Girard M.,Toulouse University Hospital Center
International Journal of Psychoanalysis | Year: 2010
In a recent paper, Fulgencio shows how Winnicott rejected the basic speculative concepts of Freud's metapsychology - Trieb, psychical apparatus and libido - and replaced them with non-speculative concepts that promoted a factual theorization. In this paper, the author examines some of Winnicott's concepts and attempts to demonstrate how, rather than replacing Freud's concepts, he provides a factual foundation for the metapsychology in the double dependence of the infant in care. Freud never actually disregards the necessity of early mothering but he takes it for granted. By differentiating between ego needs and id needs, ego-relatedness and id-relatedness, object-mother and environment-mother, Winnicott attempts to theorize what Freud takes for granted: the function of the holding environment as a framework for id-experiences and the function of object-presenting as a condition of reality-testing. Furthermore, by differentiating between pure male and pure female elements, he is also able to construct a highly speculative theorization in order to distinguish two basic principles: doing and being. Although the death drive is clearly rejected, this rejection follows from his theorization of double dependence. Consequently, the author suggests that Winnicott did not discard metapsychological concepts but theorized the conditions for using both these and the intrapsychic topography. © 2010 Institute of Psychoanalysis.
Bonneville F.,Toulouse University Hospital Center
Diagnostic and Interventional Imaging | Year: 2014
Cerebral venous thrombosis (CVT) is a potentially life-threatening emergency. The wide ranging of clinical symptoms makes the use of imaging in "slices" even more important for diagnosis. Both CT and MRI are used to diagnose the occlusion of a venous sinus, but MRI is superior to CT for detecting a clot in the cortical or deep veins. CT can show the hyperintense clot spontaneously and CT angiography the intraluminal defect. MRI also detects this thrombus, whose signal varies over time: in the acute phase, it is hypointense in T2, whilst T1 and T2 can appear falsely reassuring; in the subacute phase, it is hyperintense on all sequences (T1, T2, FLAIR, T2, diffusion). MRI easily shows the ischemic damage, even hemorrhagic, in the cerebral parenchyma in cases of CVT. Finally, imaging may reveal pathology at the origin of the CVT, such as a fracture of the skull, infection, tumor, dural fistula, or intracranial hypotension. © 2014 Éditions francąises de radiologie.
Chollet F.,Toulouse University Hospital Center
Dialogues in Clinical Neuroscience | Year: 2013
Brain plasticity is an intrinsic characteristic of the nervous system that allows continuous remodeling of brain functions in pathophysiological conditions. Although normal aging is associated with morphological modifications and decline of cerebral functions, brain plasticityis at least partially preserved in elderly individuals. A growing body of evidence supports the notion that cognitive enrichment and aerobic training induce a dynamic reorganization of higher cerebral functions, thereby helping to maintain operational skills in the elderly and reducing the incidence of dementia. The stroke model clearly shows that spontaneous brain plasticity exists after a lesion, even in old patients, and that it can be modulated through external factors like rehabilitation and drugs. Whether drugs can be used with the aim of modulating the effects of physical training or cognitive stimulation in healthy aged people has not been addressed until now. The risk:benefit ratio will be the key question with regard to the ethical aspect of this challenge. We review in this article the main aspects of human brain plasticityas shown in patients with stroke, the drug modulation of brain plasticity and its consequenceson recovery, and finally we address the question of the influence of aging on brain plasticity. © 2013 LLS SAS.
Delisle M.-B.,Toulouse University Hospital Center
Acta neuropathologica communications | Year: 2014
BACKGROUND: The accumulation of beta amyloid (Aβ) peptides, a hallmark of Alzheimer's disease (AD) is related to mechanisms leading to neurodegeneration. Among its pleiotropic cellular effects, Aβ accumulation has been associated with a deregulation of sphingolipid metabolism. Sphingosine 1-phosphate (S1P) derived from sphingosine is emerging as a critical lipid mediator regulating various biological activities including cell proliferation, survival, migration, inflammation, or angiogenesis. S1P tissue level is low and kept under control through equilibrium between its synthesis mostly governed by sphingosine kinase-1 (SphK1) and its degradation by sphingosine 1-phosphate lyase (SPL). We have previously reported that Aβ peptides were able to decrease the activity of SphK1 in cell culture models, an effect that could be blocked by the prosurvival IGF-1/IGF-1R signaling.RESULTS: Herein, we report for the first time the expression of both SphK1 and SPL by immunohistochemistry in frontal and entorhinal cortices from 56 human AD brains. Immunohistochemical analysis revealed a decreased expression of SphK1 and an increased expression of SPL both correlated to amyloid deposits in the entorhinal cortex. Otherwise, analysis of brain tissue extracts showed a decrease of SphK1 expression in AD brains whereas SPL expression was increased. The content of IGF-1R, an activator of SphK1, was found decreased in AD brains as well as S1P1, the major receptor for S1P.CONCLUSIONS: Collectively, these results highlight the importance of S1P in AD suggesting the existence of a global deregulation of S1P signaling in this disease from its synthesis by SphK1 and degradation by SPL to its signaling by the S1P1 receptor.
Minville V.,Toulouse University Hospital Center
British journal of anaesthesia | Year: 2011
The aim of this study was to assess any interaction between ondansetron and paracetamol on a model of post-fracture pain in mice. In protocol A, after fracture of the tibia, mice were assigned to four groups: paracetamol 30 mg kg 1, paracetamol 50 mg kg 1, paracetamol 100 mg kg 1, or a saline vehicle i.p. In protocol B, after fracture of the tibia, mice were randomized to receive either paracetamol (100 mg kg 1) plus saline (vehicle), paracetamol (100 mg kg 1) plus ondansetron (1 mg kg 1), paracetamol (100 mg kg 1) plus ondansetron (2 mg kg 1), saline plus ondansetron (2 mg kg 1), or saline plus saline i.p. Three tests were used to assess pain behaviour: von Frey filament application, hot-plate test, and a subjective pain scale. Rescue analgesia with morphine was administered as necessary. In protocol A, paracetamol (100 mg kg 1)-treated animals had less mechanical nociception, thermal nociception, and a lower subjective pain scale rating, when compared with those receiving paracetamol at 30 or 50 mg kg 1 or saline [ED paracetamol=46.3 (6.34) mg kg 1]. No difference was found between paracetamol (30 mg kg 1) and saline-treated animals. In protocol B, the mechanical withdrawal threshold, the thermal withdrawal latency, and the subjective pain scale were lower after injection of paracetamol (100 mg kg 1)+saline, paracetamol (100 mg kg 1)+ondansetron (1 mg kg 1), and paracetamol (100 mg kg 1)+ondansetron (2 mg kg 1), whereas in mice receiving saline+ondansetron (2 mg kg 1) or saline+saline, there was no difference. We found that paracetamol 100 mg kg 1 blocked the development of hyperalgesia and allodynia after fracture pain and ondansetron did not modify the antinociceptive effect of paracetamol in this model.