References of "Schoenen, Jean"
     in
Bookmark and Share    
Full Text
Peer Reviewed
See detailMigraine preventive drugs differentially affect cortical spreading depression in rat.
Bogdanov, Vladimir ULg; Multon, Sylvie ULg; Chauvel, Virginie ULg et al

in Neurobiology of Disease (2011), 41(2), 430-5

Cortical spreading depression (CSD) is the most likely cause of the migraine aura. Drugs with distinct pharmacological properties are effective in the preventive treatment of migraine. To test the ... [more ▼]

Cortical spreading depression (CSD) is the most likely cause of the migraine aura. Drugs with distinct pharmacological properties are effective in the preventive treatment of migraine. To test the hypothesis that their common denominator might be suppression of CSD we studied in rats the effect of three drugs used in migraine prevention: lamotrigine which is selectively effective on the aura but not on the headache, valproate and riboflavin which have a non-selective effect. Rats received for 4 weeks daily intraperitoneal injections of one of the three drugs. For valproate and riboflavin we used saline as control, for lamotrigine its vehicle dimethyl sulfoxide. After treatment, cortical spreading depressions were elicited for 2h by occipital KCl application. We measured CSD frequency, its propagation between a posterior (parieto-occipital) and an anterior (frontal) electrode, and number of Fos-immunoreactive nuclei in frontal cortex. Lamotrigine suppressed CSDs by 37% and 60% at posterior and anterior electrodes. Valproate had no effect on posterior CSDs, but reduced anterior ones by 32% and slowed propagation velocity. Riboflavin had no significant effect at neither recording site. Frontal Fos expression was decreased after lamotrigine and valproate, but not after riboflavin. Serum levels of administered drugs were within the range of those usually effective in patients. Our study shows that preventive anti-migraine drugs have differential effects on CSD. Lamotrigine has a marked suppressive effect which correlates with its rather selective action on the migraine aura. Valproate and riboflavin have no effect on the triggering of CSD, although they are effective in migraine without aura. Taken together, these results are compatible with a causal role of CSD in migraine with aura, but not in migraine without aura. [less ▲]

Detailed reference viewed: 93 (13 ULg)
Full Text
Peer Reviewed
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

Detailed reference viewed: 116 (27 ULg)
Full Text
Peer Reviewed
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)

Detailed reference viewed: 2 (0 ULg)
Full Text
See detailKynurenic acid decreases sensitivity to cortical spreading depression in rat
Chauvel, Virginie ULg; Vamos, Eniko; Pardutz, Arpat et al

Poster (2010, September)

Detailed reference viewed: 2 (0 ULg)
Full Text
See detailInvolvement of Placental growth factor in Wallerian degeneration
Chaballe, Linda ULg; Close, Pierre ULg; Sempels, Maxime ULg et al

Poster (2010, September)

Detailed reference viewed: 34 (12 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 117 (29 ULg)
Full Text
Peer Reviewed
See detailNSAIDs in the acute treatment of migraine: A review of clinical and experimental data
Párdutz, Arpad; Schoenen, Jean ULg

in Pharmaceuticals (2010), 3

Detailed reference viewed: 19 (2 ULg)
Full Text
Peer Reviewed
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

Detailed reference viewed: 17 (1 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 13 (0 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 36 (0 ULg)
See detailNeurology.
Schoenen, Jean ULg; Jansen, An

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

Detailed reference viewed: 16 (6 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 15 (2 ULg)
Full Text
Peer Reviewed
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

Detailed reference viewed: 16 (1 ULg)
Full Text
Peer Reviewed
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

Detailed reference viewed: 8 (0 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 48 (2 ULg)