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Central nervous system protection by resveratrol in streptozotocin-induced diabetic rats

The objective of the present study was to investigate the possible neuroprotective effect of resveratrol against streptozotocin-induced hyperglycaemia in the rat brain and medulla spinalis. Thirty adult male Wistar rats were divided into three groups as follows: control group, streptozotocin-induced diabetic-untreated group, and streptozotocin-induced diabetic resveratrol-treated group. Diabetes was induced by a single injection of streptozotocin (STZ) (60 mg/kg body weight). Three days after streptozotocin injection, resveratrol (10 mg/kg) was injected intraperiteonally daily over 6 weeks to the rats in the treatment group. Six weeks later, seven rats from each group were killed and the brain stem and cervical spinal cord were removed. The hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for biochemical studies (lipid peroxidation measuring malondialdehyde [MDA], xanthine oxidase [XO], nitric oxide [NO] and glutathione). MDA, XO and NO levels in hippocampus, cortex, cerebellum, brain stem and spinal cord in the streptozotocin-induced diabetic-untreated group increased significantly. Treatment with resveratrol significantly reduced MDA, XO and NO production and increased glutathione levels when compared to the streptozotocin-induced diabetic-untreated group. This study demonstrates that resveratrol is a potent neuroprotective agent against diabetic oxidative damage.

Comparative neuroprotective effect of sodium channel blockers after experimental spinal cord injury.

Spinal cord injury (SCI) results in loss of function below the lesion. Secondary injury following the primary impact includes a number of biochemical and cellular alterations leading to tissue necrosis and cell death. Influx of Na(+) ions into cells has been postulated to be a key early event in the pathogenesis of secondary traumatic and ischemic central nervous system injury. Previous studies have shown that some voltage-sensitive sodium channel blockers provide powerful neuroprotection. The purpose of the present study was to compare the neuroprotective effect of three sodium channel blockers-mexiletine, phenytoin and riluzole--after SCI. Ninety rats were randomly and blindly divided into five groups of 18 rats each: sham-operated group, trauma group (bolus injection of 1 mL physiological saline intraperiteonally [i.p.]), mexiletine treatment group (80 mg/kg, i.p.), phenytoin treatment group (200 mg/kg, i.p.) and riluzole treatment group (8 mg/kg, i.p.). Twenty-four hours after injury, the rats were killed for determination of spinal cord water content and malondialdehyde (MDA) levels. Motor function scores of six rats from each group were evaluated weekly for six weeks. Then the rats were killed for histopathological assessment. Although all the treatment groups revealed significantly lower MDA levels and spinal cord edema than the trauma group (p<0.05), the riluzole and mexiletine treatment groups were better than the phenytoin treatment group. In the chronic stage, riluzole and mexiletine treatment achieved better results for neurobehavioral and histopathological recovery than phenytoin treatment. In conclusion, all the tested Na(+) blockers had a neuroprotective effect after SCI; riluzole and mexiletine were superior to phenytoin.

Effects of resveratrol and methylprednisolone on biochemical, neurobehavioral and histopathological recovery after experimental spinal cord injury

AbstractAim:To investigate the neuroprotective effect of resveratrol in an experimental spinal cord injury (SCI) model in rats.Methods:Male Wistar albino rats weighing 200–250 g were randomized into six groups. Weight-drop trauma was performed for SCI. Group 1 underwent laminectomy alone. Group 2 underwent laminectomy followed by SCI. Groups 3, 4, 5, and 6 underwent laminectomy followed by SCI and received resveratrol (100 mg/kg), methylprednisolone (MP) (30 mg/kg), resveratrol (100 mg/kg) plus MP (30 mg/kg), and ethanol (2%), respectively. The rats were divided into two subgroups for biochemical analysis (killed at 24 h after surgery) and for neurobehavioral and histopathological evaluation (killed at 6 weeks after surgery). Posttraumatic neurological recovery after surgery was recorded weekly.Results:Groups 3 and 5 revealed significantly lower malondialdehyde, nitric oxide, xanthine oxidase, and higher glutathione levels than group 4 (P<0.05). Neurological recovery rates were significantly better in groups 3 and 5 than group 4 (P<0.05). When spinal trauma size ratios were compared, there was no significant difference between treatment groups.Conclusion:Resveratrol treatment revealed better biochemical recovery in the acute stage of trauma than MP treatment. Although resveratrol and combined treatment revealed better neurobehavioral recovery than MP treatment; resveratrol, MP, and combined treatment modalities improved histopathological recovery at the same level in the final stage of the experiment. Future studies involving different doses of resveratrol and different doses combinations with MP could promise better results as each drug has a different anti-oxidative mechanism of action.

Effect of pinealectomy and melatonin replacement on morphological and biochemical recovery after traumatic brain injury

Numerous studies showed that melatonin, a free radical scavenger, is neuroprotective. In this study, we investigated the effect of pinealectomy and administration of exogenous melatonin on oxidative stress and morphological changes after experimental brain injury.

Post-traumatic early epilepsy in pediatric age group with emphasis on influential factors

ObjectivePosttraumatic epilepsy in the pediatric age group is mostly seen within the first week. An acute posttraumatic epileptic fit, which may induce secondary insults, should be hindered. The aim of the study is to define the risk factors for posttraumatic early epilepsy (PTEE) and the indications for prophylactic therapy.MethodsIn this survey, a total of 1,785 pediatric patients—under the age of 16—are studied. The majority of the patients (1,655) were treated in Haydarpaşa Numune Hospital within the years 1993–1999. The rest, which consists of 130 patients, were treated in Inönü University Turgut Özal Medical Center between the years 2001 and 2003. The patients were categorized according to age, gender, neurological manifestations, type of trauma, cranial pathology, number and type of epileptic fits, the interval between trauma and convulsion, electroencephalogram findings, and antiepileptic therapy. All these factors were challenged due to their effect on the evolution of PTEE.ResultsOnly 149 cases had PTEE (8.4%). There was no correlation between gender and the incidence of PTEE. The data showed that 11.7% of the patients at or under the age of 3 (p=0.00072), 30.8% of the patients with severe head injury (Glasgow Coma Scale=3–8; Children’s Coma Scale = 3–8; p=0.00000), 19.3% of the patients with depressed skull fractures (p=0.00038), 13.7% of the patients with intraparenchymal hemorrhage (p=0.0000072), and 21.6% of the patients with cerebral edema (p=0.000008) had PTEE. Only 20% of the patients with PTEE had a Glasgow Outcome Scale (GOS) of 3 or less (p=0.0000075).ConclusionThose patients at or under the age of 3, with severe head injury, cerebral edema, intraparenchymal hemorrhage, or depressed skull fracture, have a higher incidence of PTEE. Moreover, because the GOS of these patients are prone to be worse, antiepileptic therapy in acute stage may be effective in preventing the secondary brain damage.

Isolated posterior spinal artery aneurysm

Isolated aneurysms of the posterior spinal artery (not associated with arteriovenous malformations) are exceptionally rare. Three cases have been reported in the literature to date. We report a case of an isolated posterior spinal artery aneurysm causing acute subarachnoidal haemorrhage. Spinal artery aneurysms are contrasted with the more common intracranial aneurysms in terms of presentation and pathogenesis.

Neuroprotective effect of etomidate on functional recovery in experimental spinal cord injury

Primary impact to the spinal cord causes rapid oxidative stress after injury. To protect neural tissue, it is important to prevent secondary pathophysiological mechanisms. Etomidate, a strong antiexcitotoxic agent, stimulates the gamma aminobutyric acid (GABA) receptors. The purpose of this study was to investigate neurobehavioral and histological recovery and to evaluate the biochemical responses to treatment of experimental spinal cord injury (SCI) in rats with etomidate or methylprednisolone (MP) or both etomidate and MP.

Do sodium channel blockers have neuroprotective effect after onset of ischemic insult

Abstract Objective: Cerebral ischemia causes a series of pathophysiologic events that may result in cerebral infarct. Some neurons are more vulnerable to ischemia, particularly pyramidal neurons in the hippocampal CA1 region. Pharmacologic intervention for treatment of cerebral ischemia aims to counteract secondary neurotoxic events or to interrupt the progression of this process. In the present study, we compare the neuroprotective effects of sodium channel blockers (mexiletine, riluzole and phenytoin) and investigate whether they have neuroprotective effect when given after ischemic insult. Methods: A transient global cerebral ischemia model was performed in this study by clipping bilateral common carotid arteries during 45 minutes. Riluzole (8 mg/kg), mexiletine (80 mg/kg) and phenytoin (200 mg/kg) were injected into the rats intraperitoneally 30 minutes before or after reperfusion. Lipid peroxidation levels and cerebral water contents were evaluated 24 hours after ischemia. Histopathologic assessment of hippocampal region was determined 7 days after ischemia. Results: Riluzole, mexiletine and phenytoin treatment after global ischemia significantly decreased water content of the ischemic brain (p<0.05 for each). No significant difference was observed in cerebral edema among the drug treatment groups (p>0.05). When pre-treatment and post-treatment groups were compared with each other, only riluzole pre-treatment group revealed better result for cerebral edema (p<0.05). Pre-treatment with these drugs revealed significantly better results for the malonyldialdehyde (MDA) level and the number of survival neuron on the hippocampal region than the post-treatment groups. Conclusion: It is demonstrated that riluzole, mexiletine and phenytoin are potent neuroprotective agents in the rat model of transient global cerebral ischemia, but they are more effective when given before onset of the ischemia.

Neuroprotective effect of mexiletine in the central nervous system of diabetic rats

Both experimental and clinical studies suggests that oxidative stress plays an important role in the pathogenesis of diabetes mellitus type 1 and type 2. Hyperglycaemia leads to free radical generation and causes neural degeneration. In the present study we investigated the possible neuroprotective effect of mexiletine against streptozotocin-induced hyperglycaemia in the rat brain and spinal cord.30 adult male Wistar rats were divided into three groups: control, diabetic, and diabetic-mexiletine treated group. Diabetes mellitus was induced by a single injection of streptozotocin (60 mg/kg body weight). Mexiletine (50 mg/kg) was injected intraperitoneally every day for six weeks. After 6 weeks the brain, brain stem and cervical spinal cord of the rats were removed and the hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for biochemical analysis (the level of Malondialdehide [MDA], Nitric Oxide [NO], Reduced Glutathione [GSH], and Xanthine Oxidase [XO] activity). MDA, XO and NO levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the diabetic group increased significantly, when compared with control and mexiletine groups (P < 0.05). GSH levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the diabetic group decreased significantly when compared with control and mexiletine groups (P < 0.05).This study demonstrates that mexiletine protects the neuronal tissue against the diabetic oxidative damage.

Bone wax can cause foreign body granuloma in the medulla oblongata

Bone wax is commonly used in neurosurgical practice as a haemostatic and sealing agent. It is a safe agent, but may lead to adverse effects such as infection, epistaxsis, allergic reaction or foreign body granuloma. There are very few reported cases of the neurological complications of remnant bone wax in the subdural or subarachnoid space. The authors report the case of a foreign body granuloma infiltration through the medulla oblongata due to remnant bone wax in the subarachnoid space after posterior fossa decompressive surgery.