Previous reports documented demonstrated that melatonin, a free radical scavenger, is important in protecting against oxidative stress-induced tissue damage after spinal cord injury (SCI). This study was undertaken to investigate the effects of pinealectomy (PX) and administration of exogenous melatonin after SCI in rats. These animals were randomized into six groups, each having 12 rats. Group 1 underwent laminectomy alone. Group 2 underwent laminectomy followed by SCI and received no medication. Group 3 underwent laminectomy followed by SCI and received melatonin. Group 4 underwent PX and laminectomy alone. Group 5 underwent PX and laminectomy followed by SCI and received no medication. Group 6 underwent PX and laminectomy followed by SCI and received melatonin. Melatonin (100 mg/kg) was given intraperitoneally immediately after trauma to the rats in the groups 3 and 6. PX caused a significant increase in the malondialdehyde (MDA), nitrite oxide (NO), glutathione (GSH), xanthine oxidase (XO) levels and decrease in GSH levels as compared with the control group. Trauma to the spinal cord results in significantly higher oxidative stress. Melatonin administration significantly reduced MDA, XO and NO levels, and increased GSH levels in the spinal cord after trauma. Exogenous melatonin treatment after trauma attenuated tissue lesion area and accelerated motor recovery rate. These findings suggest that reduction in endogenous melatonin after PX makes the rats more vulnerable to trauma and exogenous melatonin administration has an important neuroprotective effect on the level of the spinal cord.
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.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.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.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.
Although gliofibroma is a rare and incompletely characterized tumor, recent publications have revealed new aspects of this entity. The case of a 16-year-old boy who was diagnosed as having a gliofibroma is presented here, and the problems regarding nosology are discussed in the light of the recent literature.
To investigate the association between the vitamin D receptor (VDR) gene rs2228570 FokI polymorphism and the development of lumbar degenerative disc disease (LDDD) in the Turkish population.This was a prospective case-control study that included 45 patients with LDDD and 49 healthy individuals (control group). The clinical investigations of the LDDD patients consisted of neurological examinations, lumbar magnetic resonance imaging studies, visual analog scale (VAS) scores, and Oswestry Disability Index scores. The VDR gene rs2228570 FokI polymorphism was analyzed via a real-time polymerase chain reaction.Individuals with the VDR GG genotype had a significantly increased risk of LDDD, while those with the AG genotype had a significantly decreased risk. In addition, the A allele may have a protective effect against LDDD in the Turkish population. Moreover, the VAS pain results showed that the GG genotype had a significantly higher score than the others.VDR rs2228570 AG genotype is at a decreased risk and the GG genotype is at an increased risk of LDDD in the Turkish population. Since genetic polymorphisms often show ethnic differences, further functional studies are needed to evaluate the genotype and phenotype correlations in large cohorts of various ethnicities.
Sir, Idiopathic spinal cord herniation is a rare disease of middle-aged patients presenting with myelopathy. Displacement of the spinal cord is through a ventral dural defect. Surgery is the treatment of choice with different techniques ranging from direct closure to using a patch as a dural substitute.[1,2] A 72-year-old woman complaining of progressive walking difficulty, weakness of the lower extremities, and urinary incontinence was admitted to the hospital. On her neurological examination, the patient was paraparetic (right: 2/5, left: 3/5). Deep tendon reflexes were hyperactive and she were urinarily incontinent. Magnetic resonance imaging (MRI) revealed focal anterior kinking at the level of T7-8 and the cord were thinned. The posterior extramedullary space was enlarged [Figures 1, 2].Figure 1: Preoperative sagittal T2-weighted MRI: anterior kinking and atrophy of the spinal cord at T7-8 level (red arrow), subarachnoid space is enlargedFigure 2: Preoperative T2-weighted axial MRI: ventral displacement of the spinal cordThe patient was operated. Large laminectomy with microneurosurgical dentate ligament resection was performed and the spinal cord was repositioned after dural defect reparation with an allograft. Postoperatively her paraparesis was relieved. Her postoperative MRI showed the cord was repositioned [Figure 3a, b]. After three weeks, she began to ambulate with support and she was referred for physical therapy.Figure 3: (a, b): Postoperative sagittal and axial T2-weighted MRI: in the early postoperative period the cord is observed to be repositioned, although partial ventral apposition persistsIdiopathic spinal cord herniation is recognized as herniation of the spinal cord through a ventral or ventrolateral defect. Including our case, 131 patients were reviewed [Table 1]. Most frequently diagnosed between levels T3 and T7. Clinic presentation is usually as Brown-Sequard syndrome. Other presentations are monoparesis, paraparesis, sensory impairment, bowel and bladder dysfunction, impotence, and chest and back pain.[2] T4-5 is reported to be the most frequently involved level.[3] The etiology of the ventral dural defect may be idiopathic, due to trauma or iatrogenic. Pathophysiology is not thoroughly known though multiple theories have been reported. The dorsal arachnoid cyst was reported to transmit pressure from the spinal cord causing the ventral defect. MRI showed anterior kinking of the thoracic spinal cord with dorsal subarachnoid enlargement.[3]Table 1: Including our case, 131 patients were reviewedTreatment is the surgical reduction of the spinal cord and repositioning of the cord to its normal anatomic position with dural patch repair. Technically, laminectomy, dorsal durotomy with sectioning of the adhesions, and dentate ligaments are required.[4] Our patient has been surgically treated for thoracic spinal cord herniation with the dural repair. The pathogenesis of thoracic spinal cord herniation is not fully understood. Trauma due to osteophytes or calcified discs may be one of the initiating factors. Since the disease is uncommon, one must be careful about misdiagnosis. Spinal cord reposition with dural repairment may give relief in progressive myelopathic patients. Declaration of patient consent Written informed consent for submission of the paper was obtained from the patient. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
Head trauma causes two kinds of injury in the neural tissue. One is the primary injury which occurs at the time of impact. The other one is a secondary injury and is a progressive process. Free radicals are produced during oxidative reactions formed after trauma. They have been thought to be responsible in the mechanism of the secondary injury. Some studies have been conducted to demonstrate the role of free oxygen radicals in neuronal injury. The alterations in the free radical level during the early posttraumatic period and the effect of a free radical scavenger on these alterations have not been studied as a whole. We aimed to demonstrate the free oxygen radical level changes in the early posttraumatic period and the effect of melatonin, which is a potent free radical scavenger, on the early posttraumatic free radical level. A two-staged experimental head trauma study was designed. In stage one, posttraumatic free radical level changes were determined. In the second stage, the effect of melatonin on the free radical level changes in the posttraumatic period was studied. Two main groups of rats each divided into four subgroups were studied. Rats in one of the main groups underwent severe head trauma, and malondealdehyde (MDA) levels were measured in the contused cerebral tissue at different time points. Rats in the other main group also underwent the same type of trauma, and melatonin was injected intraperitoneally at different time points after trauma. The MDA level alteration in the tissue was determined after the injection of melatonin. The MDA level increased rapidly in the early posttraumatic period. But in time, it decreased in the groups with only trauma. In the melatonin-treated group, the MDA level decreased after the injection of melatonin, when injected in the early posttraumatic period, compared to the control and trauma groups. However, melatonin increased MDA to a higher level than in the groups with only trauma and the control group when injected later than 2 h after trauma. The MDA level increases in the very early posttraumatic period of cerebral trauma and decreases in time. Melatonin, which is the most potent endogenous free radical scavenger, when injected intraperitoneally to the cerebral traumatized rats in the very early posttraumatic period, causes a significant decrease in the MDA level. But, melatonin, when injected more than 2 h after trauma, increases the MDA level in experimental cerebral trauma in rats.
