Selcuk Palaoglu

Intraradicular disc herniations in the lumbar spine and a new classification of intradural disc herniations

Study design: A case report of intraradicular disc herniation. Intraradicular disc herniation is a special type of intradural disc hernations. In this report, we present the tenth case of intraradicular lumbar disc herniation and suggest a new classification for intradural disc herniations.Case Report: A 32-year-old male was admitted to hospital having experienced pain in the lower back and right leg for 1 month prior to admission. Neurological examination revealed weakness of the extensor hallucis longus, positive Laségues sign, decreased ankle reflex in his right lower extremity, and bilateral paravertebral muscle spasm. Magnetic resonance imaging (MRI) revealed a disc herniation with a posterolateral extruded fragment on the right at the level of the L5-S1 space. He underwent L5 laminectomy. During the operation, the right S1 root was found to be swollen and immobile. A longitudinal incision was made in the dura of the right S1 root and an intradural free disc fragment was removed, and the S1 root was relieved. The patient was free of pain postoperatively.Conclusion: We suggest a new classification for intradural disc herniations with this unusual case presentation and review the literature for pathogenesis, clinical picture, diagnosis and treatment.Spinal Cord (2001) 39, 545–548.

Intramedullary Epidermoid Cyst of the Cervical Spinal Cord Associated with an Extraspinal Neuroenteric Cyst

A 4-year-old girl presented with an intramedullary epidermoid cyst of the cervical spinal cord. The clinical, radiological, and surgical features and a brief critical review of the literature are included in this report. The cyst contents were removed totally in two operations. The child had a coexisting neuroenteric cyst in the posterior mediastinum. To our knowledge, this coexistence has not been previously reported. Contemporary imaging modes and prospects of the surgical treatment are discussed.

Nimodipine attenuates lipid peroxidation during the acute phase of head trauma in rats

Abstract Oxygen free radical-mediated lipid peroxidation is one of the major mechanisms of secondary damage in traumatic brain injury. We assessed the effects of nimodipine on lipid peroxidation 1 h after head trauma in rats. Nimodipine (1.5 µg/kg IV bolus injection) was given immediately after head trauma by either the carotid artery or the jugular vein. Placebo treated rats received saline by the same routes. Control rats received head trauma only. Sham-operated rats were the group without head trauma. Malondialdehyde (MDA), which is the end product of lipid peroxidation, was measured as an indicator of oxygen free radical formation in the brain tissue. The mean values for MDA in sham operated rats were 92.4±4.9 nanomoles/gram wet weight (nmol/gww) of brain tissue. In the control group, MDA content of the brain tissue was 120.8±9.4 nmol/gww. In placebo treated rats, the results were similar. In the groups receiving nimodipine via carotid artery or jugular vein, the mean values were 101.1±6.9 and 106.5±6.0 nmol/gww, respectively. These results indicate that nimodipine caused a significant decrease in lipid peroxidation when given in the acute phase of head trauma in rats. This occurred regardless of the route of injection.

Overview of vascular complications of pituitary surgery with special emphasis on unexpected abnormality

Arterial bleeding during transsphenoidal surgery for pituitary adenoma is known complication. This usually happens due to rupture of intracavernous carotid or delayed hemorrhage due to the carotico-cavernous fistula and/or pseudoaneurysm. There is also evidence that cavernous carotid aneurysms may occur with pituitary tumors, yet largest series failed to demonstrate any link between aneurysm formation and pituitary tumors. Usually such an aneurysm rupture results in formation of carotico-cavernous fistula. However, pituitary apoplexy and even epistaxis have been reported. In this paper we present a patient with recurrent pituitary adenoma and cavernous carotid artery aneurysm, which caused significant hemorrhage during the surgery. Although retrospective analysis of MRI disclosed that the patient had the aneurysm before the first surgery, it remained silent until the second operation. Therefore neurosurgeons should be very susceptive to any signal changes on preoperative MR images, especially in recurrent cases, where normal anatomical relations are disturbed by fibrotic tissue. Also, we reviewed the vascular complication of pituitary surgery based on the literature.

Medulloblastoma in a child with the metabolic disease L-2-hydroxyglutaric aciduria

L-2-Hydroxyglutaric aciduria (LHGA) is a rare autosomal recessively inherited neurodegenerative disorder. It is characterized by psychomotor retardation, progressive ataxia and typical magnetic resonance imaging findings, and presents in early infancy. On the other hand, medulloblastomas are very common solid tumors of childhood and infancy. We present a 3-year-old boy with LHGA who developed a medulloblastoma during the course of the disease. There has been no previous report of the coexistence of medulloblastomas with LHGA. Central nervous system tumors are encountered in children with other metabolic neurodegenerative disorders. The aim of this paper is to focus on the difficulties in the diagnosis and treatment of an intracranial tumor in a child already neurologically impaired due to metabolic neurodegenerative disease.

Effect of Melatonin on Cerebral Edema in Rats

OBJECTIVE Melatonin (5-methoxy-N-acetyltrypamine), a chemical naturally produced in the pineal gland, has been suggested to be a free radical scavenger and an antioxidant. In the present study, the effect of melatonin on cold-induced brain edema was evaluated by determination of cerebral water content, blood-brain barrier permeability, and areas of infarct; the effects were also studied histopathologically. METHODS Brain edema was produced in rats by creating a lesion via cortical freezing. Animals were separated into four groups: sham-operated (craniectomy only); control (cold injury); sham-vehicle (cold injury plus saline); and melatonin treatment (cold injury plus melatonin). Melatonin was administered (50 mg/kg intraperitoneally) 15 minutes after the cold injury was induced. Twenty-four hours later, tissue samples from the core, from the periphery of the cold-injured hemisphere, and from the contralateral hemisphere symmetrical to the cold injury were obtained. RESULTS Melatonin treatment reduced edema (mean +/- standard deviation; 86.22 +/- 1.54% in the control group versus 80.78 +/- 2.76% in the melatonin treatment group, P < 0.001) and blood-brain barrier permeability (45.34 +/- 2.75% in the control group versus 38.26 +/- 3.40% in the melatonin treatment group, P < 0.001) at the periphery of cold injury. Area of infarct reduced from 5.84 +/- 0.58% in the control group to 3.30 +/- 0.89% in the melatonin treatment group (P < 0.001). The effect of melatonin was also confirmed histopathologically. CONCLUSION Melatonin was found to be neuroprotective in instances of cold-induced brain edema. Thus, melatonin may be a valuable therapeutic agent in the treatment of cerebral edema.

Effect of immunomodulation with human interferon-β on early functional recovery from experimental spinal cord injury

Study Design. Electron and light microscopic changes, neutrophil infiltration, and lipid peroxidation in the spinal cord and early neurologic examination were studied in rats. Objective. To examine the effects of immunomodulator treatment with recombinant human interferon-&bgr; after spinal cord contusion injury. Summary of Backgroud Data. Immunomodulator treatment with interferon-&bgr; has been the subject of extensive studies, but mainly in relation to multiple sclerosis. Recently, it was reported that interferon-&bgr; possessed significant neuroprotection after experimental transient ischemic stroke. However, to our knowledge, there have been no previous reports about the neuroprotective effect of interferon-&bgr; after spinal cord injury. Methods. Rats were randomly allocated into 5 groups. Group 1 was control and after clinical examination, normal spinal cord samples were obtained. Group 2 was introduced 50 g/cm contusion injury. Group 3 was vehicle, immediately after trauma 1 mL of physiologic saline was injected. Group 4 was given 30 mg/kg methylprednisolone sodium succinate intraperitoneally immediately after trauma. Group 5 was given 1 × 107 IU interferon-&bgr; immediately and 0.5 × 107 IU interferon-&bgr; 4 hours after trauma. Animals were examined by inclined plane and Basso-Beattie-Bresnahan scale 24 hours after trauma. Spinal cord samples obtained following clinical evaluations. Neutrophil infiltration was evaluated by myeloperoxidase activity and lipid peroxidation was estimated by thiobarbituric acid test. Electron and light microscopic results were also performed to determine the effects of interferon-&bgr; on tissue structure. Results. Interferon-&bgr; treatment improved neurologic outcome, which was supported by decreased myeloperoxidase activity and lipid peroxidation. Electron and light microscopic results also showed preservation of tissue structure in the treatment group. Conclusions. Immunomodulator treatment with interferon-&bgr; possesses obvious neuroprotection after acute contusion injury to the rat spinal cord.

Melatonin as a free radical scavenger in experimental head trauma

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.

Metoprolol treatment decreases tissue myeloperoxidase activity after spinal cord injury in rats.

Neutrophil infiltration has been reported to play an important role in spinal cord injury (SCI). In addition to their cardioprotective effects, beta-blockers have been found to have neuroprotective effects on the central nervous system, but their effect on SCI has not yet been studied. In the current study, we investigated the effect of metoprolol on myeloperoxidase (MPO) activity, a marker of neutrophil activation, in the spinal cord after experimental SCI in rats. Rats were divided into six groups: controls received only laminectomy and spinal cord samples were taken immediately; the sham operated group received laminectomy, and spinal cord samples were taken 4h after laminectomy; the trauma only group underwent a 50g/cm contusion injury but received no medication; and three other groups underwent trauma as for the trauma group, and received 30mg/kg methylprednisolone, 1mg/kg metoprolol, or 1mL saline, respectively. All the medications were given intraperitoneally as single doses, immediately after trauma. Spinal cord samples were taken 4h after trauma and studied for MPO activity. The results showed that tissue MPO activity increased after injury. Both metoprolol and methylprednisolone treatments decreased MPO activity, indicating a reduction in neutrophil infiltration in damaged tissue. The effect of metoprolol on MPO activity was found to be similar to methylprednisolone. In view of these data, we conclude that metoprolol may be effective in protecting rat spinal cord from secondary injury.

F wave studies of neurogenic intermittent claudication in lumbar spinal stenosis

Bal S, Celiker R, Palaoglu S, Cila A: F wave studies of neurogenic intermittent claudication in lumbar spinal stenosis. Am J Phys Med Rehabil 2006;85:135–140. Objective:Lumbar spinal stenosis (LSS) may result in neurogenic claudication (NC), which is thought to be a result of transient ischemia during exercise. In this study we evaluated the changes in F wave studies before and immediately after walking stress in patients with NC. Design:Twenty-six patients with LSS who had signs and symptoms of NC and 20 healthy volunteers were included in this study. Routine motor and sensory nerve conduction studies and tibial F wave studies were performed in both groups. Immediately after walking stress test, tibial F wave studies were repeated. Exercise treadmill protocol was used for ambulation. Time to first symptoms and total ambulation time were recorded. Results:After completion of the baseline electrophysiological examination, a walking stress test was performed using a treadmill, and 16 patients (61.5%) experienced neurogenic claudication during the trial. The mean time to first symptoms was 2.0 ± 3.5 mins (minimum = 0, maximum = 14). In the control group 18 subjects (90%) completed the trial without any symptoms, and 2 (10%) subjects had to stop at an average of 10 mins because of generalized fatigue. Within 5 mins after the walking stress test, tibial F wave studies were repeated in both groups. There were significant increases in F latency values bilaterally in the patient group (P = 0.001 for both sides) but not in control subjects (P = 0.435 for right side and P = 0.122 for left side). Conclusion:Our data suggest that F wave studies after walking stress test provide more information for the diagnosis of NC.