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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 detailNeuronal Control of Astrocytes Proliferation
Rogister, Bernard ULg; Leprince, Pierre ULg; Martin, Didier ULg et al

in Fedoroff, S.; Juurlink, B. H. J.; Doucette, R. (Eds.) Biology and pathology of astrocyte-neuron interactions (1993)

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See detailNeuronal Differentiation in the Adult Brain: Cdk6 as the Molecular Regulator
Caron, Nicolas ULg; Genin, Emmanuelle ULg; Vandenbosch, Renaud ULg et al

in Hayat, Eric (Ed.) TUMORS OF THE CENTRAL NERVOUS SYSTEM (2013)

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See detailNeuronal injury in NCX3 knockout mice following permanent focal cerebral ischemia and in NCX3 knockout cortical neuronal cultures following oxygen-glucose deprivation and glutamate exposure
Cross, J. L.; Meloni, B. P.; Bakker, A. J. et al

in Journal of Experimental Stroke & Translational Medicine (2009), 2(1), 3-9

In this study we subjected NCX3 knockout and wildtype mice to permanent focal cerebral ischemia by intraluminal middle cerebral artery occlusion. Analysis of brain sections by 2,3,5-Triphenyl-2H ... [more ▼]

In this study we subjected NCX3 knockout and wildtype mice to permanent focal cerebral ischemia by intraluminal middle cerebral artery occlusion. Analysis of brain sections by 2,3,5-Triphenyl-2H-tetrazolium chloride staining, 12 hours after middle cerebral artery occlusion revealed no difference in infarct volume between NCX3 knockout and wildtype mice. In addition, we evaluated the effect of NCX3 protein knockdowri on neuronal viability in primary cortical neuronal cultures following in vitro ischemia (oxygen-glucose deprivation) and L-glutamate (glutamate) exposure. In vitro experiments revealed that neuronal viability was higher in NCX3 knockout neuronal cultures than in the wildtype cultures following ischemic and glutamate insults. The reduced sensitivity of neurons from NCX3 knockout mice to in vitro ischemia and excitotoxicity indicates that NCX3 calcium entry mode activity contributes to calcium overload and neuronal death. However our in vivo finding of e lack of differential sensitivity on infarct volume in NCX3 knockout and wildtype mice suggests that any benefit of reduced NCX3 activity is overridden following permanent focal cerebral ischemia. Taken together, these f]ndings suggest that reduced NXC3 activity limits calcium neurotoxicity during severe transient, but not during severe sustained ischemic insults. These results have important implications for the development of the NCX3 protein as a therapeutic target to reduce ischemic brain injury [less ▲]

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See detailNeuronal localization of the 25-kDa specific thiamine triphosphatase in rodent brain
Czerniecki, Jan ULg; Chanas, Grazyna; Verlaet, Myriam ULg et al

in Neuroscience (2004), 125(4), 833-840

Thiamine triphosphate (ThTP) is found in small amounts in most organisms from bacteria to mammals, but little is known about its physiological role. In vertebrate tissues, ThTP may act as a phosphate ... [more ▼]

Thiamine triphosphate (ThTP) is found in small amounts in most organisms from bacteria to mammals, but little is known about its physiological role. In vertebrate tissues, ThTP may act as a phosphate donor for the phosphorylation of certain proteins; this may be part of a new signal transduction pathway. We have recently characterized a highly specific 25-kDa thiamine triphosphatase (ThTPase) that is expressed in most mammalian tissues. The role of this enzyme may be the control of intracellular concentrations of ThTP. As the latter has been considered to be a neuroactive form of thiamine, we have studied the distribution of ThTPase mRNA and protein in rodent brain using in situ hybridization and immunohistochemistry. With both methods, we found the strongest staining in hippocampal pyramidal neurons, as well as cerebellar granule cells and Purkinje cells. Some interneurons were also labeled and many ThTPase mRNA-positive and immunoreactive cells were distributed throughout cerebral cortical gray matter and the thalamus. White matter was not significantly labeled. ThTPase immunoreactivity seems to be located mainly in the cytoplasm of neuronal perikarya. Immunocytochemical data using dissociated cultured cells from hippocampal and cerebellum showed that the staining was more intense in neurons than in astrocytes. The protein was rather uniformly located in the perikarya and dendrites, suggesting that ThTP and ThTPase may play a general role in neuronal metabolism rather than a specific role in excitability. There was no apparent correlation between ThTPase expression and selective vulnerability of certain brain regions to thiamine deficiency. (C) 2004 IBRO. Published by Elsevier Ltd. All rights reserved. [less ▲]

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See detailNeuronal migration disorders and epilepsies
Misson, Jean-Paul ULg; Dubru, Jean-Marie ULg; Leroy, Patricia et al

in Nehlig, Astrid; Motte, Jacques (Eds.) Childhood epilepsies and brain development (1999)

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See detailNeuronal migration in the murine cerebrum proceeds in parallel to raidial fibers : Analysis based upon double labeling of migrating neurons and radial fibers
Misson, Jean-Paul ULg; Austin, C.; Takahashi, T. et al

in Comptes Rendu des Journées Annuelles de la Société Belge de Pédiatrie (1990)

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See detailNeurono-Glial Interactions and Neural Plasticity
Moonen, Gustave ULg; Rogister, Bernard ULg; Leprince, Pierre ULg et al

in Coleman, Paul; Higgins, G.; Phelps, C. (Eds.) Progress In Brain research: Neuronal Plasticity in aging and dementia (1990)

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See detailNeuronotrophic Effect of Developing Otic Vesicle on Cochleo-Vestibular Neurons: Evidence for Nerve Growth Factor Involvement
Lefebvre, Philippe ULg; Leprince, Pierre ULg; Weber, T. et al

in Brain Research (1990), 507(2), 254-60

In the developing inner ear, the existence of a neuronal death and of a peripheral target-derived trophic effect on cochleovestibular neurons has been documented. Using cultures of rat cochleovestibular ... [more ▼]

In the developing inner ear, the existence of a neuronal death and of a peripheral target-derived trophic effect on cochleovestibular neurons has been documented. Using cultures of rat cochleovestibular neurons, we show that the E12 otic vesicle releases a factor promoting the survival and the neuritogenesis of these neurons, and that this effect is mimicked by NGF. The effect of the optic vesicle conditioned medium (OVCM) on cochleovestibular neurons is suppressed by anti-NGF antibodies. OVCM is neuronotrophic for NGF-sensitive sympathetic neurons, an effect that is also suppressed by anti-NGF antibodies, further demonstrating the presence of biologically active nerve growth factor. [less ▲]

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See detailNeuronotrophic factors involvement in the regeneration of adult afferent auditory neurons.
Lefebvre, P.; Weber, T.; Delrée, P. et al

Conference (1990, November 10)

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See detailLa neuropathie autonome cardiaque diabetique.
Philips, Jean-Christophe ULg; Marchand, Monique ULg; Scheen, André ULg

in Revue Médicale de Liège (2005), 60(5-6), 498-504

Cardiac autonomic neuropathy (CAN) is a common complication of diabetes mellitus, which is associated with a higher risk of morbidity and mortality. It can be detected by analyzing spontaneous (Holter) or ... [more ▼]

Cardiac autonomic neuropathy (CAN) is a common complication of diabetes mellitus, which is associated with a higher risk of morbidity and mortality. It can be detected by analyzing spontaneous (Holter) or provoked (Ewing's test battery) changes in heart rate and arterial blood pressure. Baroreflex gain is a specific index of great interest. Our laboratory has acquired a large experience in the assessment of CAN in diabetic patients. We use the Finapres, a device that allows continuous noninvasive monitoring of blood pressure and heart rate, and a special and discriminative active orthostatic manoeuvre, the "squatting" test (standing-squatting-standing). [less ▲]

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See detailLa neuropathie autonome: une complication méconnue du diabète
Philips, Jean-Christophe ULg; Marchand, Monique; Scheen, André ULg

in Association belge du diabète (2009), 52(1), 24-29

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See detailLa neuropathie avec hypersensibilite hereditaire a la pression ou neuropathie tomaculaire
Tinant, France ULg; Zeevaert, Bernard ULg; Benkirane, H. et al

in Revue Médicale de Liège (2002), 57(10), 651-4

Hereditary neuropathy liability to pressure palsies is characterized by recurring accesses of painless paralysis at the level of various nerves likely to be compressed. This affection remains ... [more ▼]

Hereditary neuropathy liability to pressure palsies is characterized by recurring accesses of painless paralysis at the level of various nerves likely to be compressed. This affection remains underdiagnosed because of its usually benign course, sometimes without any symptom. The diagnosis is supported by clinical and electrophysiological data associated with, in the majority of patients, a deletion of one of the alleles coding for protein PMP 22 on the level of the locus 17p11.2. [less ▲]

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See detailLa neuropathie diabetique: donnees epidemiologiques et predictives.
Scheen, André ULg

in Diabètes & Métabolism (1998), 24 Suppl 3

Neuropathy is a classical complication of diabetes mellitus, to the same extent as micro- and macroangiopathy. Diabetic neuropathy can be schematically divided into peripheral neuropathy, especially in ... [more ▼]

Neuropathy is a classical complication of diabetes mellitus, to the same extent as micro- and macroangiopathy. Diabetic neuropathy can be schematically divided into peripheral neuropathy, especially in the lower limbs (distal polyneuropathy), and autonomic neuropathy, present in all systems (cardiovascular, gastrointestinal, urogenital and even pulmonary abnormalities). Detection should be based on an oriented anamnesis and a careful physical examination. Complementary exams may be performed in order to confirm the diagnosis and assess the severity of the neuropathy. While the diagnosis of peripheral neuropathy is essentially based on clinical examination, that of autonomic neuropathy has been markedly facilitated by simple standardised tests for early detection of cardiac autonomic neuropathy. Depending on the terminology, the diagnostic criteria and the characteristics of the population, the prevalence of diabetic neuropathy can range from 15 to 100%. However, all studies agree that prevalence is important in both types of diabetes (Type 1 and Type 2), that it increases with age and disease duration, and that it is inversely related to the quality of glycaemic control. Detection of neuropathy is an essential step in the clinical approach to diabetic patients, mainly because of the prognosis linked to such a diagnosis, at both an early and late stage of the disease. Once neuropathy is diagnosed, the physician should provide specific advice to diabetic patients in order to prevent possible dramatic complications. [less ▲]

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See detailNeuropathie ulnaire au coude : étude combinée des muscles abductor digiti minimi et interosseus I
WANG, François-Charles ULg

in Lettre du Neurologue (La) : le Courrier du Spécialiste (2011)

Detailed reference viewed: 12 (0 ULg)