Vascular Neurosurgery - Tip s& Tricks in aneurysm clipping
Conference (2009, February 13)Detailed reference viewed: 4 (0 ULg)
International Foundation for Research in Paraplegia
Conference (2009, January 27)Detailed reference viewed: 3 (0 ULg)
Transplantation intracérébrale de cellules souches. Lesquelles ? Est-ce efficace ? Est-ce éthique ?
Scientific conference (2009, January 21)Detailed reference viewed: 7 (1 ULg)
La thrombose veineuse cérébrale (TVC).
; SCHOLTES, Félix ; 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 ▲]Detailed reference viewed: 229 (7 ULg)
NG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury.
; ; 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 ▲]Detailed reference viewed: 14 (1 ULg)
Cushing disease : Influence of microsurgery on hormonal balance
Vroonen, Laurent ; Martin, Didier ; Valdes Socin, Hernan Gonzalo et al
in European Neuroendocrine Association - Workshop : Novel insights in the management of Cushing's syndrome (2009)Detailed reference viewed: 18 (2 ULg)
Early termination of ISRCTN45828668, a phase 1/2 prospective, randomized study of sulfasalazine for the treatment of progressing malignant gliomas in adults.
Robe, Pierre ; Martin, Didier ; Nguyen-Khac, Minh-Tuan 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 ▲]Detailed reference viewed: 42 (13 ULg)
Hypopituitarisme consécutif aux atteintes cérébrales: le traumatisme cranien et l'hémorragie sous-arachnoidienne mis en cause.
Valdes Socin, Hernan Gonzalo ; Vroonen, Laurent ; Robe, Pierre et al
in Revue Médicale de Liège (2009), 64(9), 457-463
Brain injuries namely traumatic brain injuries (TBI) and subarachnoid haemorrhage (SAH) are relevant causes of acquired adult hypopituitarism, perhaps more prevalent than ever believed. TBI represent a ... [more ▼]
Brain injuries namely traumatic brain injuries (TBI) and subarachnoid haemorrhage (SAH) are relevant causes of acquired adult hypopituitarism, perhaps more prevalent than ever believed. TBI represent a major health problem with an annual incidence of 300 cases per 100.000. SAH affects six new cases per 1.000.000 habitants in USA. In Belgium we estimate nearly 30.000 new TBI cases and 600 SAH cases per year. In the English literature, TBI secondary hypopituitarism has been well documented in 14 retrospective and prospective series accounting for 1.077 cases. In all these series the main pituitary deficits were: GH (14%), ACTH (14%), gonadotrope (18%), TSH (7%) and diabetes insipidus (4%). SAH was documented as a cause of hypopituitarism in three retrospective series accounting for 110 cases and in one prospective series. In all these series main pituitary deficits were GH (25%), ACTH (15%), gonadotrope (8.5%), TSH (6%) and diabetes insipidus (4%). In this review, we analyze recent data and discuss diagnostic and treatment features of secondary hypopituitarism due TBI and SAH. [less ▲]Detailed reference viewed: 109 (7 ULg)
Les anévrysmes cérébraux – clinique. Traitement neurochirurgical. Traitement de radiologie interventionnelle
Conference (2008, December 12)Detailed reference viewed: 4 (0 ULg)
Technologie de pointe en neurochirurgie : l’IRM interventionnelle couplée à la neuronavigation.
Conference (2008, November 21)Detailed reference viewed: 5 (2 ULg)
L’hémorragie cérébrale : le coup de tonnerre dans un ciel serein
Conference (2008, October 23)Detailed reference viewed: 1 (0 ULg)
IRM interventionnelle : vers une neuronavigation en temps reel
Conference (2008, October 11)
Prise en charge médicale et neurochirurgicale de la spasticité
Scientific conference (2008, June 04)Detailed reference viewed: 15 (3 ULg)
Le diagnostic des démences : comment et pourquoi ?
Scientific conference (2008, March 19)Detailed reference viewed: 7 (0 ULg)