References of "Martin, Didier"
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See detailLes infections du rachis
Martin, Didier ULg

Scientific conference (2009, June 03)

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See detailDoes radiation treatment delay affect survival in glioblastoma ?
Robe, Pierre ULg; Nguyen Khac, Minh-Tuan ULg; Lenelle, Jacques ULg et al

Conference (2009, March 21)

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See detailLes "douleurs du petit coin" : prise en charge de la neuropathie pudendale
Martin, Didier ULg

Scientific conference (2009, March 21)

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See detailThe Gilliatt-Sumner hand: an ill-known clinical picture from cervical ribs. Report of 5 operated cases.
Dubuisson, Annie ULg; Figiel, S.; Laungani, A. et al

Conference (2009, March 21)

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See detailCombined functional neuroimaging (fMRI and MEG) for the guidance of epidural motor cortex stimulation in chronic refractory neuropathic pain: a pilot study.
Bourguignon, M.; De Tiège, X.; Baleriaux, D. et al

Conference (2009, March)

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See detailThe Gilliatt-Summer hand: an ill-know clinical picture from cervical ribs. Report of 5 operated cases
Dubuisson, Annie ULg; Figiel, S.; Laungani, A. et al

Conference (2009, March)

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See detailTips & Tricks in aneurysm clipping
Martin, Didier ULg

Conference (2009, February 13)

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See detailVascular Neurosurgery - Tip s& Tricks in aneurysm clipping
Martin, Didier ULg

Conference (2009, February 13)

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See detailInternational Foundation for Research in Paraplegia
Martin, Didier ULg

Conference (2009, January 27)

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See detailNG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury.
Buss, Armin; Pech, Katrin; Kakulas, Byron A et al

in BMC Neurology (2009), 9

BACKGROUND: A major class of axon growth-repulsive molecules associated with CNS scar tissue is the family of chondroitin sulphate proteoglycans (CSPGs). Experimental spinal cord injury (SCI) has ... [more ▼]

BACKGROUND: A major class of axon growth-repulsive molecules associated with CNS scar tissue is the family of chondroitin sulphate proteoglycans (CSPGs). Experimental spinal cord injury (SCI) has demonstrated rapid re-expression of CSPGs at and around the lesion site. The pharmacological digestion of CSPGs in such lesion models results in substantially enhanced axonal regeneration and a significant functional recovery. The potential therapeutic relevance of interfering with CSPG expression or function following experimental injuries seems clear, however, the spatio-temporal pattern of expression of individual members of the CSPG family following human spinal cord injury is only poorly defined. In the present correlative investigation, the expression pattern of CSPG family members NG2, neurocan, versican and phosphacan was studied 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 sections from control spinal cord, NG2 immunoreactivity was restricted to stellate-shaped cells corresponding to oligodendrocyte precursor cells. The distribution patterns of phosphacan, neurocan and versican in control human spinal cord parenchyma were similar, with a fine reticular pattern being observed in white matter (but also located in gray matter for phosphacan). Neurocan staining was also associated with blood vessel walls. Furthermore, phosphacan, neurocan and versican were present in the myelin sheaths of ventral and dorsal nerve roots axons. After human SCI, NG2 and phosphacan were both detected in the evolving astroglial scar. Neurocan and versican were detected exclusively in the lesion epicentre, being associated with infiltrating Schwann cells in the myelin sheaths of invading peripheral nerve fibres from lesioned dorsal roots. CONCLUSION: NG2 and phosphacan were both present in the evolving astroglial scar and, therefore, might play an important role in the blockade of successful CNS regeneration. Neurocan and versican, however, were located at the lesion epicentre, associated with Schwann cell myelin on regenerating peripheral nerve fibres, a distribution that was unlikely to contribute to failed CNS axon regeneration. The present data points to the importance of such correlative investigations for demonstrating the clinical relevance of experimental data. [less ▲]

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See detailLa thrombose veineuse cérébrale (TVC).
Servais, S; SCHOLTES, Félix ULg; Roemers, S. et al

in Revue medicale de Liege (2009), 64(1), 25-31

Cerebral venous thrombosis is a rare cause of stroke. Clinical presentation is not very specific and can be very variable. Imaging establishes the diagnosis in the majority of cases. Specially, magnetic ... [more ▼]

Cerebral venous thrombosis is a rare cause of stroke. Clinical presentation is not very specific and can be very variable. Imaging establishes the diagnosis in the majority of cases. Specially, magnetic resonance venography has high sensitivity and is presently the gold standard. Long term prognosis of cerebral venous thrombosis is generally good and few patients remain handicapped in the long term. Evolution is however unpredictable. Treatment strategies follow three axes: anti-thrombotic treatment, symptomatic measures and treatment of the cause if one is found. [less ▲]

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See detailCushing disease : Influence of microsurgery on hormonal balance
Vroonen, Laurent ULg; Martin, Didier ULg; Valdes Socin, Hernan Gonzalo ULg et al

in European Neuroendocrine Association - Workshop : Novel insights in the management of Cushing's syndrome (2009)

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See detailEarly termination of ISRCTN45828668, a phase 1/2 prospective, randomized study of sulfasalazine for the treatment of progressing malignant gliomas in adults.
Robe, Pierre ULg; Martin, Didier ULg; Nguyen-Khac, Minh-Tuan ULg et al

in BMC Cancer (2009), 9

BACKGROUND: Sulfasalazine, a NF-kappaB and x(c)-cystine/glutamate antiport inhibitor, has demonstrated a strong antitumoral potential in preclinical models of malignant gliomas. As it presents an ... [more ▼]

BACKGROUND: Sulfasalazine, a NF-kappaB and x(c)-cystine/glutamate antiport inhibitor, has demonstrated a strong antitumoral potential in preclinical models of malignant gliomas. As it presents an excellent safety profile, we initiated a phase 1/2 clinical study of this anti-inflammatory drug for the treatment of recurrent WHO grade 3 and 4 astrocytic gliomas in adults. METHODS: 10 patients with advanced recurrent anaplastic astrocytoma (n = 2) or glioblastoma (n = 8) aged 32-62 years were recruited prior to the planned interim analysis of the study. Subjects were randomly assigned to daily doses of 1.5, 3, 4.5, or 6 grams of oral sulfasalazine, and treated until clinical or radiological evidence of disease progression or the development of serious or unbearable side effects. Primary endpoints were the evaluation of toxicities according to the CTCAE v.3.0, and the observation of radiological tumor responses based on MacDonald criteria. RESULTS: No clinical response was observed. One tumor remained stable for 2 months with sulfasalazine treatment, at the lowest daily dose of the drug. The median progression-free survival was 32 days. Side effects were common, as all patients developed grade 1-3 adverse events (mean: 7.2/patient), four patients developed grade 4 toxicity. Two patients died while on treatment or shortly after its discontinuation. CONCLUSION: Although the proper influence of sulfasalazine treatment on patient outcome was difficult to ascertain in these debilitated patients with a large tumor burden (median KPS = 50), ISRCTN45828668 was terminated after its interim analysis. This study urges to exert cautiousness in future trials of Sulfasalazine for the treatment of malignant gliomas. TRIAL REGISTRATION: Current Controlled Trials ISRCTN45828668. [less ▲]

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