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  • Author or Editor: Nuket Uzum x
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Mehmet Arazi, Onder Guney, Mustafa Ozdemir, Omer Uluoglu and Nuket Uzum

✓ The authors report the case of a 53-year-old woman with monostotic fibrous dysplasia of the thoracic spine. The patient presented with a 1-month history of pain in the thoracic spinal region. En bloc resection of the lesion was successfully performed via a transthoracic approach, and a histopathological examination confirmed the diagnosis of fibrous dysplasia. At 24-month follow-up examination, pain and vertebral instability were absent.

The findings in this case illustrate that, although very rare, monostotic fibrous dysplasia of the thoracic spine should be considered in the differential diagnosis of spinal tumors. Although a consensus for management of this disease has not been achieved, the authors recommend radical removal of all involved bone as well as internal fixation or bone graft—assisted fusion to achieve long-term stabilization.

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Laurence Marshman and Karoly M. David

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Kadir Tufan, Namik Oztanir, Ebru Ofluoglu, Candan Ozogul, Nuket Uzum, Ayse Dursun, Hatice Pasaoglu and Aydin Pasaoglu

Object

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).

Methods

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.

Results

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.

Conclusions

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.

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