References of "Schoenen, Jean"
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See detailA multicentre, double-blind, randomized, placebo-controlled, parallel group study of multiple treatments of botulinum toxin type A (BoNTA) for the prophylaxis of episodic migraine headaches
Relja, M.; Poole, A. C.; Schoenen, Jean ULg et al

in Cephalalgia : An International Journal of Headache (2007), 27(6), 492-503

Our aim was to evaluate the safety and efficacy of botulinum toxin type A (BoNTA; BOTOX (R)) for prophylaxis of episodic migraine. In this double-blind, placebo-controlled study, patients were randomized ... [more ▼]

Our aim was to evaluate the safety and efficacy of botulinum toxin type A (BoNTA; BOTOX (R)) for prophylaxis of episodic migraine. In this double-blind, placebo-controlled study, patients were randomized to 225, 150 or 75 U of BoNTA or placebo after a 30-day placebo run-in for three 90-day treatment cycles. The primary efficacy end-point was the mean reduction from baseline in the frequency of migraine episodes at day 180 in the placebo non-responder stratum. All groups (N = 495) improved, with no significant differences. At day 180, the frequency of migraine episodes was reduced from baseline means of 4.3, 4.7, 4.7 and 4.4 by 1.6, 1.7, 1.5 and 1.4 for BoNTA 225 U, 150 U and 75 U and placebo, respectively. The primary end-point was not met. Treatment-related adverse events were transient and mild to moderate. BoNTA treatment was safe and well tolerated but did not result in significantly greater improvement than placebo in this study. Several factors may have confounded the results. [less ▲]

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See detailPathogénie de la maladie d'Alzheimer: les mécanismes moléculaires et cellulaires
Govaerts, L.; Schoenen, Jean ULg; Bouhy, D.

in Revue Médicale de Liège (2007), 62(4), 209-16

Alzheimer's disease is worldwide the leading cause of dementia in the elderly. Senile plaques and neurofibrillary tangles are together with neuronal loss and cortical atrophy characteristic ... [more ▼]

Alzheimer's disease is worldwide the leading cause of dementia in the elderly. Senile plaques and neurofibrillary tangles are together with neuronal loss and cortical atrophy characteristic neuropathological features of the disease. Senile plaques contain beta-amyloid (Abeta) peptide which is produced by cleavage of the amyloid precursor protein (APP) by beta- and gamma-secretases. Neurofibrillary tangles are twisted helicoidal strands of hyperphosphorylated tau protein, a microtubule-associated protein. Both pathogenic arms which we describe are interrelated and Abeta deposition seems to potentiate tau pathology. Tangle and plaque formation is influenced by various factors including reciprocal interactions, genetic factors, inflammation and reactive oxygen species. A better understanding of the cellular and molecular cascade which leads to the neuropathological lesions of Alzheimer's disease has led to novel disease-modifying treatment strategies. They yield varying, though encouraging, results and target various stages of the pathological process. Future cooperation between basic, clinical and pharmacological research should allow the development in a foreseeable future of strategies that can halt, or even prevent, this devastating disorder. [less ▲]

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See detailOccipital nerve stimulation for drug-resistant chronic cluster headache: a prospective pilot study
Magis, Delphine ULg; Allena, Marta; Bolla, Monica et al

in Lancet Neurology (2007), 6(4), 314-321

Background Drug-resistant chronic duster headache (drCCH) is a devastating disorder for which various destructive procedures have been tried unsuccessfully. Occipital nerve stimulation (ONS) is a new ... [more ▼]

Background Drug-resistant chronic duster headache (drCCH) is a devastating disorder for which various destructive procedures have been tried unsuccessfully. Occipital nerve stimulation (ONS) is a new, safe strategy for intractable headaches. We undertook a prospective pilot trial of ONS in drCCH to assess clinical efficacy and pain perception. Methods Eight patients with drCCH had a suboccipital neurostimulator implanted on the side of the headache and were asked to record details of frequency, intensity, and symptomatic treatment for their attacks in a diary before and after Continuous ONS. To detect changes in cephalic and extracephalic pain processing we measured electrical and pressure pain thresholds and the nociceptive blink reflex. Findings Two patients were pain free after a follow-up of 16 and 22 months; one of them still had occasional autonomic attacks. Three patients had around a 90% reduction in attack frequency. Two patients, one of whom had had the implant for only 3 months, had improvement of around 40%. Mean follow-up was 15.1 months (SD 9.5, range 3-22). Intensity of attacks tends to decrease earlier than frequency during ONS and, on average, is improved by 50% in remaining attacks. All but one patient were able to substantially reduce their preventive drug treatment. Interruption of ONS by switching off the stimulator or because of an empty battery was followed within days by recurrence and increase of attacks in all improved patients. ONS did not significantly modify pain thresholds. The amplitude of the nociceptive blink reflex increased with longer durations of ONS. There were no serious adverse events. Interpretation ONS could be an efficient treatment for drCCH and could be safer than deep hypothalamic stimulation. The delay of 2 months or more between implantation and significant clinical improvement suggests that the procedure ads via slow neuromodulatory processes at the level of upper brain stem or diencephalic centres. [less ▲]

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See detailGrowth-modulating molecules are associated with invading Schwann cells and not astrocytes in human traumatic spinal cord injury
Buss, A.; Pech, K.; Kakulas, B. A. et al

in Brain (2007), 130(Part 4), 940-953

Despite considerable progress in recent years, the underlying mechanisms responsible for the failure of axonal regeneration after spinal cord injury (SCI) remain only partially understood. Experimental ... [more ▼]

Despite considerable progress in recent years, the underlying mechanisms responsible for the failure of axonal regeneration after spinal cord injury (SCI) remain only partially understood. Experimental data have demonstrated that a major impediment to the outgrowth of severed axons is the scar tissue that finally dominates the lesion site and, in severe injuries, is comprised of connective tissue and fluid-filled cysts, surrounded by a dense astroglial scar. Reactive astrocytes and infiltrating cells, such as fibroblasts, produce a dense extracellular matrix (ECM) that represents a physical and molecular barrier to axon regeneration. In the human situation, correlative data on the molecular composition of the scar tissue that forms following traumatic SCI is scarce. A detailed investigation on the expression of putative growth-inhibitory and growth-promoting molecules was therefore performed in samples of post-mortem human spinal cord, taken from patients who died following severe traumatic SCI. The lesion-induced scar could be subdivided into a Schwann cell dominated domain which contained large neuromas and a surrounding dense ECM, and a well delineated astroglial scar that isolated the Schwann cell/ECM rich territories from the intact spinal parenchyma. The axon growth-modulating molecules collagen IV, laminin and fibronectin were all present in the post-traumatic scar tissue. These molecules were almost exclusively found in the Schwann cell-rich domain which had an apparent growth-promoting effect on PNS axons. In the astrocytic domain, these molecules were restricted to blood vessel walls without a co-localization with the few regenerating CNS neurites located in this region. Taken together, these results favour the notion that it is the astroglial compartment that plays a dominant role in preventing CNS axon regeneration. The failure to demonstrate any collagen IV, laminin or fibronectin upregulation associated with the astroglial scar suggests that other molecules may play a more significant role in preventing axon regeneration following human SCI. [less ▲]

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See detailInterictal habituation deficit of the nociceptive blink reflex: an endophenotypic marker for presymptomatic migraine?
Di Clemente, L.; Coppola, G.; Magis, Delphine ULg et al

in Brain : A Journal of Neurology (2007), 130(Pt 3), 765-770

Habituation of the nociception-specific blink reflex (nBR) is reduced interictally in migraine patients. This could be related to the habituation deficit of evoked cortical responses, a reproducible ... [more ▼]

Habituation of the nociception-specific blink reflex (nBR) is reduced interictally in migraine patients. This could be related to the habituation deficit of evoked cortical responses, a reproducible abnormality in migraine which has a familial character, or to central trigeminal sensitization due to repeated attacks. We compared nBR habituation in healthy volunteers devoid of personal or family history of migraine (HV), in migraine without aura patients (MO) and in healthy volunteers with a family history of migraine in first degree relatives (HV-F). We elicited the nBR by stimulating the right supraorbital region with a custom-built electrode in 16 MO between attacks, 15 HV and 14 HV-F. Habituation was measured as the percentage area-under-the-curve decrease in 10 consecutive blocks of five averaged rectified responses. nBR habituation was clearly reduced in MO and HV-F compared to HV. Percentage area under the curve decreased between the 1st and the 10th block by 55.01% in HV, 25.71% in MO (P = 0.001) and 26.73% in HV-F (P = 0.043). HV-F had the most pronounced abnormality with potentiation instead of habituation in the second block. We found a positive intraindividual correlation between attack frequency and habituation in MO (r = 0.621; P = 0.010). Migraine patients have interictally a deficient habituation of the nBR which is inversely related to attack frequency, suggesting that it is not due to trigeminal sensitization. Surprisingly, the most pronounced habituation deficit is found in asymptomatic individuals with a family history of migraine. Deficient nBR habituation could thus be a trait marker for the genetic predisposition to migraine. [less ▲]

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See detailrTMS of the occipital cortex abolishes Braille reading and repetition priming in blind subjects
Kupers, R.; Pappens, M.; MAERTENS DE NOORDHOUT, Alain ULg et al

in Neurology (2007), 68(9), 691-693

To study the functional involvement of the visual cortex in Braille reading, we applied repetitive transcranial magnetic stimulation (rTMS) over midoccipital (MOC) and primary somatosensory (SI) cortex in ... [more ▼]

To study the functional involvement of the visual cortex in Braille reading, we applied repetitive transcranial magnetic stimulation (rTMS) over midoccipital (MOC) and primary somatosensory (SI) cortex in blind subjects. After rTMS of MOC, but not SI, subjects made significantly more errors and showed an abolishment of the improvement in reading speed following repetitive presentation of the same word list, suggesting a role of the visual cortex in repetition priming in the blind. [less ▲]

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See detailOestrogen-modulated increase of calmodulin-dependent protein kinase II (CamKII) in rat spinal trigeminal nucleus after systemic nitroglycerin
Pardutz, A.; Hoyk, Z.; Varga, H. et al

in Cephalalgia : An International Journal of Headache (2007), 27(1), 46-53

Migraine can be triggered by systemic administration of the nitric oxide (NO) donor nitroglycerin (NTG) and by abrupt falls in plasma oestradiol. Calmodulin-dependent protein kinase II (CamKII) present in ... [more ▼]

Migraine can be triggered by systemic administration of the nitric oxide (NO) donor nitroglycerin (NTG) and by abrupt falls in plasma oestradiol. Calmodulin-dependent protein kinase II (CamKII) present in superficial dorsal horns is thought to play a role in sensitization of central nociceptors, a phenomen present in migraineurs. We therefore examined in rats the expression of CamKII in the caudal trigeminal nucleus (TNC) after subcutaneous NTG (10 mg/kg) and its modulation by oestrogen. In male rats and in ovariectomized females, after 4 h NTG increased significantly CamKII expression in the superficial layers of TNC, but not in the upper thoracic spinal cord. NTG had no effect on CamKII expression in oestradiol-treated ovariectomized animals. Thus NTG, i.e. NO, selectively enhances CamKII in the rat TNC and oestradiol blocks this effect. These data may help to understand the mechanisms by which NO triggers migraine attacks and oestrogens influence migraine severity. [less ▲]

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See detailA randomized double-blind placebo-controlled trial of thioctic acid in migraine prophylaxis
Magis, Delphine ULg; Ambrosini, Anna; Sandor, Peter et al

in Headache (2007), 47(1), 52-57

BACKGROUND: Impaired mitochondrial phosphorylation potential may play a role in migraine pathogenesis. Metabolic enhancers, such as riboflavin or coenzyme Q, are effective in migraine prophylaxis and ... [more ▼]

BACKGROUND: Impaired mitochondrial phosphorylation potential may play a role in migraine pathogenesis. Metabolic enhancers, such as riboflavin or coenzyme Q, are effective in migraine prophylaxis and quasi-devoid of adverse effects. Thioctic acid (-lipoic acid) is another substance known to enhance energy metabolism in mitochondria and to be beneficial in diabetic neuropathy. OBJECTIVE: After an open pilot study suggesting its therapeutic antimigraine potentials, we embarked therefore in a randomized controlled trial of thioctic acid (Thioctacid) in migraine prophylaxis steered by the Belgian Headache Society. METHODS: Five Belgian centers recruited 54 migraineurs (43 migraine without aura, 11 with aura; mean age 38 +/- 8 years; 7 males). After a 1-month single-blinded run-in period, 44 patients received either placebo (n = 18) or thioctic acid 600 mg p.o./day (n = 26) for 3 months. RESULTS: Statistical analysis was carried out on an intention-to-treat basis. Monthly attack frequency tended to be reduced between run-in and the 3rd month of treatment in the thioctic acid group compared to placebo (P= .06). The proportion of 50% responders was not significantly different between thioctic acid (30.8%) and placebo (27.8%). Within-group analyses showed a significant reduction of attack frequency (P= .005), headache days (P= .009), and headache severity (P= .03) in patients treated with thioctic acid for 3 months, while these outcome measures remained unchanged in the placebo group. No adverse effects were reported. For logistical reasons this trial was interrupted before the planned 80 patients were enrolled. CONCLUSION: Albeit underpowered, this study tends to indicate that thioctic acid may be beneficial in migraine prophylaxis. Before any firm conclusion can be drawn, however, a large multicenter trial is necessary. [less ▲]

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See detailMatrix metalloproteinases and their inhibitors in human traumatic spinal cord injury.
Buss, Armin; Pech, Katrin; Kakulas, Byron A et al

in BMC Neurology (2007), 7

BACKGROUND: Matrix metalloproteinases (MMPs) are a family of extracellular endopeptidases that degrade the extracellular matrix and other extracellular proteins. Studies in experimental animals ... [more ▼]

BACKGROUND: Matrix metalloproteinases (MMPs) are a family of extracellular endopeptidases that degrade the extracellular matrix and other extracellular proteins. Studies in experimental animals demonstrate that MMPs play a number of roles in the detrimental as well as in the beneficial events after spinal cord injury (SCI). In the present correlative investigation, the expression pattern of several MMPs and their inhibitors has been investigated in the human spinal cord. METHODS: An immunohistochemical investigation in post mortem samples of control and lesioned human spinal cords was performed. All patients with traumatic SCI had been clinically diagnosed as having "complete" injuries and presented lesions of the maceration type. RESULTS: In the unlesioned human spinal cord, MMP and TIMP immunoreactivity was scarce. After traumatic SCI, a lesion-induced bi-phasic pattern of raised MMP-1 levels could be found with an early up-regulation in macrophages within the lesion epicentre and a later induction in peri-lesional activated astrocytes. There was an early and brief induction of MMP-2 at the lesion core in macrophages. MMP-9 and -12 expression peaked at 24 days after injury and both molecules were mostly expressed in macrophages at the lesion epicentre. Whereas MMP-9 levels rose progressively from 1 week to 3 weeks, there was an isolated peak of MMP-12 expression at 24 days. The post-traumatic distribution of the MMP inhibitors TIMP-1, -2 and -3 was limited. Only occasional TIMP immuno-positive macrophages could be detected at short survival times. The only clear induction was detected for TIMP-3 at survival times of 8 months and 1 year in peri-lesional activated astrocytes. CONCLUSION: The involvement of MMP-1, -2, -9 and -12 has been demonstrated in the post-traumatic events after human SCI. With an expression pattern corresponding largely to prior experimental studies, they were mainly expressed during the first weeks after injury and were most likely involved in the destructive inflammatory events of protein breakdown and phagocytosis carried out by infiltrating neutrophils and macrophages, as well as being involved in enhanced permeability of the blood spinal cord barrier. Similar to animal investigations, the strong induction of MMPs was not accompanied by an expression of their inhibitors, allowing these proteins to exert their effects in the lesioned spinal cord. [less ▲]

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See detailMigraine without aura
Fumal, Arnaud ULg; Schoenen, Jean ULg

in Schmidt, R. R.; Wilis, W. D. (Eds.) Encyclopedia of Pain (2007)

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See detailCost estimates of brain disorders in Belgium
Schoenen, Jean ULg; Gianni, F.; Schretlen, L. et al

in Acta Neurologica Belgica (2006), 106(4), 208-214

This article presents the data on cost of the major brain disorders in Belgium which were retrieved from "Cost of Disorders of the Brain in Europe" study sponsored by the European Brain Council and ... [more ▼]

This article presents the data on cost of the major brain disorders in Belgium which were retrieved from "Cost of Disorders of the Brain in Europe" study sponsored by the European Brain Council and performed by Stockholm Health Economics. The disorders selected were : addiction, depression, anxiety disorders, brain tumours, dementia, epilepsy, migraine and other headaches, multiple sclerosis, Parkinson's disease, psychotic disorders, stroke and trauma. Figures for prevalence of disorders and direct medical, direct non-medical and indirect costs are based on data coming from available electronic data bases, or when missing for Belgium, best possible estimates or extrapolated data were used. All economic data were transformed to E's for 2004 and adjusted for purchasing power parity (PPP). The results show that the total number of people with any brain disorder in Belgium amounts to 2,9 million in 2004, the most prevalent being anxiety disorders 1.1 million, migraine 860 000, addiction (any) 800.000 and depression 500.000 cases. The total cost of all included brain disorders in Belgium was estimated at 10.6 billion Euros. Most costly per case are brain tumours, multiple sclerosis, stroke and dementia. Because of their higher prevalence, however, depression, dementia, addiction, anxiety disorders and migraine have the highest total costs. Taken together, brain disorders consume 4% of the gross national product and cost each citizen of Belgium E 1029 per year The drug costs for brain disorders constitute only 10% of the total drug market in Belgium, and only 4% of the total cost of brain disorders in Belgium. This should be compared to the cost estimates and to a previous study which showed that brain disorders are responsible for 35% of the total burden of all disorders in Europe. This study suggests therefore that the direct healthcare resources, including expenses for drug therapies, allocated to brain disorders in Belgium are not leveled to the indirect costs and burden of these disorders. A comparison with data available from a direct prospective study in demented Belgian patients suggests that the mathematical estimates presented here reflect quite accurately the real average cost for dementia, although there are large variations depending on disease severity. As, in addition, subjects with brain disorders face collateral costs which have not been taken into account and may vary between countries, it seems worthwhile to conduct, in cooperation with patients associations, a complementary survey in the Belgian ecosystem to establish the cost profile of representative patients for the major brain disorders. Such a survey is being organized by a task force of the Belgian Brain Council. [less ▲]

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See detailEffects of vagal nerve stimulation in the rat orofacial formalin model of pain
Multon, S.; Scholsem, M.; Legrain, C. et al

Conference (2006, November 10)

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See detailEffects of vagal nerve stimulation in the rat orofacial formalin model of pain
Multon, Sylvie ULg; Scholsem, Martin; LEGRAIN, Caroline ULg et al

Poster (2006, November)

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See detailHypothalamic stimulation in chronic cluster headache: a pilot study of efficacy and mode of action
Schoenen, Jean ULg; Di Clemente, L.; Vandenheede, Michel et al

in Cephalalgia : An International Journal of Headache (2006, November), 26(11), 1352

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See detailLong-term depression of trigeminal nociceptive evoked potentials by supraorbital 1Hz electrical stimulations is deficient in migraineurs but not in tension-type headache patients
Magis, Delphine ULg; Bolla, M.; De Pasqua, Victor ULg et al

in Cephalalgia : An International Journal of Headache (2006, November), 26(11), 1386

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See detailLong term follow-up study of occipital nerve stimulation (ONS) for refractory chronic cluster headache: drastic change from short term outcome
Magis, Delphine ULg; Remacle, J. M.; Schoenen, Jean ULg

in Cephalalgia : An International Journal of Headache (2006, November), 26(11), 1398

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See detailEffects of vagal nerve stimulation in the rat orofacial formalin model of pain
Multon, Sylvie ULg; Scholsem, Martin; LEGRAIN, Caroline ULg et al

in Book of Abstracts of the 36th Annual Meeting Society for Neuroscience (Oct 2006) (2006, October)

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See detailTowards a definition of intractable headache for use in clinical practice and trials
Goadsby, P. J.; Schoenen, Jean ULg; Ferrari, M. D. et al

in Cephalalgia : An International Journal of Headache (2006), 26(9), 1168-1170

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