References of "Schoenen, Jean"
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See detailLe laboratoire d’Anatomie : un banc d’essai des nouvelles technologies
Bonnet, Pierre ULg; Carlier, Alain ULg; Radermecker, Marc ULg et al

in Revue Médicale de Liège (2010), 65(Synthèse 2010), 35-40

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See detailEffect of kynurenic acid on sensitivity to cortical spreading depression in rats
Chauvel, Virginie ULg; Vamos, Eniko; Pardutz, Arpat et al

Poster (2010, October)

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See detailKynurenic acid decreases sensitivity to cortical spreading depression in rat
Chauvel, Virginie ULg; Vamos, Eniko; Pardutz, Arpat et al

Poster (2010, September)

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See detailInvolvement of Placental growth factor in Wallerian degeneration
Chaballe, Linda ULg; Close, Pierre ULg; Sempels, Maxime ULg et al

Poster (2010, September)

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See detailSTEM CELLS IN THE ADULT RAT SPINAL CORD: PLASTICITY AFTER INJURY AND TREADMILL TRAINING EXERCISE.
Foret, Ariane ULg; Quertainmont, Renaud ULg; Botman, O. et al

in Journal of Neurochemistry (2010), 112(3), 762-772

ABSTRACT Ependymal cells located around the central canal of the adult spinal cord are considered as a source of neural stem cells (NSCs) and represent an interesting pool of endogenous stem cells for ... [more ▼]

ABSTRACT Ependymal cells located around the central canal of the adult spinal cord are considered as a source of neural stem cells (NSCs) and represent an interesting pool of endogenous stem cells for repair strategies. Physical exercise is known to increase ependymal cell proliferation, while improving functional recovery. In this work, we further characterized those endogenous NSCs within the normal and injured adult rat spinal cord and investigated the effects of treadmill training using immunohistochemical and behavioural studies. In uninjured untrained rats, Sox-2, a NSC marker, was detected in all ependymal cells of the central canal, and also scattered throughout the parenchyma of the spinal cord. Within the lesion, Sox-2 expression increased transiently, while the number of nestin-positive ependymal cells increased with a concomitant enhancement of proliferation, as indicated by the mitotic markers Ki67 and BrdU. Exercise, which improved functional recovery and autonomous micturition, maintained nestin expression in both injured and uninjured spinal cords, with a positive correlation between locomotor recovery and the number of nestin-positive cells. [less ▲]

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See detailNSAIDs in the acute treatment of migraine: A review of clinical and experimental data
Párdutz, Arpad; Schoenen, Jean ULg

in Pharmaceuticals (2010), 3

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See detailHoneycomb-like appearance of dilated Virchow-Robin spaces.
Ruiz Miyares, F. J.; Deleu, D.; Akhtar, N. et al

in Acta Neurologica Belgica (2010), 110(1), 116-7

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See detailChanges in visual-evoked potential habituation induced by hyperventilation in migraine.
Coppola, G.; Curra, A.; Sava, Simona ULg et al

in Journal of Headache & Pain (2010)

Hyperventilation is often associated with stress, an established trigger factor for migraine. Between attacks, migraine is associated with a deficit in habituation to visual-evoked potentials (VEP) that ... [more ▼]

Hyperventilation is often associated with stress, an established trigger factor for migraine. Between attacks, migraine is associated with a deficit in habituation to visual-evoked potentials (VEP) that worsens just before the attack. Hyperventilation slows electroencephalographic (EEG) activity and decreases the functional response in the occipital cortex during visual stimulation. The neural mechanisms underlying deficient-evoked potential habituation in migraineurs remain unclear. To find out whether hyperventilation alters VEP habituation, we recorded VEPs before and after experimentally induced hyperventilation lasting 3 min in 18 healthy subjects and 18 migraine patients between attacks. We measured VEP P100 amplitudes in six sequential blocks of 100 sweeps and habituation as the change in amplitude over the six blocks. In healthy subjects, hyperventilation decreased VEP amplitude in block 1 and abolished the normal VEP habituation. In migraine patients, hyperventilation further decreased the already low block 1 amplitude and worsened the interictal habituation deficit. Hyperventilation worsens the habituation deficit in migraineurs possibly by increasing dysrhythmia in the brainstem-thalamo-cortical network. [less ▲]

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See detailEFNS guideline on the treatment of tension-type headache - Report of an EFNS task force.
Bendtsen, L.; Evers, S.; Linde, M. et al

in European Journal of Neurology (2010)

Background: Tension-type headache (TTH) is the most prevalent headache type and is causing a high degree of disability. Treatment of frequent TTH is often difficult. Objectives: To give evidence-based or ... [more ▼]

Background: Tension-type headache (TTH) is the most prevalent headache type and is causing a high degree of disability. Treatment of frequent TTH is often difficult. Objectives: To give evidence-based or expert recommendations for the different treatment procedures in TTH based on a literature search and the consensus of an expert panel. Methods: All available medical reference systems were screened for the range of clinical studies on TTH. The findings in these studies were evaluated according to the recommendations of the EFNS resulting in level A, B or C recommendations and good practice points. Recommendations: Non-drug management should always be considered although the scientific basis is limited. Information, reassurance and identification of trigger factors may be rewarding. Electromyography (EMG) biofeedback has a documented effect in TTH, whilst cognitive-behavioural therapy and relaxation training most likely are effective. Physical therapy and acupuncture may be valuable options for patients with frequent TTH, but there is no robust scientific evidence for efficacy. Simple analgesics and non-steroidal anti-inflammatory drugs are recommended for the treatment of episodic TTH. Combination analgesics containing caffeine are drugs of second choice. Triptans, muscle relaxants and opioids should not be used. It is crucial to avoid frequent and excessive use of analgesics to prevent the development of medication-overuse headache. The tricyclic antidepressant amitriptyline is drug of first choice for the prophylactic treatment of chronic TTH. Mirtazapine and venlafaxine are drugs of second choice. The efficacy of the prophylactic drugs is often limited, and treatment may be hampered by side effects. [less ▲]

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See detailNeurology.
Schoenen, Jean ULg; Jansen, An

in Acta neurologica Belgica (2010), 110(4), -

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See detailFactors predicting the probability of relapse after discontinuation of migraine preventive treatment with topiramate.
Schoenen, Jean ULg; Reuter, Uwe; Diener, Hans*-Christoph et al

in Cephalalgia : An International Journal of Headache (2010), 30(11), 1290-5

INTRODUCTION: Demographic and clinical variables were examined in a post hoc analysis of the PROlonged Migraine Prevention with Topiramate (PROMPT) study to determine potential contribution to relapse ... [more ▼]

INTRODUCTION: Demographic and clinical variables were examined in a post hoc analysis of the PROlonged Migraine Prevention with Topiramate (PROMPT) study to determine potential contribution to relapse. METHODS: After a six-month open-label (OL) topiramate phase, patients were randomised to continue topiramate or switch to placebo in a six-month double-blind (DB) phase. 'Relapse' was investigated in terms of change in monthly migraine days after randomisation compared with the month before randomisation, and was analysed during the first ('initial relapse') and last month ('sustained relapse') of the DB phase. More than 40 potential predicting factors were entered into analyses of variance and covariance. RESULTS: For initial relapse, variable-by-treatment interactions were significant for the Headache Impact Test (HIT-6) at DB baseline, and decline in acute medication intake or reporting of 'anxiety' in the OL phase. For sustained relapse, no statistically significant interactions were observed. CONCLUSION: Relapse after topiramate discontinuation in migraine prophylaxis appears to be unaffected by patient characteristics or baseline migraine frequency. [less ▲]

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See detailBotulinum toxin in headache treatment: finally a promising path?
Schoenen, Jean ULg

in Cephalalgia : An International Journal of Headache (2010), 30(7), 771-3

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See detailAlmotriptan efficacy in migraine with allodynia: a rebuttal to Burstein and Jakubowski's critique of Schoenen et al.
Schoenen, Jean ULg; Vandenheede, Michel

in Cephalalgia : An International Journal of Headache (2010), 30(9), 1147-8

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See detailGenome-wide association study of migraine implicates a common susceptibility variant on 8q22.1.
Anttila, Verneri; Stefansson, Hreinn; Kallela, Mikko et al

in Nature Genetics (2010), 42(10), 869-73

Migraine is a common episodic neurological disorder, typically presenting with recurrent attacks of severe headache and autonomic dysfunction. Apart from rare monogenic subtypes, no genetic or molecular ... [more ▼]

Migraine is a common episodic neurological disorder, typically presenting with recurrent attacks of severe headache and autonomic dysfunction. Apart from rare monogenic subtypes, no genetic or molecular markers for migraine have been convincingly established. We identified the minor allele of rs1835740 on chromosome 8q22.1 to be associated with migraine (P = 5.38 x 10, odds ratio = 1.23, 95% CI 1.150-1.324) in a genome-wide association study of 2,731 migraine cases ascertained from three European headache clinics and 10,747 population-matched controls. The association was replicated in 3,202 cases and 40,062 controls for an overall meta-analysis P value of 1.69 x 10(1)(1) (odds ratio = 1.18, 95% CI 1.127-1.244). rs1835740 is located between MTDH (astrocyte elevated gene 1, also known as AEG-1) and PGCP (encoding plasma glutamate carboxypeptidase). In an expression quantitative trait study in lymphoblastoid cell lines, transcript levels of the MTDH were found to have a significant correlation to rs1835740 (P = 3.96 x 10, permuted threshold for genome-wide significance 7.7 x 10. To our knowledge, our data establish rs1835740 as the first genetic risk factor for migraine. [less ▲]

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See detailAbnormal cortical responses to somatosensory stimulation in medication-overuse headache.
Coppola, Gianluca; Curra, Antonio; Di Lorenzo, Cherubino et al

in BMC neurology (2010), 10

BACKGROUND: Medication-overuse headache (MOH) is a frequent, disabling disorder. Despite a controversial pathophysiology convincing evidence attributes a pivotal role to central sensitization. Most ... [more ▼]

BACKGROUND: Medication-overuse headache (MOH) is a frequent, disabling disorder. Despite a controversial pathophysiology convincing evidence attributes a pivotal role to central sensitization. Most patients with MOH initially have episodic migraine without aura (MOA) characterized interictally by an absent amplitude decrease in cortical evoked potentials to repetitive stimuli (habituation deficit), despite a normal initial amplitude (lack of sensitization). Whether central sensitization alters this electrophysiological profile is unknown. We therefore sought differences in somatosensory evoked potential (SEP) sensitization and habituation in patients with MOH and episodic MOA. METHODS: We recorded median-nerve SEPs (3 blocks of 100 sweeps) in 29 patients with MOH, 64 with MOA and 42 controls. Episodic migraineurs were studied during and between attacks. We measured N20-P25 amplitudes from 3 blocks of 100 sweeps, and assessed sensitization from block 1 amplitude, and habituation from amplitude changes between the 3 sequential blocks. RESULTS: In episodic migraineurs, interictal SEP amplitudes were normal in block 1, but thereafter failed to habituate. Ictal SEP amplitudes increased in block 1, then habituated normally. Patients with MOH had larger-amplitude block 1 SEPs than controls, and also lacked SEP habituation. SEP amplitudes were smaller in triptan overusers than in patients overusing nonsteroidal anti-inflammatory drugs (NSAIDs) or both medications combined, lowest in patients with the longest migraine history, and highest in those with the longest-lasting headache chronification. CONCLUSIONS: In patients with MOH, especially those overusing NSAIDs, the somatosensory cortex becomes increasingly sensitized. Sensory sensitization might add to the behavioral sensitization that favors compulsive drug intake, and may reflect drug-induced changes in central serotoninergic transmission. [less ▲]

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