Résultat de la rééducation sur l’évolution motrice et fonctionnelle au cours du traitement de la tuberculose vertébrale

Objectives. – To evaluate the result of rehabilitation on motor and functional improvement in spinal tuberculosis.Methods. – Prospective case study. Data were collected from 47 patients with spinal tuberculosis medically and/or surgically treated, and rehabilitated over a period of 6 months, after spinal decompression and fusion. The main outcome measures were motor development of the patients was evaluated at the beginning, in the 1st week, in the 3rd month, and in the 6th month. Functional development of the patients was evaluated at the beginning and in the 6th month. Functional assessment was made according to Modified Barthel Index (MBI), and motor examination was make according to American Spinal Injury Association (ASIA).Results. – The study population consisted of 47 patients (22 males and 25 females) mean age 37.9 ± 18.3 years (range 5–76 years). The most common site of spinal tuberculosis was the thoracic region. Localized back pain, paraparesis, sensory dysfunction and fever were typical clinical manifestations. Surgical management was performed as anterior or posterior drainage of abscess and/or stabilization of the spine. The rehabilitation program was performed in all patients during the preoperative, early postoperative and late postoperative 6th month periods. Muscle-strengthening exercises on necessary localization such as pectoral, abdominal, lower extremities, truncal and sacrospinal extansors were started for the rehabilitation. The motor score for the lower limbs and the MBI scores for activities of daily living (ADL) and mobility improved significantly (P < 0.001). The self-care and mobility categories of the MBI on admission were 14.8% severely dependent and 10.6% independent. However, at the end of the rehabilitation program, 4.2% were severely dependent and 70.2% independent.Conclusion. – Early diagnosis and appropriate medical and/or surgical treatment together with a rehabilitation program will improve the life quality of patients with spinal tuberculosis.     

Dissection postopératoire de l’artère vertébrale en deux temps

The diagnosis of perioperative vertebral artery dissection can be difficult because of non-specific clinical signs. We report a case revealed by a tegmento-thalamic stroke after an abdominal second surgical look. The interest of this observation is related to a particular evolution in two steps separated by a 2-month-interval and an intercurrent cervical manipulation. After the second anesthesia, neck pain associated with a third cranial nerve palsy and a supranuclear ophtalmoplegia revealed a tegmento-thalamic ischemic stroke due to vertebral artery dissection. We discuss here the different factors possibly involved in the pathophysiology of postoperative vertebral artery dissection: positioning, cervical manipulation, subclavian central venous access and cisplatin toxicity. Vertebral artery dissection should be discussed in case of postoperative neck pain, especially with non-typical symptomatology.     

La cascade ischémique cérébrale

The pathophysiology of ischaemia depends on the residual cerebral blood flow. As a result, it is different in global ischaemia, when compared with focal ischaemia, where the centre area is surrounded with an area called an ischaemic penumbra. Ischaemia results from a sudden failure in the oxygen and glucose supply. Oxidative phosphorylation fails, a major event that is responsible for all the other reactions. Anaerobic metabolism produces lactate and H⁺. Cell membrane ionic pumps are inactivated, which results in a breakdown of ionic homeostasis. Ca⁺⁺ and Na⁺ penetrate into the cells, as K⁺ is released. The energy failure causes an extracellular accumulation of excitatory amino-acids, thus eliciting a hyperstimulation of the NMDA receptors. These receptors are hyperactivated as a result of the deterioration in the control systems with, especially, the blockade of the NMDA receptor by Mg⁺⁺. As a consequence, there is a massive entry of Ca⁺⁺ into the cell, inducing a series of enzymatic reactions involving phospholipases, proteases and endonucleases. Reperfusion will cause toxic lesions by producing free radicals, due to the action of arachidonic acid, xanthine oxidase and nitric oxide. The decrease in cell energetic supplies, as well as the overactivation of enzymes and the production of free radicals, result in cell death.     

Hypothermie modérée et protection cérébrale

To define the part played by mild-to-moderate hypothermia in neuroprotection, it is necessary to take into account the thermoregulatory responses that occur in the normal human as the change in central temperature exceeds 0.2 °C. The mechanisms induced by cold are cutaneous vasoconstriction and shivering. They must be suppressed before starting controlled hypothermia. In these conditions, controlled moderate hypothermia between 32 and 35 °C dœs not seem to have deleterious side-effects, especially on coagulation. Caution is needed with the analysis of the numerous papers reporting experiments concerning the effects of moderate hypothermia in animals with induced cerebral ischaemia because of significant differences in the study designs. These differences concern mainly the time of onset of hypothermia, viz before or after ischaemia, the fact that the ischaemia is either global or focal, that it is caused by vascular occlusion posttraumatic or initiated by hypo or hyperglycemia. Some differences are also existing in the criteria used to appreciate the neuronal damage, as well as in the level of temperature and the site where it is measured. The mechanism of neuroprotectionfrom moderate hypothermia seems to be not only a decrease in cerebral metabolism, but also involves a specific action on some intra-cellular events such as the blocking of the release of glutamate and of lipid peroxydation in brain tissue. An indirect proof of the neuroprotective effect of moderate hypothermia is the increase in the neuronal damage induced by moderate hyperthermia. It is conceivable that moderate hypothermia could exert a better neuroprotective effect than the drugs having this reputation, such as barbiturates, isoflurane and propofol. The possible induction of hypothermia into experiments concerning barbiturate or isoflurane protection could even explain the protection observed, as this has been proven for anti NMDA, MK-801. The few clinical studies already published do not show obvious differences allowing to recommend moderate hypothermia as a standard technique among the therapeutic modalities used for cerebral protection for intracerebral vascular surgery or cerebral resuscitation after severe head trauma. However, the experimental results are strong enough to justify futur controlled clinical studies. The prevention of brain hyperthermia may also emerge as a major objective of resuscitative intervention.