P J Blanchet

Université de Montréal, Montréal, Quebec, Canada

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Publications (77)280.86 Total impact

  • Souha Mahmoudi, Daniel Lévesque, Pierre J. Blanchet
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    ABSTRACT: Tardive dyskinesia (TD) is a delayed and potentially irreversible motor complication arising in patients chronically exposed to centrally active dopamine D2 receptor antagonists, including antipsychotic drugs and metoclopramide. The classical dopamine D2 receptor supersensitivity hypothesis in TD, which stemmed from rodent studies, lacks strong support in humans. To investigate the neurochemical basis of TD, we chronically exposed adult capuchin monkeys to haloperidol (median, 18.5 months; n = 11) or clozapine (median, 6 months; n = 6). Six unmedicated animals were used as controls. Five haloperidol-treated animals developed mild TD movements, and no TD was observed in the clozapine group. Using receptor autoradiography, we measured striatal dopamine D1, D2, and D3 receptor levels. We also examined the D3 receptor/preprotachykinin messenger RNA (mRNA) co-expression, and quantified preproenkephalin mRNA levels, in striatal sections. Unlike clozapine, haloperidol strongly induced dopamine D3 receptor binding sites in the anterior caudate-putamen, particularly in TD animals, and binding levels positively correlated with TD intensity. Interestingly, the D3 receptor upregulation was observed in striatonigral neurons. In contrast, D2 receptor binding was comparable to controls, and dopamine D1 receptor binding was reduced in the anterior putamen. Enkephalin mRNA widely increased in all animals, but to a greater extent in TD-free animals. These results suggest for the first time that upregulated striatal D3 receptors correlate with TD in nonhuman primates, adding new insights to the dopamine receptor supersensitivity hypothesis. The D3 receptor could provide a novel target for drug intervention in human TD. © 2014 International Parkinson and Movement Disorder Society
    Movement Disorders 05/2014; · 5.63 Impact Factor
  • Pierre J Blanchet, Pierre H Rompré
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    ABSTRACT: Parkinsonism (or Parkinson's syndrome [PS]) remains common in patients exposed to antipsychotic drugs. One clinical tool used in its detection and follow-up, the Simpson-Angus Scale (SAS), has been under revision lately. We further examined the discriminative power of the SAS to detect PS and its efficacy as a measure of PS intensity in chronic schizophrenia. Fifty-six outpatients between 50 and 75 years of age, under stable antipsychotic drug therapy, provided consent to undergo an evaluation along the SAS and Unified Parkinson's Disease Rating Scale III motor subsection, split according to the presence or absence of PS defined in the UK Parkinson's Disease Society Brain Bank (UKPDSBB) criteria or Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria. The identification rate for PS was 39.3% based on UKPDSBB criteria applied to the Unified Parkinson's Disease Rating Scale III, compared with 62.5% and 87.5% according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria and SAS cutoff value greater than 0.3, respectively. Median SAS scores for PS and PS-free participants were comparable. The SAS yielded high sensitivity (90.9%) but low specificity (17.7%). κ Values generally revealed only slight agreement between the group allocation provided by the SAS and the UKPDSBB criteria. Receiver operating characteristic curve for screening performance of the SAS provided poor prediction of subject status. The SAS lacks specificity and constitutes an imperfect detection and measurement tool for PS in older adults. Raising the cutoff score would avoid inflation in PS identification. The scale is probably best used as a measure of change relative to baseline score following an intervention, but results should be interpreted with caution.
    Journal of clinical psychopharmacology 10/2013; · 5.09 Impact Factor
  • Souha Mahmoudi, Pierre J Blanchet, Daniel Lévesque
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    ABSTRACT: Tardive dyskinesia (TD) is a delayed and potentially irreversible motor complication arising in patients chronically exposed to antipsychotic drugs. As several modern (so-called atypical) antipsychotic drugs are common offenders, combined with the widening clinical indications for prescription as well as exposure of vulnerable individuals, TD will remain a significant drug-induced unwanted side effect. In addition, the pathophysiology of TD remains elusive and therapeutics are difficult. Based on rodent experiments, we have previously shown that the transcriptional factor Nur77 (also known as nerve growth factor inducible gene B or Nr4a1) is induced in the striatum following antipsychotic drug exposure as part of a long-term neuroadaptive process. To confirm this, we exposed adult capuchin (Cebus apella) monkeys to prolonged treatments with haloperidol (median 18.5 months, N = 11) or clozapine (median 6 months, N = 6). Six untreated animals were used as controls. Five haloperidol-treated animals developed mild TD movements similar to those found in humans. No TD was observed in the clozapine group. Postmortem analysis of Nur77 expression measured by in situ hybridization revealed a stark contrast between the two drugs, as Nur77 mRNA levels in the caudate-putamen were strongly upregulated in animals exposed to haloperidol but were spared following clozapine treatment. Interestingly, within the haloperidol-treated group, TD-free animals showed higher Nur77 expression in putamen subterritories compared with dyskinetic animals. This suggests that Nur77 expression might be associated with a reduced risk of TD in this experimental model and could provide a novel target for drug intervention.
    European Journal of Neuroscience 03/2013; · 3.75 Impact Factor
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    Abdul Qayyum Rana, Zishan M Chaudry, Pierre J Blanchet
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    ABSTRACT: The aim of this review is to assess new, emerging, and experimental treatment options for tardive dyskinesia (TD). The methods to obtain relevant studies for review included a MEDLINE search and a review of studies in English, along with checking reference lists of articles. The leading explanatory models of TD development include dopamine receptor supersensitivity, GABA depletion, cholinergic deficiency, neurotoxicity, oxidative stress, changes in synaptic plasticity, and defective neuroadaptive signaling. As such, a wide range of treatment options are available. To provide a complete summary of choices we review atypical antipsychotics along with resveratrol, botulinum toxin, Ginkgo biloba, tetrabenazine, clonazepam, melatonin, essential fatty acids, zonisamide, levetiracetam, branched-chain amino acids, drug combinations, and invasive surgical treatments. There is currently no US Food and Drug Administration-approved treatment for TD; however, prudent use of atypical antipsychotics with routine monitoring remain the cornerstone of therapy, with experimental treatment options available for further management.
    Drug Design, Development and Therapy 01/2013; 7:1329-1340. · 3.49 Impact Factor
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    ABSTRACT: Tardive dyskinesia remains an elusive and significant clinical entity that can possibly be understood via experimentation with animal models. We conducted a literature review on tardive dyskinesia modeling. Subchronic antipsychotic drug exposure is a standard approach to model tardive dyskinesia in rodents. Vacuous chewing movements constitute the most common pattern of expression of purposeless oral movements and represent an impermanent response, with individual and strain susceptibility differences. Transgenic mice are also used to address the contribution of adaptive and maladaptive signals induced during antipsychotic drug exposure. An emphasis on non-human primate modeling is proposed, and past experimental observations reviewed in various monkey species. Rodent and primate models are complementary, but the non-human primate model appears more convincingly similar to the human condition and better suited to address therapeutic issues against tardive dyskinesia.
    Behavioral and Brain Functions 03/2012; 8:12. · 2.79 Impact Factor
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    ABSTRACT: Tardive dyskinesia (TD) is a neurological motor complication eventually arising in one-third of patients chronically exposed to antipsychotic drugs. Some orodental peripheral factors have been reported to influence TD. To measure orodental factors such as temporomandibular joint function, static occlusal contacts, and denture condition, and attempt correlations with orofacial TD intensity. In this exploratory cross-sectional pilot study, 31 subjects between 30 and 75 years of age were divided in two groups displaying minimal to mild, or moderate to severe orofacial TD, respectively, and underwent a detailed oral, dental, and prosthetic evaluation to capture various aspects of oral health compared between the two groups. Blinded video-based TD ratings along a validated scale were obtained to compare dentulous and edentulous subjects, and contrast TD intensity in complete denture wearers with and without their own prostheses. None of the factors examined tightly correlated with orofacial TD intensity. However, edentulism was associated with a higher median orofacial TD rating compared to the dentulous group (p = 0.001). Further, a significant intra-subject difference was observed in the edentulous subjects rated with their own complete dentures in place or not (p = 0.028), the dentures attenuating the mean orofacial ratings by 21.8 ± 7.3%. Of all orodental factors considered, only edentulism and complete denture wearing influenced oral TD expression, calling for the close monitoring of the dental status in antipsychotic drug-exposed patients to prevent tooth loss. Further studies to measure the impact of an adequate prosthodontic rehabilitation in edentulous subjects with orofacial TD seem warranted.
    Journal of psychiatric research 03/2012; 46(5):684-7. · 3.72 Impact Factor
  • Pierre J Blanchet, Louise Normandeau, Pierre H Rompré
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    ABSTRACT: Drug-induced parkinsonism (DIP) is seen in one third of patients exposed to antipsychotic drugs and may lead to complications related to dysphagia and falls. Aside from skilled neurological examination, no tool has been validated to facilitate detection and follow-up. In this pilot study, three validated screening instruments were tested in an age-biased cohort of schizophrenia patients, including four items of the Liverpool University Neuroleptic Side-Effects Rating Scale (LUNSERS) and two brief questionnaires designed for community survey of parkinsonism. Fifty-six subjects living with chronic schizophrenia between 50 and 75 years of age underwent a motor evaluation along the original Unified Parkinson's Disease Rating Scale-section III and answered questions along the selected screening instruments, and results compared to those of 16 patients with Parkinson's disease (PD) and 15 neurologically unimpaired volunteers. Odds ratios, sensitivity, specificity, and their 95% confidence intervals, were calculated. All three screening instruments correctly identified the PD state and distinguished PD from healthy participants. Eighteen (32%) schizophrenic patients displayed objective motor signs of parkinsonism. A single item of the LUNSERS (shakiness) significantly distinguished DIP from DIP-free patients, with a sensitivity of 61.1% and a specificity of 83.3%. The positive predictive value was 63.5% and the negative predictive value was 81.9%. The two other screening methods showed insufficient predictive value. Apart from a single query on shakiness, none of the tools examined were adequate to screen for DIP in patients treated for schizophrenia. A different instrument is necessary to monitor this important adverse effect in schizophrenia.
    Schizophrenia Research 02/2012; 137(1-3):230-3. · 4.59 Impact Factor
  • Schizophrenia Research 07/2011; 136(1-3):162-3. · 4.59 Impact Factor
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    ABSTRACT: Chunking of single movements into integrated sequences has been described during motor learning, and we have recently demonstrated that this process involves a dopamine-dependant mechanism in animal (Levesque et al. in Exp Brain Res 182:499–508, 2007; Tremblay et al. in Behav Brain Res 198:231–239, 2009). However, there is no such evidence in human. The aim of the present study was to assess this question in Parkinson’s disease (PD), a neurological condition known for its dopamine depletion in the striatum. Eleven PD patients were tested under their usual levodopa medication (ON state), and following a 12-h levodopa withdrawal (OFF state). Patients were compared with 12 healthy participants on a motor learning sequencing task, requiring pressing fourteen buttons in the correct order, which was determined by visual stimuli presented on a computer screen. Learning was assessed from three blocks of 20 trials administered successively. Chunks of movements were intrinsically created by each participant during this learning period. Then, the sequence was shuffled according to the participant’s own chunks, generating two new sequences, with either preserved or broken chunks. Those new motor sequences had to be performed separately in a fourth and fifth blocks of 20 trials. Results showed that execution time improved in every group during the learning period (from blocks 1 to 3). However, while motor chunking occurred in healthy controls and ON-PD patients, it did not in OFF-PD patients. In the shuffling conditions, a significant difference was seen between the preserved and the broken chunks conditions for both healthy participants and ON-PD patients, but not for OFF-PD patients. These results suggest that movement chunking during motor sequence learning is a dopamine-dependent process in human. KeywordsParkinson-Dopamine-Striatum-Motor learning-Movement-Sequence learning
    Experimental Brain Research 09/2010; 205(3):375-385. · 2.22 Impact Factor
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    ABSTRACT: Le sommeil est un état physiologique et comportemental caractérisé par une isolation partielle de l’environnement. Lors du sommeil, un événement perturbateur comme la douleur peut provoquer une réaction de microéveil brève et inconsciente vers un réveil comportemental caractérisé par une réactivation thalamocorticale complète et un niveau plus élevé de conscience. Le sommeil devient alors fragmenté et les plaintes de douleur se trouvent souvent exacerbées. La continuité oscillatoire de 90–110 minutes, rythme ultradien du sommeil léger et profond (non-REM: rapid eye movement) vers le sommeil paradoxal (REM), est alors rompue. Chez un patient souffrant de céphalée, on observe trois périodes durant lesquelles surviennent les crises en relation avec le sommeil: 1) dans les heures avant l’initiation du sommeil, 2) durant et, 3) après le sommeil. La céphalée de tension et la migraine, la céphalée de type hypnique, l’algie vasculaire de la face (cluster headache) et l’hémicrânie paroxystique chronique peuvent survenir en relation avec le sommeil. Soulignons que la céphalée du réveil est parfois associée à du bruxisme (serrement et grincement des dents), à un abus de médications antalgiques, à de l’hypertension, à un trouble de l’humeur ou à des réductions du flux respiratoire lors du sommeil. Les céphalées suite à un traumatisme crânien sont fréquentes et causent de l’insomnie, des réveils subits et prématurés et surtout des matins pénibles avec délai de phase circadienne. Dans le contexte d’une céphalée survenant en relation avec l’insomnie ou la somnolence diurne, la recherche de troubles respiratoires du sommeil, d’intrusions sous forme de mouvements périodiques des membres ou de bruxisme est indiquée. La polygraphie peut être effectuée en laboratoire ou en ambulatoire. La gestion de ces céphalées suit les grands principes de la médecine contemporaine tout en visant une hygiène du sommeil maximale par thérapie cognitive et comportementale, le maintien d’un rythme circadien idéal, la prise de mélatonine, la correction du phénomène respiratoire. La prise d’hypnotique ne semble pas un traitement de choix à long terme. Sleep is a physiological and behavioral state where the person is partly isolated from the external environment. In the presence of sleep intrusions such as pain, sleep becomes fragmented. The non REM to REM ultradian oscillations, occurring every 90 to 110 minutes, are then disrupted by several brief and transient arousals (rise in cardiac, brain, muscle, and respiratory activities). The pain reports from these individuals tend to be exacerbated by the loss of sleep continuity. Tension headache, migraine, and cluster headache may occur before sleep (delaying sleep onset), during sleep (e.g., migraine, hypnic headache, cluster headache, and chronic paroxysmal hemicrania), or upon awakening (e.g., breathing disorder, bruxism, pain medication overuse, and arterial hypertension). Minor traumatic brain injury is frequently associated with headache and circadian sleep disturbances. Little is known on how to manage sleep-related headaches. A polygraphic search for breathing disturbances or periodic limb movements is recommended if the complaints are recurrent and associated with daytime somnolence. Use of breathing or oral devices is helpful if an upper airway resistance is present or if apnea-hypopnea is observed. Cognitive and behavioral approaches related to sleep hygiene and lifestyle are valuable. Hypnotic medications probably have limited long-term value. Mots clésSommeil-Céphalée-Migraine-Microéveils-Rythme circadien-Traumatisme crânien KeywordsSleep-Headache-Migraine-Arousal-Circadian rhythm-Brain trauma
    Douleur et Analgésie 01/2010; 23(3):175-180. · 0.09 Impact Factor
  • Douleur Et Analgesie - DOULEUR ANALG. 01/2010; 23(1).
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    ABSTRACT: This study examined discrete motor irregularities in ballistic aiming movements in patients with atypical parkinsonian syndromes (APS). Nine patients with APS were compared to 9 patients with idiopathic Parkinson's disease (PD) and 9 controls on ballistic arm extension movements performed on a digitizing tablet without visual feedback and without accuracy constraints. Patients with APS showed a higher number of irregularities in the acceleration and jerk time series compared to PD patients and controls. No difference was found between PD patients and controls. These discrete irregularities were not associated with general motor impairment, tremor, akinesia, or rigidity. These results suggest that atypical parkinsonism is associated with movement irregularities in ballistic movements, which may help differentiate APS from PD.
    Parkinsonism & Related Disorders 01/2009; 15(7):542-5. · 3.27 Impact Factor
  • P.-J. Blanchet, B. Lalonde, G.-J. Lavigne
    Douleur Et Analgesie - DOULEUR ANALG. 01/2009; 22(2):103-111.
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    ABSTRACT: Motor learning disturbances have been shown in diseases involving dopamine insufficiency such as Parkinson's disease and schizophrenic patients under antipsychotic drug treatment. In non-human primates, motor learning deficits have also been observed following systemic administration of raclopride, a selective D2-receptor antagonist. These deficits were characterized by persistent fluctuations of performance from trial to trial, and were described as difficulties in consolidating movements following a learning period. Moreover, it has been suggested that these raclopride-induced fluctuations can result from impediments in grouping separate movements into one fluent sequence. In the present study, we explore the hypothesis that such fluctuations during movement consolidation can be prevented through the use of sumanirole - a highly selective D2 agonist - if administered before raclopride. Two monkeys were trained to execute a well known sequence of movements, which was later recalled under three pharmacological conditions: (1) no drug, (2) raclopride, and (3) sumanirole+raclopride. The same three pharmacological conditions were repeated with the two monkeys, trained this time to learn new sequences of movements. Results show that raclopride has no deleterious effect on the well known sequence, nor the sumanirole+raclopride co-administration. However, results on the new sequence to be learned revealed continuous fluctuations of performances in the raclopride condition, but not in the sumanirole+raclopride condition. These fluctuations occurred concurrently with a difficulty in merging separate movement components, known as a "chunking deficit". D2 receptors seem therefore to be involved in the consolidation of new motor skills, and this might involve the chunking of separate movements into integrated motor sequences.
    Behavioural brain research 12/2008; 198(1):231-9. · 3.22 Impact Factor
  • D Mongeon, P Blanchet, J Messier
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    ABSTRACT: Increasing evidence suggests that the pathophysiology of movement disorders in Parkinson's disease (PD) includes deficits in sensory processing and integration. However, the exact nature of these deficits and the ability of dopamine medication to correct them have not been thoroughly examined in previous studies. For instance, it remains unclear whether PD patients have globally impaired sensorimotor integration functions or selective deficiencies in processing proprioception. We evaluated the specific deficits of PD patients in sensorimotor integration and proprioceptive processing by testing their ability to perform three-dimensional (3D) reaching movements in four conditions in which the sensory signals defining target and hand positions (visual and/or proprioceptive) varied. Ten healthy subjects and 11 PD patients, ON dopamine medication and in the OFF state, were tested. PD patients in the OFF state showed a greater mean level of 3D errors relative to controls when the only available sensory information about target and hand position came from proprioception, but this difference did not reach significance. This indicates that deficient proprioception is not an early key feature of PD. Interestingly, the inaccuracies of a number of PD subjects further increased in the ON medicated state relative to healthy controls when reaching to proprioceptively-defined targets, and this between group difference was statistically significant. However, dopamine medication did not consistently degrade the reaching accuracy of PD patients, with both negative and positive effects on accuracy of reaching to proprioceptive-defined targets. Together, these findings indicate that dopamine replacement therapy not only did not normalize sensorimotor performance to the level of controls, but also induced deficits in the processing of proprioceptive information in some of the PD patients tested. Furthermore, the diversity of effects of medication on accuracy of reaching to proprioceptively-defined targets supports the idea that dysfunction of dopaminergic circuits within the basal ganglia is not primarily responsible for the proprioceptive processing deficits of PD patients.
    Neuroscience 11/2008; 158(2):426-40. · 3.12 Impact Factor
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    ABSTRACT: Oral dyskinesias occur in elderly individuals in relation to drug use (tardive dyskinesia, TD) or edentulousness (edentulous orodyskinesia, EOD) but their characterization remains incomplete. Our aim was to investigate whether magnetic resonance techniques such as diffusion-weighted imaging (DWI) and magnetization transfer imaging (MTI) of the brain could be used to differentiate dyskinetic patients from control subjects. Eight drug-treated patients with TD, 12 EOD patients, 8 drug-treated patients without TD, and 10 control subjects were recruited and examined by DWI and MTI. Measurements in the caudate nucleus, putamen, and globus pallidus yielded globally different apparent diffusion coefficient (ADC) values between drug treated patients with TD and control subjects but the magnetization transfer ratios showed no significant variations. The discrimination between dyskinetic patients and control subjects offered by ADC values was however slightly poorer than the discrimination offered by the previously published choline/creatine ratios measured by MR spectroscopy in the basal ganglia. The results are consistent with the pathophysiological hypothesis of damage to cholinergic interneurons.
    Movement Disorders 06/2008; 23(9):1281-5. · 5.63 Impact Factor
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    ABSTRACT: To characterize postural stability control and levodopa responsiveness in early Parkinson's disease (PD). Postural sway was studied during quiet stance in ten patients within six years of PD onset, both before (OFF) and after (ON) regular oral levodopa dosing. Postural sway was recorded using a force platform during 30 sec with eyes open, and six dependent variables were examined. Mild baseline subclinical changes in postural sway were recorded in our patients. Clear benefit was observed in five out of six characteristics (mean sway, transversal sway, sagittal sway, sway intensity, and sway area) in the ON condition. Postural control mechanisms are affected early in PD and modulated by dopamine.
    The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques 04/2008; 35(1):65-8. · 1.33 Impact Factor
  • F. Lobbezoo, P. Blanchet, G. J. Lavigne
    Citizenship Studies - CITIZENSH STUD. 01/2008;
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    ABSTRACT: Results obtained in patients with schizophrenia have shown that antipsychotic drugs may induce motor learning deficits correlated with the striatal type-2 dopamine receptors (D(2)R) occupancy. Other findings suggest that the role of the striatum in motor learning could be related to a process of "chunking" discrete movements into motor sequences. We therefore hypothesized that a D(2)R blocking substance, such as raclopride, would affect motor learning by specifically disrupting the grouping of movements into sequences. Two monkeys were first trained to perform a baseline-overlearned sequence (Seq. A) drug free. Then, a new sequence was learned (Seq. B) and the overlearned sequence was recalled OFF-drug (Seq. A recall OFF-drug). The effect of raclopride was then assessed on the learning of a third sequence (Seq. C), and on the recall of the overlearned sequence (Seq. A recall ON-drug). Results showed that performance related to the overlearned sequence remained the same in the three experimental conditions (Seq. A, Seq. A recall OFF-drug, Seq. A recall ON-drug), whether the primates received raclopride or not. On the other hand, new sequence learning was significantly affected during raclopride treatment (Seq. C), when compared with new sequence learning without the effect of any drug (Seq. B). Raclopride-induced disturbances consisted in performance fluctuations, which persisted even after many days of trials, and prevented the monkeys from reaching a stable level of performance. Further analyses also showed that these fluctuations appeared to be related to monkeys' inability to group movements into single flowing motor sequences. The results of our study suggest that dopamine is involved in the stabilization or consolidation of motor performances, and that this function would involve a chunking of movements into well-integrated sequences.
    Experimental Brain Research 11/2007; 182(4):499-508. · 2.22 Impact Factor
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    ABSTRACT: Oral dyskinesias may occur spontaneously or be induced by medications such as antipsychotics and antidepressants. In this study, single voxel proton magnetic resonance spectroscopy was used to compare metabolite levels in the striatum for (1) 12 patients with drug-induced tardive dyskinesia (TD), (2) 12 patients with spontaneous oral dyskinesia (SOD), (3) 8 antidepressant-treated patients without TD, and (4) 8 control subjects. Statistically significant reductions in the choline/creatine (Cho/Cr) ratio were measured for the drug-treated patients with TD (-13%, P = 0.020) and SOD patients (-12%, P = 0.034) relative to control subjects. In comparison with antidepressant-treated patients without TD, drug-treated patients with TD showed a non statistically significant reduction in Cho/Cr (-11%, P = 0.079). All other metabolite ratios (N-acetylaspartate (NAA)/Cr, myo-inositol (mI)/Cr, glutamine + glutamate (Glx)/Cr, macromolecule + lipid (MM+Lip)/Cr, NAA/Cho) were unaffected by either type of dyskinesia. The observed Cho/Cr reduction in dyskinesia patients suggests decreased membrane phosphatidylcholine turnover, which provides free choline as precursor of molecules responsible for cellular signal transduction.
    Movement Disorders 06/2007; 22(7):957-62. · 4.56 Impact Factor

Publication Stats

2k Citations
280.86 Total Impact Points

Institutions

  • 2003–2014
    • Université de Montréal
      • • Department of Stomatology
      • • Faculty of Pharmacy
      • • Faculty of Dentistry
      Montréal, Quebec, Canada
  • 2007–2013
    • Université du Québec à Montréal
      • Department of Psychology
      Montréal, Quebec, Canada
  • 2011
    • Hôpital Louis-H. Lafontaine
      Montréal, Quebec, Canada
  • 2005–2008
    • Université Victor Segalen Bordeaux 2
      Burdeos, Aquitaine, France
  • 2004
    • Centre hospitalier de l'Université de Montréal (CHUM)
      Montréal, Quebec, Canada
  • 1996–2003
    • National Institutes of Health
      • Branch of Experiemental Therapeutics
      Bethesda, MD, United States
  • 1995–2001
    • Laval University
      • Faculté de Médecine
      Québec, Quebec, Canada
  • 1999
    • Hôpital du Sacré-Coeur de Montréal
      • Center for Advanced Research in Sleep Medicine
      Montréal, Quebec, Canada
  • 1998–1999
    • Centre Hospitalier Universitaire de Québec (CHUQ)
      Québec, Quebec, Canada
    • University Hospital of Ioannina
      Yannina, Epirus, Greece