References of "PARMENTIER, Eric"
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See detailSuccessful treatment of hand dystonia with Botulinum Toxin in a DYT12 patient
DEPIERREUX, Frédérique ULiege; PARMENTIER, Eric ULiege; HARDY, Pierre-Yves et al

Poster (2019, May 11)

We present the case of a young boy suffering from DYT12 (Rapid-onset dystonia-parkinsonism), presenting with generalized dystonia. Left hand dystonia has been treated successfully with botulinum toxin ... [more ▼]

We present the case of a young boy suffering from DYT12 (Rapid-onset dystonia-parkinsonism), presenting with generalized dystonia. Left hand dystonia has been treated successfully with botulinum toxin, under double guidance techniques (EMG and ultrasound) [less ▲]

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See detailCorrelation between deep brain stimulation effects on freezing of gait and audio-spinal reflex
Parmentier, Eric ULiege; De Pasqua, Victor; D'Ostilio, Kévin et al

in Clinical Neurophysiology (2018), 129

Detailed reference viewed: 46 (3 ULiège)
See detailMaladie de Parkinson: actualités thérapeutiques
DEPIERREUX, Frédérique ULiege; PARMENTIER, Eric ULiege

Conference given outside the academic context (2016)

Cette conférence reprend les dernières guidelines et publications récentes au sujet du traitement de la maladie de Parkinson

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See detailLes troubles du contrôle des impulsions associés au traitement dopaminergique substitutif antiparkinsonien
DEPIERREUX, Frédérique ULiege; CREMERS, Julien ULiege; SKAWINIAK, Eva ULiege et al

in Revue Médicale de Liège (2013), 68(mai-juin), 221-225

Summary : In some patients, impulse control behaviours can be triggered by dopaminergic replacement therapy, particularly dopamine agonist drugs: hobbyism, punding (stereotyped behaviours), compulsive ... [more ▼]

Summary : In some patients, impulse control behaviours can be triggered by dopaminergic replacement therapy, particularly dopamine agonist drugs: hobbyism, punding (stereotyped behaviours), compulsive buying, binge eating disorder, pathological gamgling, hypersexuality, hedonistic homeostatic dysregulation syndrome ... The pathogenesis of these behaviours is not well understood, but likely involves aberrant changes in the dopaminergic pathways that mediate motivation i.e., a dopaminergic “overdose” in meso-cortico-limbic circuits. An early diagnosis is difficult, but mandatory to prevent the occurrence of devastating familial, marital, professional, socio-economic, medical and medico-legal consequences. Their management is not yet well standardized. Patients and caregivers should be warned about impulse control behaviours before starting dopamine agonists and monitoring for such behaviours while on therapy is requested. [less ▲]

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See detailThe Day George Avellis Met Miller Fisher – About the Unsual Presentation of an Anti-GQ1b IgG Antibody Syndrome
PHAN BA, Remy ULiege; Parmentier, Eric ULiege; LIEVENS, Isabelle ULiege et al

Poster (2013, March)

Objective: OBJECTIVE: To describe the clinical, laboratory and electrophysiological features of a patient who presented an Avellis syndrome as the initial feature of Miller Fisher syndrome (MFS ... [more ▼]

Objective: OBJECTIVE: To describe the clinical, laboratory and electrophysiological features of a patient who presented an Avellis syndrome as the initial feature of Miller Fisher syndrome (MFS). Background: BACKGROUND: Anti-GQ1b Ig antibodies are associated with an increasing spectrum of neurological disorders, including MFS and Guillain-Barre syndrome (GBS). Design/Methods: DESIGN/METHODS: Clinical case description. Results: RESULTS: A 67-year old woman was seen for subacute dysphagia and dysphonia, preceded by rapidly worsening paresthesia of the extremities and face, with a history of upper respiratory tract infection two weeks before admission. Nasotracheal examination showed a left velopalatine and left vocal cord paresis. Twelve hours later, sensory ataxia appeared and deep tendon reflexes weakened. Diffuse paresis affecting predominantly the axial muscles developped. Oculomotricity was preserved. Brain MRI was normal, while EMG suggested a mild sensory neuropathy. Within hours, dysphagia worsened and dyspnea appeared, prompting ICU admission for airway support. She developed a proximal paresis and dysautonomia, global areflexia. CSF findings were unremarkable. IVIg were administered at a dose of 0.2g/kg per day during five days. Control EMG showed signs of polyradiculoneuropathy. She gradually recovered and was discharged at home after 32 days, with only a slight velopalatal paresis and a mild fatigue. Anti-ganglioside antibodies screen was positive for IgG-GM3, GD1b, GD3, GQ1b, GT1a and GT1b. In front of this clinical and biological picture, the diagnosis of atypical MFS was retained. Thirty day after discharge, both clinical and electrophysiological parameters were normalised. Conclusions: CONCLUSIONS: This case highlights that (i) MFS can show atypical presentation (here a pure Avellis syndrome, never reported in the context of the anti-GQ1b syndrome to our knowledge) and should be considered in front of an isolated impaired cranial nerve function, even in the absence of the classical triad of ophtalmoplegia, areflexia and ataxia, and (ii) that the boundaries between MFS and GBS are usually neater in textbooks than in real life. [less ▲]

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