommer, Sebastian Hartter, and Wolfgang H. Jost. "Pramipexole Extended Release: A Novel Treatment Option in Parkinson's Disease." Parkinson's Disease 2010 (2010): 1–7. http://dx.doi.org/10.4061/2010/612619.

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Pramipexole, the most commonly prescribed dopamine agonist worldwide, meanwhile serves as a reference substance for evaluation of new drugs. Based on numerous clinical data and vast experiences, efficacy and safety profiles of this non-ergoline dopamine agonist are well characterized. Since October 2009, an extended-release formulation of pramipexole has been available for symptomatic treatment of Parkinson's disease. Pramipexole administration can be cut down from three times to once a day due to the newly developed extended-release formulation. This is considerable progress in regard to minimizing pill burden and enhancing compliance. Moreover, the 24 h continuous drug release of the once-daily extended-release formulation results in fewer fluctuations in plasma concentrations over time compared to immediate-release pramipexole, given three times daily. The present study summarizes pharmacokinetics and all essential pharmacological and clinical characteristics of the extended-release formulation. In addition, it provides all study data, available so far, with regard to transition and de-novo administration of extended-release formulation for patients with Parkinson's disease. It further compares efficacy and safety data of immediate-release pramipexole with the extended-release formulation of pramipexole.

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Merlino, Giovanni, Simone Lorenzut, Martina Sommaro, Gian Luigi Gigli, and Mariarosaria Valente. "Pharmacotherapy of Restless Legs Syndrome with Pramipexole." Clinical Medicine Insights: Therapeutics 2 (January 2010): CMT.S3580. http://dx.doi.org/10.4137/cmt.s3580.

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Restless Legs Syndrome (RLS) is one of the most common neurological diseases characterized by an urge to move the legs, often associated with unpleasant sensations relieved by movement. It is engendered by rest, and is worse in the evening or at night. Patients affected by severe RLS should be treated pharmacologically. Dopamine-agonists represent the first-line treatment for RLS symptoms. Pramipexole is a non-ergot derived dopamine agonist with a high selectivity for D2 and D3 receptors. At doses comprised between 0.125 and 0.75 mg, pramipexole improves subjective symptoms and objective signs of primary RLS even after the first administration. In addition, pramipexole seems to be safe and well tolerated. However, physicians should be aware that augmentation and compulsive behaviours might occur in their RLS patients treated with pramipexole. Further studies are needed to confirm the efficacy of pramipexole in uremic RLS and in children affected by the sleep disorder.

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Zhou, Haiyan, Shuhua Li, Hongmei Yu, Shenggang Sun, Xinhua Wan, Xiaodong Zhu, Chun-Feng Liu, et al. "Efficacy and Safety of Pramipexole Sustained Release versus Immediate Release Formulation for Nocturnal Symptoms in Chinese Patients with Advanced Parkinson’s Disease: A Pilot Study." Parkinson's Disease 2021 (March 3, 2021): 1–12. http://dx.doi.org/10.1155/2021/8834950.

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Objective. To explore the efficacy and safety of pramipexole sustained release (SR) versus pramipexole immediate release (IR) in treating nocturnal symptoms in levodopa-treated Chinese patients with advanced Parkinson’s disease (PD) and sleep disturbances. Method. SUSTAIN was an open-label, randomised, active-controlled parallel group exploratory pilot study (NCT03521635). A total of 98 patients were randomly allocated (1 : 1) to either pramipexole SR (n = 49) or pramipexole IR (n = 49) groups. The primary endpoint was a change from baseline in PD Sleep Scale 2nd version (PDSS-2) total score at 18 weeks. A reduction in score represents improvement. Secondary endpoints included Nocturnal Hypokinesia Questionnaire, Scales for Outcomes in PD Sleep Scale, Early Morning Off (EMO), Epworth Sleepiness Scale, PD Questionnaire-8, and responder rates as measured by PDSS-2 total score (<18), EMO scores (≥1 point change), Clinical Global Impression Improvement scale, and Patient Global Impression-Improvement scale. Other endpoints included motor complications (MDS-UPDRS part IV) score. Adverse events were evaluated for each group. Results. The mean pramipexole dose for both groups was 1.5 mg/day at week 18, and the mean changes in PDSS-2 total score for pramipexole SR and IR were –13.7 (95% CI –16.0 to –11.4) and –14.4 (–16.8 to –12.0) (difference of 0.7; p = 0.688 ). Change from baseline for both groups achieved the minimal clinical important difference threshold (MCID = –3.44). No significant difference was observed in change from baseline for other measures of sleep-related disturbances or responder rates. For motor complications, a greater improvement in MDS-UPDRS part IV score was observed in pramipexole SR over IR (–3.4 vs –2.3; treatment group difference: –1.1; p = 0.036 ). Both groups had comparable safety profiles. Conclusion. In Chinese patients with advanced PD and sleep disturbances, pramipexole SR and IR have similar benefits in the treatment of nocturnal symptoms and safety, and an improvement from baseline in nocturnal symptoms was observed regardless of pramipexole formulation.

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Henry, E. "Une expérience clinique du pramipexole chez 64 patients déprimés uni ou bipolaires suivis en ambulatoire." European Psychiatry 30, S2 (November 2015): S58. http://dx.doi.org/10.1016/j.eurpsy.2015.09.162.

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Du fait de l’analogie entre apathie et dépression [1,2], nous avons utilisé le pramipexole [3] chez 64 patients déprimés (39 patients présentant une dépression uni ou bipolaire, 25 patients présentant des troubles dysthymiques). Tous les patients, depuis trois mois au moins, prenaient un traitement par inhibiteur sélectif de la recapture de la sérotonine (ISRS) maintenu sans modification. Il s’agit d’une étude rétrospective portant sur quatre années d’utilisation du pramipexole La sévérité de la dépression a été cotée par le patient sur l’échelle de Hamilton 21 items et par l’investigateur sur l’échelle Montgomery and Asberg Depression Rating Scale (MADRS). Tous les patients ont été revus un à deux mois après l’introduction du pramipexole. La posologie du pramipexole a été de 1,4 mg par jour atteinte en 16 jours. Les critères d’amélioration ont été définis comme l’obtention d’un score inférieur à 10 sur l’échelle de Hamilton et un score inférieur à 10 sur l’échelle MADRS. Parmi les 25 patients présentant un trouble dysthymique, 3 patients ont été améliorés Parmi les 39 patients présentant une dépression uni- ou bipolaire, 35 ont été améliorés. L’amélioration chez ces 38 patients est survenue 10 à 15 jours après le début du traitement. Tous les patients améliorés présentaient une variation franche de l’humeur au cours de la journée avec moindre intensité de la souffrance en fin de journée. La médiane de suivi a été de 23 mois. Les nausées (5 patients) et la somnolence (6 patients) n’ont pas nécessité de modification dans la progression de la posologie. Deux patients ont présenté un épisode maniaque résolutif en 5 à 10 jours après l’arrêt du pramipexole, 1 patient a présenté des hallucinations visuelles résolutives 15 jours après l’arrêt du pramipexole et 1 patient a présenté un priapisme résolutif dès l’arrêt du pramipexole. Aucun cas d’addiction au pramipexole n’a été observé. Au total, le pramipexole semble être un traitement bien toléré et efficace chez les patients présentant une dépression dans le cadre d’un trouble uni ou bipolaire. Il ne semble pas avoir d’indication lors de troubles dysthymiques.

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Hajian, Sepideh, Mohammad Reza Rajabpoor Nikfam, and Zahra Esmayeilzad. "Comparison of the effects of pramipexole and gabapentin on the treatment of restless leg syndrome in end-stage chronic renal failure patients undergoing hemodialysis." Journal of Nephropathology 9, no. 3 (February 12, 2020): e25-e25. http://dx.doi.org/10.34172/jnp.2020.25.

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Introduction: Despite the high prevalence of restless legs syndrome (RLS) in hemodialysis patients, few studies have investigated the effect of pramipexole and gabapentin on the severity of RLS in these patients. Objectives: The study aimed to evaluate the effects of pramipexole and gabapentin on the treatment of RLS in end-stage chronic renal failure patients undergoing hemodialysis. Patients and Methods: Using the diagnostic criteria the presence of RLS was investigated in all hemodialysis patients admitted to the dialysis ward of Bu Ali Sina and Velayat hospitals in Qazvin, Iran. Out of 162 patients, 96 patients had RLS and 60 patients with moderate to severe RLS were enrolled in the study. The selected patients were randomly divided into two groups including pramipexole (0.18 mg daily) and gabapentin (100 mg daily). The two groups were treated for 4 weeks. Results: The prevalence of RLS was 59% (96 out of 162 patients). After the intervention, the severity of RLS was significantly decreased in all patients and also in each of the pramipexole and gabapentin groups (P<0.001). Moreover, after the intervention, the rate of improvement in RLS severity in the pramipexole group (16.8 ± 6.5) was significantly higher than that in the gabapentin group (13.0 ± 7.3; P=0.036). Conclusion: The findings of the study showed that the severity of RLS in hemodialysis patients undergoing 4 weeks of treatment with pramipexole or gabapentin was significantly reduced; in addition, the rate of improvement in RLS severity was higher in pramipexole group.

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Hauser, Robert A., Mark Forrest Gordon, Yoshikuni Mizuno, Werner Poewe, Paolo Barone, Anthony H. Schapira, Olivier Rascol, Catherine Debieuvre, and Mandy Fräßdorf. "Minimal Clinically Important Difference in Parkinson’s Disease as Assessed in Pivotal Trials of Pramipexole Extended Release." Parkinson's Disease 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/467131.

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Background. The minimal clinically important difference (MCID) is the smallest change in an outcome measure that is meaningful for patients.Objectives. To calculate the MCID for Unified Parkinson’s Disease Rating Scale (UPDRS) scores in early Parkinson’s disease (EPD) and for UPDRS scores and “OFF” time in advanced Parkinson’s disease (APD).Methods. We analyzed data from two pivotal, double-blind, parallel-group trials of pramipexole ER that included pramipexole immediate release (IR) as an active comparator. We calculated MCID as the mean change in subjects who received active treatment and rated themselves “a little better” on patient global impression of improvement (PGI-I) minus the mean change in subjects who received placebo and rated themselves unchanged.Results. MCIDs in EPD (pramipexole ER, pramipexole IR) for UPDRS II were −1.8 and −2.0, for UPDRS III −6.2 and −6.1, and for UPDRS II + III −8.0 and −8.1. MCIDs in APD for UPDRS II were −1.8 and −2.3, for UPDRS III −5.2 and −6.5, and for UPDRS II + III −7.1 and −8.8. MCID for “OFF” time (pramipexole ER, pramipexole IR) was −1.0 and −1.3 hours.Conclusions. A range of MCIDs is emerging in the PD literature that provides the basis for power calculations and interpretation of clinical trials.

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Eisenreich, W., and W. Jost. "Pramipexol Retard: Eine neue Therapieoption bei Morbus Parkinson." Nervenheilkunde 29, no. 10 (2010): 675–81. http://dx.doi.org/10.1055/s-0038-1628823.

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ZusammenfassungPramipexol ist der meistverordnete Dopaminagonist weltweit und darf mittlerweile als Referenzsubstanz bei der Bewertung neuer Substanzen angesehen werden. Das Wirksamkeits- und Sicherheitsprofil dieses non-ergolinen Dopaminagonisten ist aufgrund umfangreicher klinischer Daten und Erfahrungen gut charakterisiert. Seit Oktober 2009 steht in Deutschland Pramipexol in retardierter Form zur symptomatischen Behandlung des Morbus Parkinson zur Verfügung. Die notwendige dreimal tägliche Einnahme von Pramipexol lässt sich durch die neu entwickelte Retardform auf eine Einmalgabe pro Tag reduzieren. Dies ist ein wesentlicher therapeutischer Fortschritt im Hinblick auf eine Reduktion der Tablettenlast und bessere Compliance der Patienten. Bei einer kontinuierlichen Wirkstofffreigabe über 24 Stunden zeigt die Retardform zudem weniger Fluktuationen im Plasmakonzentrationsverlauf als eine dreimal tägliche Gabe des unretardierten Pramipexol. Die vorliegende Arbeit fasst die wesentlichen pharmakologischen, pharmakokinetischen und klinischen Merkmale der Retardform zusammen, stellt die Studiendaten zur Um- und Neueinstellung auf Pramipexol Retard bei idiopathischem Parkinson-Syndrom vor und vergleicht die Wirksamkeits- und Sicherheitsdaten der unretardierten versus der retardierten Pramipexol-Formulierungen.

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Al-Rifai, Nafisah, Anas Alshishani, Bahruddin Saad, Anas Rasras, Jalal Zahra, Shadi Madieh, and Fouad Darras. "Synthesis, Isolation, Identification and Characterization of a Drug-Excipient Interaction Degradation Impurity in Pramipexole by HPLC, LC/MS and NMR." Separations 10, no. 1 (December 22, 2022): 7. http://dx.doi.org/10.3390/separations10010007.

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A drug-excipient interaction impurity associated with the degradation process of pramipexole was isolated. The impurity was detected during the stability study of pramipexole extended-release tablets. It was found at a relative retention time of 0.88 with respect to pramipexole, using the pramipexole gradient HPLC-UV detection method described in the USP. The structure of the impurity was identified and fully characterized using high resolution mass spectrometry, IR and NMR techniques, as presented herein. The degradation impurity was identified as (S)-N2-(methoxymethyl)-N6-propyl-4,5,6,7-tetrahydro-1,3-benzothiazole-2,6-diamine. The drug-excipient interaction mechanism of its formation was proposed. An efficient and straightforward synthetic approach was developed to prepare the degradation impurity to confirm its proposed degradation pathway and structure.

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Custodio, Nilton, Rosa Montesinos, David Lira, and Hernando Torres. "Hipersexualidad asociada a pramipexol, en el tratamiento de síntomas parkinsonianos: revisión de la literatura, a propósito de 3 casos." Anales de la Facultad de Medicina 71, no. 1 (May 7, 2011): 51. http://dx.doi.org/10.15381/anales.v71i1.72.

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Introducción: Los desórdenes del control de los impulsos han sido reportados en pacientes con enfermedad de Parkinson (EP), así como en usuarios de agonistas dopaminérgicos. Comunicamos tres casos de pacientes con síntomas parkinsonianos e hipersexualidad, un desorden del control de los impulsos, asociado al uso de pramipexol. Casos clínicos: Caso 1: Varón de 62 años de edad con EP en tratamiento con levodopa/carbidopa, que requirió inicio de pramipexol; a los doce meses presentó hipersexualidad que remitió parcialmente con escitalopram. Caso 2: Varón de 66 años de edad con EP en tratamiento con levodopa/carbidopa, entacapona y clonazepam; requirió inicio de pramipexol y a los dieciséis meses presentó hipersexualidad, que remitió totalmente con escitalopram. Caso 3: Varón de 45 años de edad con parkinsonismo secundario a encefalitis esclerosante aguda en tratamiento con risperidona, amitriptilina y clonazepam; requirió inicio de pramipexol; a los dos meses presentó hipersexualidad, recibió escitalopram, pero la hipersexualidad solo desapareció al disminuir la dosis de pramipexol; se inició levodopa/carbidopa y reapareció la hipersexualidad, que desapareció con la disminución de la dosis de levodopa/carbidopa. Conclusiones: Pramipexol podría estar asociado a hipersexualidad; pero, es necesario tener en cuenta las características relacionadas a cada enfermedad, así como los factores individuales. La hipersexualidad podría mejorar con el escitalopram, siendo necesario tratar los síntomas asociados.

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Bueno Sanya, L., A. Bermejo Pastor, H. Andreu Gracia, O. De Juan Viladegut, L. Olivier Mayorga, and I. Pacchiarotti. "The use of pramipexole in drug-induced parkinsonism: A case study on a patient with bipolar depression." European Psychiatry 65, S1 (June 2022): S411—S412. http://dx.doi.org/10.1192/j.eurpsy.2022.1044.

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Introduction Pramipexole is a dopaminergic agonist used in the treatment of Parkinson’s disease and restless leg syndrome. Although there is a lack of pharmacological options to treat drug-induced parkinsonism, not many studies have been made on the use of pramipexole in its management. There is also evidence on pramipexole effectiveness on major depressive episodes, particularly for bipolar and treatment-resistant depression. Objectives To describe a case of drug-induced parkinsonism treated with pramipexole in a complex patient with bipolar disorder type I and obsessive-compulsive disorder, long-term treated with antipsychotics and valproate. Methods We present the case of a 51-year-old woman admitted in our psychiatric inpatient unit mainly to treat a bipolar depression. She also presented a parkinsonian syndrome, and a neurological study was conducted. As a negative DaTSCAN concluded its cause to be pharmacological, we decided to stop lurasidone and initiated pramipexole. Results Guidelines suggest that drug-induced parkinsonism should be managed by discontinuing causative drugs or switching to another agent. However, we decided to use pramipexole with the aim of not only treating the parkinsonian syndrome but helping manage the depressive episode. We observed a remission of the depressive symptoms and an improvement in the parkinsonian symptoms. Conclusions Although the best way to treat drug-induced parkinsonism is to avoid its causative agents, in clinical practice it is not always possible as some patients have resistant and complex psychiatric syndromes. We suggest considering pramipexole in its management, especially when dealing with a patient with a comorbid unipolar or bipolar depression. Further research is necessary to clarify its utility. Disclosure No significant relationships.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1382 (December 2011): 29. http://dx.doi.org/10.2165/00128415-201113820-00108.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1386 (January 2012): 31. http://dx.doi.org/10.2165/00128415-201213860-00109.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1389 (February 2012): 35. http://dx.doi.org/10.2165/00128415-201213890-00128.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1389 (February 2012): 35. http://dx.doi.org/10.2165/00128415-201213890-00129.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1395 (March 2012): 33. http://dx.doi.org/10.2165/00128415-201213950-00113.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1173 (October 2007): 22–23. http://dx.doi.org/10.2165/00128415-200711730-00066.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1188 (February 2008): 19. http://dx.doi.org/10.2165/00128415-200811880-00062.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1190 (February 2008): 21. http://dx.doi.org/10.2165/00128415-200811900-00068.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1193 (March 2008): 23–24. http://dx.doi.org/10.2165/00128415-200811930-00070.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1129 (November 2006): 18. http://dx.doi.org/10.2165/00128415-200611290-00061.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1139 (February 2007): 19. http://dx.doi.org/10.2165/00128415-200711390-00061.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1156 (June 2007): 22. http://dx.doi.org/10.2165/00128415-200711560-00070.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1159 (July 2007): 24. http://dx.doi.org/10.2165/00128415-200711590-00074.

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&NA;. "Pramipexole." Inpharma Weekly &NA;, no. 1164 (November 1998): 7. http://dx.doi.org/10.2165/00128413-199811640-00010.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1365 (August 2011): 37. http://dx.doi.org/10.2165/00128415-201113650-00137.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1365 (August 2011): 37. http://dx.doi.org/10.2165/00128415-201113650-00138.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 808 (July 2000): 10. http://dx.doi.org/10.2165/00128415-200008080-00023.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1403 (May 2012): 28–29. http://dx.doi.org/10.2165/00128415-201214030-00094.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1403 (May 2012): 29. http://dx.doi.org/10.2165/00128415-201214030-00097.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1416 (August 2012): 36. http://dx.doi.org/10.2165/00128415-201214160-00117.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1200 (May 2008): 26–27. http://dx.doi.org/10.2165/00128415-200812000-00074.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1213 (August 2008): 28. http://dx.doi.org/10.2165/00128415-200812130-00081.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1101 (May 2006): 16–17. http://dx.doi.org/10.2165/00128415-200611010-00044.

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Dooley, Mukta, and Anthony Markham. "Pramipexole." Drugs & Aging 12, no. 6 (1998): 495–514. http://dx.doi.org/10.2165/00002512-199812060-00007.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1257 (June 2009): 36. http://dx.doi.org/10.2165/00128415-200912570-00115.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1267 (August 2009): 26–27. http://dx.doi.org/10.2165/00128415-200912670-00077.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1269 (September 2009): 28. http://dx.doi.org/10.2165/00128415-200912690-00081.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1270 (September 2009): 31. http://dx.doi.org/10.2165/00128415-200912700-00098.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1231 (December 2008): 24–25. http://dx.doi.org/10.2165/00128415-200812310-00072.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1251 (May 2009): 29. http://dx.doi.org/10.2165/00128415-200912510-00086.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1252 (May 2009): 36. http://dx.doi.org/10.2165/00128415-200912520-00124.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1311 (July 2010): 35. http://dx.doi.org/10.2165/00128415-201013110-00120.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1311 (July 2010): 35. http://dx.doi.org/10.2165/00128415-201013110-00121.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1311 (July 2010): 35. http://dx.doi.org/10.2165/00128415-201013110-00123.

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&NA;. "Pramipexole." Reactions Weekly &NA;, no. 1312 (July 2010): 37. http://dx.doi.org/10.2165/00128415-201013120-00129.

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