[Post-traumatic vegetative states].
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Biomedical subjects
Publications and source records attributed to E Richer.
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In 25 cases of post traumatic vegetative state persisting 3 months after the initial injury, deep brain stimulation (DBS) has been used with the aim to activate the cortex and the hope to produce some degree of functional recovery. Electrodes were stereotaxically implanted in the centrum medianum-parafascicularis complex. Bipolar stimulation was provided daily from 8 a.m. to 8 p.m. In 12 cases no changes occurred in the clinical features and overall behaviour. DBS was given up after 2 months. All these patients with a follow-up of 1 to 10 years, remained in a permanent vegetative state, 4 of them eventually deceased. In 13 cases, following 1 to 3 weeks of DBS a definite improvement was obtained with recovery of some degree of consciousness and interpersonal relationship. However all these patients, with 1 to 12 years follow-up remained severely disabled. 2 of them deceased from intercurrent causes. The practical meaning of these clinical results are questioned. We consider that the absence of response to DBS is an important argument to predict the irreversibility of post traumatic vegetative state. It is not certain that DBS is directly responsible for positive changes observed, some degree of long-term spontaneous recovery being already documented in such patients. However it seems likely that DBS accelerates recovery and possibly improves the final level of performances.
We have studied the electrophysiological evolution, with the aid of long-term, quantitative E.E.G. (Holter method) and sensory evoked potentials (visual, auditory and somatosensory) on 25 severe traumatic head injury patients (initial Glasgow scale--between 3 and 5) aged from 5 to 42 years having evolved towards a persistent vegetative state and being object of a protocol of thalamic stimulation. Electrophysiological exploration was practised before placement of the stimulation, then at 2 weeks, 1 month, 2 months and finally 3 months after. The electrophysiological parameters appear to have no predictive value on the clinical evolution after stimulation. However, changes such as long-term quantitative EEG as well as evoked potentials mostly precede clinical progress when present. Cortical evoked potentials are the first to change significantly (J15) followed by long-term quantitative EEG and brain stem evoked potentials (J30); the latter improving more completely. Also the consideration of the chronobiological aspects of the recordings of the long term EEG allow the proposal of "waking targeted" stimulations at the most favorable moments of the nyctohemeral period.
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It has never been formally established whether eclampsia can come on more than 48 hours after delivery. We report a case of a patient who had convulsions together with transitory raised blood pressure coming on 14 days after her delivery. MRI was carried out 24 hours after the attack and showed pathological sub-cortical images and there was a hyper signal at T2. This is now a well known feature and has been described in the course of typical eclampsia fits. On the other hand MRI is able to eliminate a certain number of differential diagnoses such as cerebral thrombophlebitis, cerebral vascular accidents and tumours. A cerebral blood flow study and a trans-cranial Doppler flow study showed (as far as we know for the first time) a lessening in perfusion and in speed of flow giving rise to lowered blood circulation in that part of the brain and suggestive of vascular spasm. This observation makes it very likely that eclamptic crises can occur two weeks after delivery and favours a vascular spasm being the origin of these crises.
Ovarian abscess is very rare and is usually a complication of acute purulent salpingitis. It can however rarely be isolated. Wilson and Black found 28 cases of 75,262 women who were admitted to the Department of Gynaecology and Obstetrics in Philadelphia between 1948 and 1963. There are only 120 cases in the literature. We report here two cases of abscess of the ovary which were operated in our department at an interval of one month.
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The coordinator draws conclusions on the symposium day devoted to the teams. After defining "team" he gives several thoughts on the team's work its advantages and its difficulties. During this day the teams talked about their questions and their certainties in the various fields of their work. They also discussed their hard ships and their need of psychological support which the hospital departments do not have the means to satisfy.
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.
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This study will consider the course and final outcome of severe traumatic coma (Glasgow coma scale score 5-3 at admission). Intensive rehabilitation programs aimed at functional recovery must be undertaken from the very beginning. The importance of retraining of axial motricity is stressed. Successive stages of evolution and various neurological syndromes disclosed during the awakening period are described. Even in the case of these very severe brain injuries, a considerable amount of recovery is possible and leads to a normal socio-economic status in 62% of the cases. 22% however will remain bound to some type of sheltered life. Functional outcome is not related to the depth of initial coma but rather to the length of comatose period. It can be safely predicted only at the awakening phase, the neurological status reached at this time reflecting rather well the overall extent and severity of brain lesions. Neurophysiological mechanisms likely to support the functional recovery after this type of trauma are discussed.
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CDP Choline, a metabolic precursor of phospholipids, has been tested against placebo in a controlled randomized double blind study concerning 60 cases of severe head injuries (wide-spread cerebral contusions and/or severe concussion). In the treated group, a shortening of the comatose period and an acceleration of neurological deficits recovery have been observed. These results are tentatively attributed to an effect of the drug against brain edema, already documented on experimental models.
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