Hemostasis vs. epidural fibrosis?: A comparative study on an experimental rat model of laminectomy.

AIM: The aim of this study was to evaluate the histopathological and biochemical impact and effectiveness of two hemostatic agents, Ankaferd blood stopper (ABS) and Microporous Polysaccharide Hemospheres (MPH), on epidural fibrosis in an experimental rat laminectomy model. MATERIAL AND METHODS: Twenty adult Wistar albino rats were divided into MPH-treated (n=6), ABS-treated (n=6) and control (n=8) groups. Laminectomy of the lumbar spine was performed in all animals and treatment groups were exposed to MPH and ABS while closure was applied in control group as per usual. Epidural fibrosis was evaluated in all groups macroscopically, histopathologically, biochemically and with electron microscopy four weeks later. RESULTS: Statistically, it was found that MPH-treated group had significantly less epidural fibrosis compared to ABS-treated and control groups. CONCLUSION: We compared two hemostatic agents for their propensity to cause adhesions in the present study. Our results show that MPH significantly reduces epidural scar formation and dural adhesion in a rat model of laminectomy while ABS increases postoperative fibrosis.

[Bilateral epidural hematoma in a patient with human immunodeficiency virus infection: a case report]. / Human immunodeficiency virus ile enfekte bir hastada gelisen iki tarafli epidural hematom: Olgu sunumu.

Intracranial epidural haematomas are almost always secondary to head traumas and usually occur unilaterally. Bilateral intracranial epidural haematomas are rare, but the mortality is very high. In our case, we report a bilateral epidural haematoma in a 32 year old, HIV infected male patient who came to the emergency service with a head trauma because of a motor vehicle-pedestrian accident. The occurrence of bilateral epidural haematoma in an HIV infected patient is a rare condition as a result of head trauma in a lateral direction on one side. As a result of the vasculopathy and coagulopathy, which are complications of HIV infection, the cerebral vessels have a fragile structure that leads to complications that facilitate the development of contralateral intracranial epidural haematoma together.

AR-A014418 as a glycogen synthase kinase-3 inhibitor: anti-apoptotic and therapeutic potential in experimental spinal cord injury.

OBJECTIVES: We aimed to investigate the effects of AR-A014418, a strong inhibitor specific to GSK-3beta, on neuronal apoptosis and neuroprotection in the traumatic SCI model. MATERIALS AND METHODS: In this study, three groups were generated from 36 Wistar rats; (1) control, (2) spinal cord trauma group created by clip compression technique after laminectomy, and (3) AR-A014418 (4mg/kg, i.p., DMSO) treatment group after laminectomy and spinal cord trauma. The TUNEL assay for apoptosis detection, immunohistochemical staining for bax and TGF-beta were applied in spinal cord tissues. For light microscopic examination, necrotic, and apoptotic cells were counted, and PMNL counting was applied to detect inflammation. Functional recovery was tested by field locomotor test in the 3rd and 7th days following surgery. RESULTS: In the trauma group, diffuse hemorrhage, cavitation, necrosis and edematous regions, degeneration in motor neurons and leukocyte infiltration were observed in gray matter. In the AR-A014418-treated groups, healthy cells were observed in more places compared to the trauma groups, however, cavitation, hemorrhagic, and edematous areas were seen in gray matter. In the AR-A014418-treatment groups, the number of apoptotic cells in the 3rd and 7th days (respectively; p<0.05, p<0.01), were significantly decreased compared to the trauma groups, as were the levels of bax (p<0.01) and TGF-beta 1 immunoreactivity. Results of the locomotor test were significantly increased in the treatment group (p<0.001) as compared to the trauma group. CONCLUSIONS: In this experimental spinal cord trauma model study neural apoptosis was significantly triggered in secondary damage developed after trauma, however, neurological healing was expedited by preventing mitochondrial apoptosis and reducing the inflammation by the potent inhibitor AR-A014418, which is GSK-3beta selective.

Correlation between leptin and pro-inflammatory cytokines in cortical contusion injury model.

BACKGROUND: The present study aimed to investigate time-dependent changes in leptin concentrations in brain tissue following experimental traumatic brain injury and to examine the relationship with cytokines. METHODS: After circular craniectomy, 33 male Wistar-albino rats were positioned on a stereotaxic frame and subjected to cortical contusion injury and then divided into 3 groups based on the depth of deformation as: 0 mm (sham controls, n=3), 1.5 mm (moderate injury, n=15) and 2.7 mm (severe injury, n=15). Animals were sacrificed on the 1st, 3rd and 5th days post-injury. RESULTS: One day after moderate injury, interleukin-1 beta (IL-1ß), IL-6, tumor necrosis factor-alpha (TNF-?), and leptin levels were found to be markedly increased in the brain tissue. On the 3rd and 5th days, the levels returned to the shamcontrol levels. Following severe injury, IL-1ß, IL-6 and TNF-? levels increased in correlation after the 1st day and reached the sham-control levels on the same days. However, leptin tissue levels decreased on the 1st and 3rd days and normalized to the sham-control levels on the 5th day. CONCLUSION: Our results showed that the release of leptin is decreased in the early stage of severe injury. Thus, leptin replacement may play an important role in therapy in cases with severe traumatic brain injury.

A rare emergency condition in neurosurgery: foot drop due to Paget's disease.

Paget's disease is a chronic, focal skeletal disorder that usually affects the pelvis and spine. Spinal cases are generally asymptomatic; in the symptomatic cases, the neurological dysfunctions are related to non-compressive vascular defects, hemorrhage, sarcomatoid degeneration, spinal stenosis, or pathological fractures, primarily in the lumbar region. The Neurosurgeon should have a fundamental understanding of the complications of Paget's disease and should be familiar with the indications for treatment, as well as available medical and surgical therapies. In the present paper, we report a case of Paget's disease that presented with an isolated foot drop due to a pathological fracture of L5 vertebra, and then discuss the therapeutic strategies presented in the literature.

Neuroprotective effects of Ac.YVAD.cmk on experimental spinal cord injury in rats.

BACKGROUND: Apoptosis as a cell death mechanism is important in numerous diseases, including traumatic SCI. We evaluated the neuroprotective effects of Ac.YVAD.cmk and functional outcomes in a rat SCI model. METHODS: Thirty rats were randomized into 3 groups of 10: sham-operated, trauma only, and trauma plus Ac.YVAD.cmk treatment. Trauma was produced in the thoracic region by a weight-drop technique. Group 3 rats received Ac.YVAD.cmk (1 mg/kg, ip) 1 minute after trauma. The rats were killed at 24 hours and 5 days after injury. Efficacy was evaluated with light microscopy and TUNEL staining. Functional outcomes were assessed with the inclined plane technique and a modified version of the Tarlov grading system. RESULTS: At 24 hours postinjury, the respective mean number of apoptotic cells in groups 1, 2, and 3 were 0, 5.26 +/- 0.19, and 0.97 +/- 0.15. Microscopic examination of group 2 tissues showed widespread hemorrhage, edema, necrosis, and polymorphic nuclear leukocyte infiltration and vascular thrombi. Group 3 tissues revealed similar features, but cavitation and demyelination were less prominent than those in group 2 samples at this period. At 5 days postinjury, the respective mean inclined plane angles in groups 1, 2, and 3 were 65.5 +/- 2.09, 42.00 +/- 2.74, and 52.5 +/- 1.77. Motor grading of animals revealed a similar trend. These differences were statistically significant (P < .05). CONCLUSIONS: Ac.YVAD.cmk inhibited posttraumatic apoptosis in a rat SCI model. This may provide the basis for development of new therapeutic strategies for the treatment of SCI.

The effects of resveratrol on vasospasm after experimental subarachnoidal hemorrhage in rats.

BACKGROUND: Cerebral vasospasm remains a major cause of morbidity and mortality in patients with SAH. Although many pharmacologic agents and chemicals have been used to prevent and treat CV, the pathogenesis of that condition has not been established. We investigated the efficacy of resveratrol, a stilbene polyphenol and tyrosine kinase inhibitor that occurs naturally in grapes and red wine, in a murine basilar artery vasospasm model. METHODS: Forty-two Wistar albino rats were used in this study. The rats were divided into 3 groups of 14 animals each: the sham-operated control group (group 1), the vasospasm group (group 2), and the treatment group (group 3). In groups 2 and 3, autologous blood (0.3 mL) was injected into the cisterna magna. After that injection, the rats in group 3 received an intravenous injection of resveratrol (10 mg/kg) for 72 hours. The evaluation of the response to both the injection of autologous blood and treatment was based on biochemical markers in tissue and serum and on light microscopic findings from the basilar artery, which were collected at different intervals after experimental SAH. RESULTS: Endothelin-1 levels in brain tissue and serum were higher in the vasospasm group than in the control group (P < .05). In group 3 rats, the administration of resveratrol resulted in significantly lower ET-1 values than those in group 2. Brain and serum lipid peroxidation levels were markedly elevated in group 2 rats but decreased significantly after resveratrol treatment in group 3 rats (P < .05). Superoxide dismutase expression in brain tissue and serum was lower in group 2 rats than in sham-operated controls, and a significant increase in the SOD level was associated with resveratrol treatment. On examination via light microscopy 72 hours after SAH, the mean perimeters of the arterial lumen in groups 1, 2, and 3 were 719 +/- 16, 411.6 +/- 9, and 590.1 +/- 5.6 microm, respectively. The mean thickness of the arterial wall was as follows: in group 1, 11.1 +/- 0.8 microm; in group 2, 16.1 +/- 1.2 microm; and (after resveratrol treatment) in group 3, 13.4 +/- 0.6 microm. CONCLUSIONS: The results of our study showed that resveratrol induced the relaxation of smooth muscle in the wall of the basilar artery and may be provided with neuroprotection against cerebral ischemia in a rat model. These effects may be associated with the antioxidant and vasodilatory effects of resveratrol, which could prove to be an agent prophylactic against CV and to be therapeutic for individuals who experience that event.

The neuroprotective effects of z-DEVD.fmk, a caspase-3 inhibitor, on traumatic spinal cord injury in rats.

BACKGROUND: Apoptosis is one of the most important forms of cell death seen in a variety of physiological and pathological conditions, including traumatic injuries. This type of cell death occurs via mediators known as caspases. Previous studies have investigated the roles that apoptosis and different caspases play in the pathogenesis of secondary damage after spinal cord injury (SCI). The aim of this research was to assess the neuroprotective effect of z-DEVD.fmk, a caspase-3 inhibitor, in a rat model of SCI. METHODS: Forty-five Wistar albino rats were studied in 3 groups of 15 animals: sham-operated control animals (group 1); trauma-only control animals (group 2); and rats subjected to trauma + z-DEVD.fmk treatment (group 3). Spinal cord injury was produced at the thoracic level using the weight-drop technique. Responses to injury and the efficacy of z-DEVD.fmk were assessed by light microscopy and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling staining in cord tissues collected at 4 and 24 hours posttrauma. Five rats from each group were used to assess functional recovery at 7 days after SCI. The functional evaluations were done using the inclined-plane technique and a modified Tarlov motor grading scale. RESULTS: At 4 hours postinjury, the mean apoptotic index in groups 1, 2, and 3 was 0, 33.01+/-6.62, and 16.40+/-4.91, respectively. The group 3 count was significantly lower than the group 2 count (P<.01). At 24 hours postinjury, light microscopic examination of group 2 tissues showed widespread hemorrhage, necrosis, polymorphonuclear leukocyte infiltration, and vascular thrombi. The group 3 tissues showed similar features. The prominent findings in group 2 were hemorrhage and necrosis, whereas the prominent findings in group 3 were focal hemorrhage and leukocyte infiltration. The mean inclined-plane angles in groups 1, 2, and 3 were 64.5 degrees+/-1.0 degrees, 41.5 degrees+/-1.3 degrees, and 47 degrees+/-2.0 degrees, respectively. Motor scale results in all groups showed a similar trend. CONCLUSION: Local application of z-DEVD.fmk after SCI in rats reduces secondary tissue injury and helps preserve motor function. These effects can be explained by inhibition of apoptotic death in all cell types in the spinal cord.