✓The treatment of spinal tuberculosis is a challenging and controversial problem. The authors present the rare case of an 8-month-old infant with dorsolumbar junction tuberculosis. The child did not sit or stand and a hump was noted on his back. Radiological evaluations demonstrated destruction by a tuberculous abscess of the T-12 and L-1 vertebral bodies, extending into the psoas muscles and spinal canal. In addition to medical therapy, radical debridement and grafting were performed via an anterolateral approach. The follow-up period was 2 years. The difficulties in the management of spinal tuberculosis in infants are discussed.
Kadir Tufan, Fikret Dogulu, Ozgur Kardes, Namik Oztanir and M. Kemali Baykaner
Kadir Tufan, Namik Oztanir, Ebru Ofluoglu, Candan Ozogul, Nuket Uzum, Ayse Dursun, Hatice Pasaoglu and Aydin Pasaoglu
Lamotrigine is an antiepileptic drug that inhibits presynaptic voltage-gated sodium channels and reduces the presynaptic release of glutamate in pathological states. Neuroprotective effects of this drug have already been demonstrated in cerebral ischemia models. The aim of the present study was to determine the effects of presynaptic glutamate release inhibition on experimental spinal cord injury (SCI).
A total of 66 adult Wistar rats were randomly allocated into 6 groups. Group I was the control group used to obtain normal blood samples and spinal cord specimens. Spinal cord injury was introduced by using the extradural clip compression technique, but no medication was given to Group II (trauma group) rats. Group III was treated with vehicle, and the same amount of dimethyl sulfoxide used in treatment groups was administered to these rats. A dose of 50 mg/kg lamotrigine was administered intraperitoneally to Group IV (pretreatment), Group V (peritreatment), and Group VI (posttreatment) rats 30 minutes before, during, and 30 minutes after SCI, respectively. Oxidative stress parameters and transmission electron microscopic findings were examined.
Blockade of presynaptic release of glutamate by lamotrigine treatment yielded protective effects on the spinal cord ultrastructure even when administered after the SCI, but it prevented oxidative stress only when it was administered before or during the SCI.
Currently, no available agent has been identified, that can block all the glutamate receptors at the same time. To prevent excitotoxicity in SCI, inhibiting glutamate release from the presynaptic buttons instead of blocking the postsynaptic glutamate receptors seems to be a more rational approach. Further research, such as neurobehavioral assessment, is warranted to demonstrate the probable neuroprotective effects of presynaptic glutamate release inhibition in SCI.