References of "Schoenen, Jean"
     in
Bookmark and Share    
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 24 (0 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 50 (3 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 12 (2 ULg)
See detailMigraine without aura
Fumal, Arnaud ULg; Schoenen, Jean ULg

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

Detailed reference viewed: 19 (3 ULg)
Full Text
Peer Reviewed
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 ▲]

Detailed reference viewed: 15 (1 ULg)
Peer Reviewed
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)

Detailed reference viewed: 6 (3 ULg)
Full Text
Peer Reviewed
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)

Detailed reference viewed: 4 (0 ULg)
Full Text
Peer Reviewed
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

Detailed reference viewed: 9 (0 ULg)
Full Text
Peer Reviewed
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

Detailed reference viewed: 10 (6 ULg)
Full Text
Peer Reviewed
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

Detailed reference viewed: 21 (3 ULg)
Full Text
Peer Reviewed
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)

Detailed reference viewed: 4 (0 ULg)
Full Text
Peer Reviewed
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

Detailed reference viewed: 16 (2 ULg)
Full Text
Peer Reviewed
See detailAnimal models of migraine: looking at the component parts of a complex disorder
Bergerot, A.; Holland, P. R.; Akerman, S. et al

in European Journal of Neuroscience (2006), 24(6), 1517-1534

Animal models of human disease have been extremely helpful both in advancing the understanding of brain disorders and in developing new therapeutic approaches. Models for studying headache mechanisms ... [more ▼]

Animal models of human disease have been extremely helpful both in advancing the understanding of brain disorders and in developing new therapeutic approaches. Models for studying headache mechanisms, particularly those directed at migraine, have been developed and exploited efficiently in the last decade, leading to better understanding of the potential mechanisms of the disorder and of the action for antimigraine treatments. Model systems employed have focused on the pain-producing cranial structures, the large vessels and dura mater, in order to provide reproducible physiological measures that could be subject to pharmacological exploration. A wide range of methods using both in vivo and in vitro approaches are now employed; these range from manipulation of the mouse genome in order to produce animals with human disease-producing mutations, through sensitive immunohistochemical methods to vascular, neurovascular and electrophysiological studies. No one model system in experimental animals can explain all the features of migraine; however, the systems available have begun to offer ways to dissect migraine's component parts to allow a better understanding of the problem and the development of new treatment strategies. [less ▲]

Detailed reference viewed: 68 (4 ULg)
Full Text
Peer Reviewed
See detailTranscranial magnetic stimulation of the visual cortex induces somatotopically organized qualia in blind subjects
Kupers, R.; Fumal, Arnaud ULg; Maertens De Noordhout, Alain ULg et al

in Proceedings of the National Academy of Sciences of the United States of America (2006), 103(35), 13256-13260

After loss of a particular sensory channel, the deprived cortex can be activated by inputs from other sensory modalities. It is not known whether activation of the rewired cortex evokes subjective ... [more ▼]

After loss of a particular sensory channel, the deprived cortex can be activated by inputs from other sensory modalities. It is not known whether activation of the rewired cortex evokes subjective experiences characteristic of that cortex or consistent with the rerouted sensory information. In a previous study, blind subjects were trained to perform visual tasks with a tongue display unit, a sensory substitution device that translates visual displays into electrotactile tongue stimulation. This cross-modal sensory stimulation activated their visual cortices. We now extend this finding by using transcranial magnetic stimulation to examine the perceptual correlates of training-induced plastic responses. We find that blind subjects proficient with the use of the tongue display unit report somatopicaily organized tactile sensations that are referred to the tongue when transcranial magnetic stimulation is applied over the occipital cortex. No such sensations were evoked in trained, blindfolded, seeing control subjects who performed the sensory substitution task equally well. These data show that the perceptual correlate of activity in a given cortical area reflects the characteristics of its novel sensory input source. [less ▲]

Detailed reference viewed: 21 (2 ULg)
Full Text
Peer Reviewed
See detailMigraine with Urticaria
Fumal, Arnaud ULg; Cremers, Julien ULg; Ambrosini, A. et al

in Neurology (2006), 67(4), 682

Detailed reference viewed: 12 (1 ULg)
Full Text
Peer Reviewed
See detailDelayed GM-CSF treatment stimulates axonal regeneration and functional recovery in paraplegic rats via an increased BDNF expression by endogenous macrophages
Bouhy, Delphine; Malgrange, Brigitte ULg; Multon, Sylvie ULg et al

in FASEB Journal (2006), 20(8), 12391241

Macrophages (monocytes/microglia) could play a critical role in central nervous system repair. We have previously found a synchronism between the regression of spontaneous axonal regeneration and the ... [more ▼]

Macrophages (monocytes/microglia) could play a critical role in central nervous system repair. We have previously found a synchronism between the regression of spontaneous axonal regeneration and the deactivation of macrophages 3-4 wk after a compression-injury of rat spinal cord. To explore whether reactivation of endogenous macrophages might be beneficial for spinal cord repair, we have studied the effects of granulocyte-macrophage colony stimulating factor (GM-CSF) in the same paraplegia model and in cell cultures. There was a significant, though transient, improvement of locomotor recovery after a single delayed intraperitoneal injection of 2 mu g GM-CSF, which also increased significantly the expression of Cr3 and brain-derived neurotrophic factor ( BDNF) by macrophages at the lesion site. At longer survival delays, axonal regeneration was significantly enhanced in GMCSF-treated rats. In vitro, BV2 microglial cells expressed higher levels of BDNF in the presence of GM-CSF and neurons cocultured with microglial cells activated by GM-CSF generated more neurites, an effect blocked by a BDNF antibody. These experiments suggest that GM-CSF could be an interesting treatment option for spinal cord injury and that its beneficial effects might be mediated by BDNF.-Bouhy, D., Malgrange, B., Multon, S., Poirrier, A. L., Scholtes, F., Schoenen, J., Franzen, R. Delayed GM-CSF treatment stimulates axonal regeneration and functional recovery in paraplegic rats via an increased BDNF expression by endogenous macrophages. [less ▲]

Detailed reference viewed: 30 (5 ULg)
Full Text
Peer Reviewed
See detailNeurophysiological features of the migrainous brain
Schoenen, Jean ULg

in Neurological Sciences (2006), 27(Suppl. 2), 77-81

Migraine is a disorder in which central nervous system (CNS) dysfunction might play a pivotal role. As there are no consistent structural disturbances, clinical neurophysiology methods seem particularly ... [more ▼]

Migraine is a disorder in which central nervous system (CNS) dysfunction might play a pivotal role. As there are no consistent structural disturbances, clinical neurophysiology methods seem particularly suited to study its pathophysiology. This chapter will focus on a review of neurophysiological studies that have provided an insight into migraine pathogenesis. The results are in part contradictory, which may be due to the methodology, patient selection or timing of study. Nonetheless, quantitative electroencephalography and magnetoencephalography recordings during migraine attacks provide strong, though indirect, evidence favouring the occurrence of spreading cortical depression during attacks of migraine with, and possibly without, aura. Evoked cortical potential and nociceptive blink reflex studies demonstrate that lack of habituation during repetitive stimulation is a reproducible CNS dysfunction interictally in both migraine with and without aura. Transcranial magnetic stimulations show excitability changes of the visual cortex. The interictal migrainous CNS dysfunction is likely to play a role in migraine pathogenesis, has a familial character and undergoes periodic modulations with quasi-normalisation just before, during an attack and after treatment with certain prophylactic agents. In addition, neurophysiological methods have revealed subclinical abnormalities of cerebellar function and neuromuscular transmission, which may improve phenotyping of migraineurs for genetic and therapeutic studies. [less ▲]

Detailed reference viewed: 17 (0 ULg)
Full Text
Peer Reviewed
See detailLes céphalées par abus d'antalgiques et d'anti-migraineux
Fumal, Arnaud ULg; Magis, Delphine ULg; Schoenen, Jean ULg

in Revue Médicale de Liège (2006), 61(4), 217-22

Medication overuse headache (MOH) insidiously evolves from episodic migraine or tension-type headache because of overconsumption of analgesics, ergotamine or triptans. It affects 1-2% of the general ... [more ▼]

Medication overuse headache (MOH) insidiously evolves from episodic migraine or tension-type headache because of overconsumption of analgesics, ergotamine or triptans. It affects 1-2% of the general population, but 15-20% of patients attending specialized headache centers. The precise neurobiologic mechanisms underlying this complication of episodic headaches are not well understood. Abnormalities of central monoaminergic systems have been suggested and substance dependence is more frequent in personal and family histories of affected subjects. In a recent FDG-PET study of 16 migraineurs with MOH before and after analgesics withdrawal we found a persistent hypometabolism of the medial orbitofrontal cortex, comparable to the one described after withdrawal in substance abuse. The orbitofrontal cortex plays a pivotal role in drive, decision-making and drug dependence. We postulate that its hypoactivity predisposes certain migraineurs to MOH and to relapse after withdrawal. There is no unique management strategy for these patients, but medication withdrawal is a prerequisite for the effectiveness of preventive treatments and headache improvement. [less ▲]

Detailed reference viewed: 68 (4 ULg)
Full Text
Peer Reviewed
See detailOrbitofrontal cortex involvement in chronic analgesic-overuse headache evolving from episodic migraine
Fumal, Arnaud ULg; Laureys, Steven ULg; Di Clemente, Laura et al

in Brain (2006), 129(Pt 2), 543-550

The way in which medication overuse transforms episodic migraine into chronic daily headache is unknown. To search for candidate brain areas involved in this process, we measured glucose metabolism with ... [more ▼]

The way in which medication overuse transforms episodic migraine into chronic daily headache is unknown. To search for candidate brain areas involved in this process, we measured glucose metabolism with 18-FDG PET in 16 chronic migraineurs with analgesic overuse before and 3 weeks after medication withdrawal and compared the data with those of a control population (n = 68). Before withdrawal, the bilateral thalamus, orbitofrontal cortex (OFC), anterior cingulate gyrus, insula/ventral striatum and right inferior parietal lobule were hypometabolic, while the cerebellar vermis was hypermetabolic. All dysmetabolic areas recovered to almost normal glucose uptake after withdrawal of analgesics, except the OFC where a further metabolic decrease was found. A subanalysis showed that most of the orbitofrontal hypometabolism was due to eight patients overusing combination analgesics and/or an ergotamine-caffeine preparation. Medication overuse headache is thus associated with reversible metabolic changes in pain processing structures like other chronic pain disorders, but also with persistent orbitofrontal hypofunction. The latter is known to occur in drug dependence and could predispose subgroups of migraineurs to recurrent analgesic overuse. [less ▲]

Detailed reference viewed: 13 (0 ULg)