[Increased prevalence of rectocolonic polyadenomas in patients with acromegaly. Preliminary results in 15 patients].
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Biomedical subjects
Publications and source records attributed to F Cohadon.
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This work describes the control exerted by dicarboxylate carrier and succinate dehydrogenase activities on the oxidative phosphorylations in rabbit brain mitochondria as an edema develops. Vasogenic edema leads to an uncompetitive inhibition of succinate dehydrogenase activity and to a large decrease of oxidative phosphorylations linked to succinate utilisation. Naftidrofuryl treatment in vivo restores both a high succinate dehydrogenase activity and a normal respiratory rate. In order to quantify the control of oxidative phosphorylations by the succinate dehydrogenase step, we applied the control analysis (Kacser, H. and Burns, J.A. (1973) in Rate Control of Biological Processes (Davies, D.D., ed.), pp. 65-104, Cambridge University Press, London; Heinrich, R. and Rapoport, T.A. (1974) Eur. J. Biochem. 42, 89-95). By using two inhibitors, one (phenylsuccinate) acting only on the dicarboxylate carrier and another (malonate) acting on both the dicarboxylate carrier and the succinate dehydrogenase, a method was developed to calculate the control coefficients of these two steps. The main result is that in mitochondria isolated from normal tissue succinate dehydrogenase exerted no control, but in the course of edema this enzymatic step became a controlling one: a transition from zero to a high control coefficient (0.5) was observed from the onset of intracellular edema for the threshold value of water/dry-weight tissue of 4.6.
This paper describes the resumption of motor activity during the successive stages of recovery following severe traumatic coma and discusses the likely mechanisms of such resumption. Even in severe brain injury a considerable amount of motor recovery is possible and leads to a normal level of function in half of the cases. The impairment of voluntary movements is often transitory and recovers spontaneously but in cases of persistent deficits probably from direct lesion of the pyramidal tract re-education efforts are relatively inefficient. The disorders of reflex and semi-automatic motor activity subserving tonic adjustments, gait and locomotion are nearly constant and often severe. The recovery of this basal function is the most important to attain and to secure and this can be achieved through extensive and prolonged retraining of reflex activity. Presumably these disorders are not caused by direct lesions of brainstem structures but rather to a functional denervation akin to spinal shock. A resumption of function in the denervated groups of neurons should necessitate the reopening of silent synapses and/or a structural reorganisation of synaptic connections, this dynamic process being highly influenced by retraining.
Within the tissue surrounding the necrotic lesion, following a cryogenic injury of the brain, there is a definite activation of phospholipase A2 (at 2 and 4 hr post lesion) that accounts, at least in part, for the phospholipid breakdown. There is also an activation of cholinephosphotransferase (at 2 hr post lesion) that may correspond to an early process of phospholipid resynthesis. Oral CDP-choline in this model is able to completely inhibit the activation of phospholipase A2, but has no detectable effect on cholinephosphotransferase activity. The beneficial effect of CDP-choline might be explained by a prevention of destruction rather than by an enhancement of reconstruction of phospholipids.
This paper investigates the kinetic parameters of Na+-K+-ATPase in glial, neuronal, and synaptosomal enriched fractions isolated from rabbit cerebral cortex. Under normal conditions, kinetic parameters-Vmax and KK+0.5- of Na+-K+-ATPase are the same in the three fractions, suggesting that this enzyme behaves as the same molecular entity. Following a cryogenic lesion, the alterations of these parameters appear to be different in the different fractions. These data suggest that the same enzyme exhibits various responses when exposed to the same pathological event. The dissimilar lipid composition of the Na+-K+-ATPase environment, and/or different adaptative responses to abnormal ion concentrations in glial, neuronal, and synaptosomal fractions could account for these different responses.
Following cryogenic lesions of the brain in the rabbit, ictal activity appears within min with a maximum at 2 h. Brain edema increases rapidly between 2-4 h with a maximum at 8 h. The glutamate concentration reaches 209% of control in the perilesional area at 2 h and the time course of glutamate/GABA ratio parallels the time course of epileptic activity. The impairment of Na+-K+-ATPase activity (rise of KMapp for K+) in the glial fraction coincides with the increase of edema. A positive correlation is found between the total amount of ictal activity and the total amount of edema in individual animals, suggesting that epilepsy may enhance edema formation.
Edematous reactions surrounding brain lesions are less extensive in old patients. There also is a general tendency of the aging brain to be vulnerable to osmotic stress, to yield space, and to collapse. In order to elucidate these clinical phenomena, brain sodium, potassium and water, brain osmolarity, and Na+-K+-ATPase activity were studied in old and young rats following three experimental aggressions: cold induced vasogenic edema, osmotically induced edema, and osmotically induced dehydration. This study supports the hypothesis that: (a) extracellular edema is slightly smaller in the aged brain, but cellular swelling is relatively greater and (b) that protective adaptation of brain volume to acute osmotic changes is less efficient and slower in the aged brain.
Brain edema (BE), defined as an increase in tissue water content leading to an increase in tissue volume, is a common histopathologic response associated with a number of acute and subacute brain lesions. In some cases BE is a result of an unbalance of physical forces, hydrostatic or osmotic gradients driving the water in the tissue (hypertensive encephalopathy, hydrocephaly, plasma hypoosmolarity). In most cases however BE is associated with complex brain tissue alterations. According to Klatzo (1967) two physiopathological types can be described: vasogenic edema follows a breakdown of blood brain barrier to proteins. Edema fluid enlarges the extra-cellular space and spreads within the white matter; cytotoxic edema is an intra-cellular retention of water due to various disorders of ionic balance across the plasmic cell membrane. In both cases the hydrostatic gradient between the vascular lumen and the tissue plays a major role in the amount and spread of the edema fluid. In both cases also, toxic substances produced by tissue destruction act as factors of secondary damage causing more blood brain barrier lesions and/or cellular membrane alterations and eventually enhance edema. In various pathological conditions vasogenic and cytotoxic edema are associated: edema around circumscribed lesions such as hematomas, traumatic contusions, tumors, abscesses is basically a vasogenic edema with a secondary cytotoxic component. Ischemic edema is initially a pure cytotoxic phenomenon with a secondary osmotic edema and lately a vasogenic component. The formation of BE leads to an increase in tissue pressure which may reduce local cerebral blood flow. If blood supply is already impaired this can lead to energy shortage and further tissue destruction. If the bulk of edema is large enough intracranial pressure rises up, brain shifts and herniations may occur. Hypertonic solutions and corticoids are the more widely used drugs against brain edema. Hypertonic solutions remove water from the normal brain and hence may reduce intracranial pressure rather than treat edema. Corticoids, through various discrete mechanisms interfere with some toxic substances, enhance energetic metabolism and allow tissue restitution with a rather limited effect on edema itself.
One hundred chronic subdural haematomas in the adult are presented in a retrospective study, looking for correlations between results and aetiological, clinical, radiological and therapeutic elements. Only four parameters are correlated with results: headache and isodensity on C.T. Scan are good prognostic factors (p less than 0.02 and p less than 0.04 respectively); on the other hand chronic alcoholism (p less than 0.03) and even more postoperative pneumatocele (p less than 0.007) are correlated with a poor result. Pneumatocele is due to intracranial hypotension which is the major factor promoting formation and development of chronic subdural haematoma occurring in aged population.
Brain water content and Na/K-ATPase activity have been compared in two groups of rats aged 60 +/- 5 days (group I) and 630 +/- 10 days (group II). In group II control animals, brain water content (p less than 0.001) and Na/K-ATPase activity (p less than 0.02) were found to be significantly reduced. Following a cryogenic lesion of the brain, the increase in water content was larger in group I (not significant), whereas impairment of Na/K-ATPase activity was much more pronounced in group II (p less than 0.001).
The functional status of GABA synapses together with tissue levels of other putative neurotransmitter amino acids was studied in epileptogenic foci (identified by stereo-EEG) removed neurosurgically from 14 epileptic patients unresponsive to anti-epileptic medication. L. glutamic acid decarboxylase was lower than normal in epileptogenic cortical tissue from 10 to 12 patients. 3H-GABA-"A" receptor binding was low in all epileptogenic tissue examined. GABA levels were unchanged, whereas glutamate was increased in 7 patients. These studies confirm previous observations that there is a decreased functional activity of GABA synapses in a high proportion of epileptogenic foci. Therefore these data indicate that there is indeed an imbalance between excitatory and inhibitory neurotransmitter systems.
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One hundred and ninety-two cases of supratentorial astrocytic tumors are classified in 4 groups according to the presence or absence in the pathological material of simple morphological criteria: abnormal cellular density, nuclear pleomorphism, neovascularization, necrosis. Each one of these criteria is strongly correlated with prognosis. Nevertheless only a simple classification in low and high grade lesions has a definite predictive value. A multivariate analysis utilizing Cox's hazard function confronts these histological findings with a number of clinical and etiological possible factors of prognosis. Age and performance status at the time of diagnosis are the best predictors of survival time. The clinical use of a predictive model derived from Cox's function analysis is discussed.
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The authors report the late results of thermocoagulation of the gasserian ganglion in 939 patients operated by 3 different neurosurgical teams, (Bologna, Bordeaux, Marseille). It has been assessed that the results are comparable among the 3 teams and that percutaneous selective thermocoagulation represents a simple and low-risk technique with a high rate of efficacity.
On May 12th 1984 a meeting on stereotactic biopsies of intraencephalic lesions has been held in Marseilles. All French Neurosurgeons and Neuropathologists involved with this technique were present. This report presents, in one hand, the result of an investigation on 3 052 BS and, in the other hand, the synthesis of discussions held on the limits and dangers of the BS, morphology of the biopsy instrument, means of the definition of the target and the microscopic histologic technics and results.
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