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See detailLa neuroinvasion dans les maladies à prions: étude de l'interface neuroimmune FDC - système nerveux sympathique
Demonceau, Caroline ULg

Doctoral thesis (2013)

Prion diseases are neurodegenerative diseases affecting the central nervous system (CNS) wherein the PrPd disease-associated prion infectious agent is an abnormal isoform of PrPc host-encoded cellular ... [more ▼]

Prion diseases are neurodegenerative diseases affecting the central nervous system (CNS) wherein the PrPd disease-associated prion infectious agent is an abnormal isoform of PrPc host-encoded cellular prion protein. The process through which the prion infectious agent is transferred to the CNS, the neuroinvasion, is still unknown, but secondary lymphoid organs seem to play an important role in prion amplification prior the invasion of the associated peripheral nervous system (PNS). In particular, modifications of follicular dendritic cells (FDC) and sympathetic nervous system (SNS) of lymphoid organs could influence the speed of neuroinvasion, and thus the length of the disease incubation period. It was shown that the lack of mature FDC prevents the replication of the infectious agent in secondary lymphoid organs. Likewise, sympathectomy delays the onset of the disease, and enhances sympathetic innervation reduces the incubation period. In mice, the relative positioning of FDC and sympathetic neural fibres plays a role in the incubation period following scrapie inoculation. This study thus focuses on the neuroimmune interface between FDC and sympathetic neural fibres. First, the number of close interactions between FDC and sympathetic neural fibres of five mouse strains with the same Prnpa genotype was estimated to check if it could explain the different incubation period observed after inoculation of primary bovine spongiform encephalopathy (BSE) infected-brain. Then we checked if scrapie infection, by oral or intraperitoneal route, could influence this neuroimmune interface between FDC and sympathetic neural fibres within Peyer’s patches (PP) and spleen of the C57BL/6 mouse strain. In the first part of this work, co-localizations between FDC and sympathetic neural fibres were observed in vivo within germinal centers (GC) of mouse spleen. Among the five mouse strains exhibiting the same Prnpa genotype, three strains (RIII-1, RIII-2 and 129/Ola) showed an incubation period about 100 days shorter than those of C57BL and C57BL/6 mouse strains when inoculated with primary BSE. Moreover, amplification by FDC seems an obligatory process before subsequent neuroinvasion as an intracerebral inoculation doesn’t reduce the incubation period observed with an intraperitoneal inoculation. A meticulous analysis revealed that the density of close interactions between FDC and sympathetic neural fibres is not higher for the three mouse strains with a shorter incubation period. However, these three mouse strains with a shorter incubation period after primary BSE inoculation have a higher proportion of FDC networks with close interactions than the mouse strains with a longer incubation period. These results suggest that it is not the quantity of sympathetic neural fibres close to FDC, but rather the percentage of FDC with close sympathetic neural endings that could influence the incubation period of prions diseases. In the second part of this work, it came out that prion infection did not result in neuronal loss within the PNS like observed in the CNS, and also did not modify the FDC-SNS neuroimmune interface of secondary lymphoid organs where PrPd deposits are observed within germinal centers. For a single mouse strain orally infected with scrapie, neither FDC networks hypertrophy nor sympathetic neural fibres closer than 10 μm from a FDC network were observed within GC of PP. Moreover, in our conditions, the prion strain did not seem to alter the neuroimmune interface between FDC and SNS in PP that could explain the different incubation periods observed with the 139A and ME7 scrapie strains. To check if prion infection does not modify the FDC-SNS neuroimmune interface, close interactions between FDC and sympathetic neural fibres already shown in the spleen were analyzed in the same mouse strain intraperitoneally infected with the 139A scrapie strain. In that case as well, no differences were observed in FDC network hypertrophy, in the in vivo density of sympathetic neural fibres closer than 10 μm from a FDC network, or in the proportion of well innervated FDC networks, compared to control mice. An in vitro model of coculture of splenic FDC from the same C57BL/6 mouse strain with nerve cells from dorsal root ganglia (DRG) also yielded similar results. FDC isolated from scrapie 139A infected mice exhibited the same neuritogenic or neurotrophic effects than FDC isolated from control mice. During these experiments, it was also noted that young-adult or middle-age mice showed both the same mean density of close interactions between FDC and SNS. However, with age, even if the splenic volume occupied by FDC networks halved, the proportion of FDC networks with close interactions almost doubled. It would be very interesting to check this last parameter in old mice that show some delay in neuroinvasion of prion disease but also to evaluate if this percentage of well innervated FDC network contributes to the prion pathogenesis within the spleen. In conclusion, scrapie 139A and ME7 strains don’t modify FDC-SNS neuroimmune interface of secondary lymphoid organs, not allowing explaining the different incubation period observed with equivalent infectious doses. Moreover, following an oral inoculation of prion, neuroinvasion within PP would not involve direct contact between FDC and sympathetic nerves, but rather another process still to be determined or implying other nerve fibres and/or mobile cells such as macrophages or dendritic cells. However, in the spleen, the percentage of FDC networks with close sympathetic neural fibres – rather than the number of sympathetic neural fibres close to the FDC network – observed for a given age, species and Prnp genotype at the time of inoculation could play a role in the different incubation periods observed for the same prion strain. The cellular compounds involved in the specific FDC microenvironment still have to be determined for each cell implied in the neuroinvasion process. [less ▲]

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See detailNeurokinin-1 receptor antagonists in the prevention of postoperative nausea and vomiting
Diemunsch, P.; Joshi, G. P.; Brichant, Jean-François ULg

in British Journal of Anaesthesia (2009), 103(1), 7-13

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See detailNeuroleptiques à longue durée d'action. III. Etude pilote du penfluridol (R16341)
Bobon, Jean; Mélon, Jean; Mormont, Christian ULg et al

in Acta Psychiatrica Belgica (1970), 70

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See detailNeuroleptiques à longue durée d'action: III. Etude pilote du penfluridol (R16341) : données psychométriques
Mormont, Christian ULg

in Acta Psychiatrica Belgica (1972), 72(5), 595-601

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See detailNeurological aspects of developmental oro-linguo-facial disorders
Misson, Jean-Paul ULg; Evrard, Philippe

Conference (1984)

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See detailNeurological complications of acute and persistent Epstein-Barr virus infection in paediatric patients
Häusler, M.; Ramaekers, Vincent ULg; Doenges, M. et al

in Journal of Medical Virology (2002), 68(2), 253-263

Neurological complications of Epstein-Barr virus (EBV) have been reported almost exclusively in the course of acute primary infections. The role of EBV in paediatric neurological disease was investigated ... [more ▼]

Neurological complications of Epstein-Barr virus (EBV) have been reported almost exclusively in the course of acute primary infections. The role of EBV in paediatric neurological disease was investigated prospectively over a 2-year period, searching for acute primary, chronic, and reactivated EBV infections. Active EBV infections were diagnosed in 10/48 patients, including two with acute primary EBV infections (cranial neuritis and cerebellitis), one with chronic active infection (T/NK cell lymphoma with cranial neuritis), and seven with reactivated infections. Among these seven patients, three showed "Alice in Wonderland" syndrome, one facial nerve palsy, one progressive macrocephaly, and two prolonged encephalitic illness. The prognosis was good except for the patient with lethal T/NK cell lymphoma and the two girls with encephalitic illness. Despite steroid treatment, these girls suffered prolonged cognitive impairment and epileptic seizures. Both developed left-sided hippocampal atrophy, and one of them hippocampal sclerosis. Like primary infections, reactivated EBV infections cause neurological complications in a considerable number of paediatric patients, lead to serious long-term complications, and may contribute to the pathogenesis of hippocampal lesions. © 2002 Wiley-Liss, Inc. [less ▲]

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See detailNeurological picture. Extreme unilateral widening of Virchow-Robin spaces
Fumal, Arnaud ULg; Maertens De Noordhout, Alain ULg; Collignon, Laurent

in Journal of Neurology, Neurosurgery & Psychiatry (2009), 80(1), 64-65

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See detailNeurologie des équidés
Amory, Hélène ULg

Learning material (2011)

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See detailNeurology.
Schoenen, Jean ULg; Jansen, An

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

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See detailNeuromodulation in cluster headache.
Fontaine, Denys; Vandersteen, Clair; MAGIS, Delphine ULg et al

in Advances and technical standards in neurosurgery (2015), 42

Medically refractory chronic cluster headache (CH) is a severely disabling headache condition for which several surgical procedures have been proposed as a prophylactic treatment. None of them have been ... [more ▼]

Medically refractory chronic cluster headache (CH) is a severely disabling headache condition for which several surgical procedures have been proposed as a prophylactic treatment. None of them have been evaluated in controlled conditions, only open studies and case series being available. Destructive procedures (radiofrequency lesioning, radiosurgery, section) and microvascular decompression of the trigeminal nerve or the sphenopalatine ganglion (SPG) have induced short-term improvement which did not maintain on long term in most of the patients. They carried a high risk of complications, including severe sensory loss and neuropathic pain, and consequently should not be proposed in first intention.Deep brain stimulation (DBS), targeting the presumed CH generator in the retro-hypothalamic region or fibers connecting it, decreased the attack frequency >50 in 60 % of the 52 patients reported. Complications were infrequent: gaze disturbances, autonomic disturbances, and intracranial hemorrhage (2).Occipital nerve stimulation (ONS) was efficient (decrease of attack frequency >50 %) in about 70 % of the 60 patients reported, with a low risk of complications (essentially hardware related). Considering their respective risks, ONS should be proposed first and DBS only in case of ONS failure.New on-demand chronically implanted SPG stimulation seemed to be efficient to abort CH attacks in a pilot controlled trial, but its long-term safety needs to be further studied. [less ▲]

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See detailNeuromodulation in migraine: state of the art and perspectives.
MAGIS, Delphine ULg

in Expert review of medical devices (2015)

Migraine is a highly prevalent and disabling disease. The drugs prescribed for migraine prophylaxis can have intolerable side effects or can be ineffective. Neuromodulation techniques are increasingly ... [more ▼]

Migraine is a highly prevalent and disabling disease. The drugs prescribed for migraine prophylaxis can have intolerable side effects or can be ineffective. Neuromodulation techniques are increasingly used in neurology. Transcutaneous supraorbital nerve stimulation is effective in episodic migraine prevention, whereas vagus nerve stimulation provides interesting results in acute migraine therapy. Transcranial stimulation techniques gave variable, and sometimes contradictory, results. The visual cortex is the target of choice in migraine: studies in migraine prevention and aura acute treatment are encouraging. These noninvasive therapies appear safe with a low rate of side effects. Available studies of invasive occipital nerve stimulation in chronic migraine gave modest results; but invasive occipital nerve stimulation offers a new hope to highly disabled patients who failed to respond to any other treatment. In the future, neuromodulation will probably take an increasing place in migraine treatment, as add-on therapy or alternative to medications, especially because of its attractive safety profile. [less ▲]

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See detailNeuromodulation of chronic headaches: position statement from the European Headache Federation
Martelletti, P; Jensen, R; Antal, A et al

in Journal of Headache & Pain (2013), 14

The medical treatment of patients with chronic primary headache syndromes (chronic migraine, chronic tension-type headache, chronic cluster headache, hemicrania continua) is challenging as serious side ... [more ▼]

The medical treatment of patients with chronic primary headache syndromes (chronic migraine, chronic tension-type headache, chronic cluster headache, hemicrania continua) is challenging as serious side effects frequently complicate the course of medical treatment and some patients may be even medically intractable. When a definitive lack of responsiveness to conservative treatments is ascertained and medication overuse headache is excluded, neuromodulation options can be considered in selected cases.Here, the various invasive and non-invasive approaches, such as hypothalamic deep brain stimulation, occipital nerve stimulation, stimulation of sphenopalatine ganglion, cervical spinal cord stimulation, vagus nerve stimulation, transcranial direct current stimulation, repetitive transcranial magnetic stimulation, and transcutaneous electrical nerve stimulation are extensively published although proper RCT-based evidence is limited. The European Headache Federation herewith provides a consensus statement on the clinical use of neuromodulation in headache, based on theoretical background, clinical data, and side effect of each method. This international consensus further gives recommendations for future studies on these new approaches.In spite of a growing field of stimulation devices in headaches treatment, further controlled studies to validate, strengthen and disseminate the use of neurostimulation are clearly warranted. Consequently, until these data are available any neurostimulation device should only be used in patients with medically intractable syndromes from tertiary headache centers either as part of a valid study or have shown to be effective in such controlled studies with an acceptable side effect profile. [less ▲]

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See detailNeuromorphic reinforcement learning
Dethier, Julie ULg; Ernst, Damien; Sepulchre, Rodolphe

Conference (2012, March 29)

Living organisms are able to successfully perform challeng- ing tasks such as perception, classification, association, and control. In hope for similar successes in artificial systems, neuromorphic ... [more ▼]

Living organisms are able to successfully perform challeng- ing tasks such as perception, classification, association, and control. In hope for similar successes in artificial systems, neuromorphic engineering uses neurophysiological models of perception and information processing in biological sys- tems to emulate their functions but also resemble their struc- ture [1]. In this abstract, we focus on the basal ganglia (BG), brain region in control of primitive functions of the nervous system, and specifically on their involvement in action selec- tion and reinforcement learning (RL). We hypothesize that neuromorphic-inspired systems will greatly benefit the RL community. [less ▲]

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See detailNeuromuscular transmission in migraine patients with prolonged aura
Ambrosini, Anna; MAERTENS DE NOORDHOUT, Alain ULg; SCHOENEN, Jean ULg

in Acta Neurologica Belgica (2001), 101(3), 166-70

P/Q Ca2+ channels are genetically abnormal in most cases of familial hemiplegic migraine (FHM) and may be involved in other types of migraine. They are also found at the neuromuscular junctions, where ... [more ▼]

P/Q Ca2+ channels are genetically abnormal in most cases of familial hemiplegic migraine (FHM) and may be involved in other types of migraine. They are also found at the neuromuscular junctions, where they control stimulation-induced acetylcholine release. Prolonged aura is a very frequent clinical feature in FHM patients. The objective of this study was thus to explore neuromuscular transmission in migraine with typical and prolonged aura patients. We performed single fiber electromyography (SFEMG) in such patients and compared them to a group of healthy volunteers. Results were expressed as mean jitter (MCD) and percentage of single endplate abnormalities. Mean MCD was on average comparable in controls and migraineurs. By contrast, single endplate abnormalities were only found in patients (p < 0.01), especially in those with prolonged aura (p < 0.001). These results suggest subtle impairment of neuromuscular transmission in a subgroup of migraineurs characterized by prolonged aura, which might be due to dysfunctioning P/Q Ca(2+)-channels. [less ▲]

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See detailNeuromuscular transmission in migraine: a single-fiber EMG study in clinical subgroups.
Ambrosini, Anna; Maertens De Noordhout, Alain ULg; Schoenen, Jean ULg

in Neurology (2001), 56(8), 1038-43

OBJECTIVE: To search for impairment of neuromuscular transmission by single-fiber electromyography (SFEMG) in patients with common forms of migraine. BACKGROUND: P/Q Ca(2+) channels are genetically ... [more ▼]

OBJECTIVE: To search for impairment of neuromuscular transmission by single-fiber electromyography (SFEMG) in patients with common forms of migraine. BACKGROUND: P/Q Ca(2+) channels are genetically abnormal in most cases of familial hemiplegic migraine (International Headache Society [IHS] code 1.2.3) and may be involved in other types of migraine. Besides in the brain, these channels are found in motor nerve endings, where they control stimulation-induced acetylcholine release. If they are functionally abnormal, the neuromuscular transmission might be impaired. METHODS: Sixty-two migraineurs (18 without aura, IHS code 1.1; 19 with typical aura, IHS code 1.2.1; 10 with prolonged aura, IHS code 1.2.2; 15 with and without aura) and 16 healthy control subjects underwent stimulation SFEMG. Results were expressed as the mean value of consecutive differences (MCD) and percentage of single-fiber abnormalities (abnormal jitter or impulse blocking). RESULTS: Average MCD was comparable in control subjects and migraineurs (17.1 +/- 2.6 versus 17.5 +/- 4.7 microsec). By contrast, single-fiber abnormalities were found in 17 patients but in none of the control subjects (p = 0.036). Most of these patients had unilateral sensorimotor symptoms and/or aphasia and/or loss of balance during the aura. SFEMG abnormalities were significantly correlated with the occurrence of these clinical features and with a diagnosis of migraine with prolonged aura. CONCLUSIONS: Stimulation SFEMG shows mild abnormalities of neuromuscular transmission in a subgroup of migraineurs with aura, characterized by clinical features frequently found in human P/Q Ca(2+) channelopathies. These abnormalities might thus be due to genetically modified P/Q Ca(2+) channels. [less ▲]

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See detailNeuron-Specific Enolase as a Marker of in Vitro Neuronal Damage. Part I: Assessment of Neuron-Specific Enolase as a Quantitative and Specific Marker of Neuronal Damage
Hans, Pol ULg; Bonhomme, Vincent ULg; Collette, Julien ULg et al

in Journal of Neurosurgical Anesthesiology (1993), 5(2), 111-6

Enolase in cerebrospinal fluid is a sensitive marker for many types of neurological injuries including head injury and ischemia. We assessed neuron-specific enolase (NSE) as a quantitative and specific ... [more ▼]

Enolase in cerebrospinal fluid is a sensitive marker for many types of neurological injuries including head injury and ischemia. We assessed neuron-specific enolase (NSE) as a quantitative and specific biochemical marker of neuronal damage in an experimental model of kainate neurotoxicity. Rat hippocampal cultures were treated with various concentrations of kainate. NSE release into the culture medium was compared with neuronal death estimated either by direct cell counting or by lactate dehydrogenase (LDH) release, largely used to quantify neuronal injury. A dose-response relationship was observed between kainate concentration and the amount of NSE released (r = -0.69; p < 0.05) as well as a significant correlation between NSE release and neuronal death (r = 0.64; p < 0.05). Likewise, a significant correlation was found between LDH and NSE release (r = 0.85; p < 0.05). The specificity of NSE as an indicator of neuronal death was demonstrated using immunocyto-chemistry labeling and measurement of NSE release by pure astrocyte cultures. We concluded that NSE is a reliable, quantitative, and specific marker of neuronal injury. [less ▲]

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See detailNeuron-Specific Enolase as a Marker of in Vitro Neuronal Damage. Part II: Investigation of the Astrocyte Protective Effect against Kainate-Induced Neurotoxicity
Bonhomme, Vincent ULg; Hans, Pol ULg; Collette, Julien ULg et al

in Journal of Neurosurgical Anesthesiology (1993), 5(2), 117-20

The protective effect of astrocytes on hippocampal neurons against kainate-induced toxicity was investigated using neuron-specific enolase as an indicator of neuronal death. Astrocyte-rich and astrocyte ... [more ▼]

The protective effect of astrocytes on hippocampal neurons against kainate-induced toxicity was investigated using neuron-specific enolase as an indicator of neuronal death. Astrocyte-rich and astrocyte-poor mixed rat hippocampal cultures were submitted to various concentrations of kainate. At each kainate concentration, the amount of NSE released by neurons was significantly greater in astrocyte-poor than in astrocyte-rich cultures (p < 0.05). This protective effect was not observed when neuronal survival was tested on astrocyte-poor cultures in astrocyte-conditioned culture medium with or without 10(-4) M kainate. In conclusion, astrocytes significantly attenuate kainate toxicity on hippocampal neurons, and this effect is not mediated by a diffusible factor. [less ▲]

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See detailNeuron-Specific Enolase as a Predictor of Death or Poor Neurological Outcome After Out-of-Hospital Cardiac Arrest and Targeted Temperature Management at 33 degrees C and 36 degrees C.
Stammet, Pascal ULg; Collignon, Olivier; Hassager, Christian et al

in Journal of the American College of Cardiology (2015), 65(19), 2104-14

BACKGROUND: Neuron-specific enolase (NSE) is a widely-used biomarker for prognostication of neurological outcome after cardiac arrest, but the relevance of recommended cutoff values has been questioned ... [more ▼]

BACKGROUND: Neuron-specific enolase (NSE) is a widely-used biomarker for prognostication of neurological outcome after cardiac arrest, but the relevance of recommended cutoff values has been questioned due to the lack of a standardized methodology and uncertainties over the influence of temperature management. OBJECTIVES: This study investigated the role of NSE as a prognostic marker of outcome after out-of-hospital cardiac arrest (OHCA) in a contemporary setting. METHODS: A total of 686 patients hospitalized after OHCA were randomized to targeted temperature management at either 33 degrees C or 36 degrees C. NSE levels were assessed in blood samples obtained 24, 48, and 72 h after return of spontaneous circulation. The primary outcome was neurological outcome at 6 months using the cerebral performance category score. RESULTS: NSE was a robust predictor of neurological outcome in a baseline variable-adjusted model, and target temperature did not significantly affect NSE values. Median NSE values were 18 ng/ml versus 35 ng/ml, 15 ng/ml versus 61 ng/ml, and 12 ng/ml versus 54 ng/ml for good versus poor outcome at 24, 48, and 72 h, respectively (p < 0.001). At 48 and 72 h, NSE predicted neurological outcome with areas under the receiver-operating curve of 0.85 and 0.86, respectively. High NSE cutoff values with false positive rates </=5% and tight 95% confidence intervals were able to reliably predict outcome. CONCLUSIONS: High, serial NSE values are strong predictors of poor outcome after OHCA. Targeted temperature management at 33 degrees C or 36 degrees C does not significantly affect NSE levels. (Target Temperature Management After Cardiac Arrest [TTM]; NCT01020916). [less ▲]

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See detailNeuronal and glial expression of the inducible HSP70 in forebrain ischemia
Xu, D.; Plumier, Jean-Christophe ULg; Robertson, Harold A. et al

Poster (1995)

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See detailNeuronal and psychological underpinnings of pathological gambling
Singer, Bryan F.; Anselme, Patrick ULg; Robinson, Mike J.F. et al

in Frontiers in Behavioral Neuroscience (2014), 8, 230

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