Murteza Cakir

The feasibility of dual-energy CT in differentiation of vertebral compression fractures

OBJECTIVE To prospectively evaluate the ability of dual-energy CT (DECT), compared with MRI, to identify vertebral compression fractures in acute trauma patients. METHODS This institutional review board-approved study included 23 consecutive patients with 32 vertebral fractures who underwent both DECT and MRI of the spine between February 2014 and September 2014. A total of 209 vertebrae were evaluated for the presence of abnormal bone marrow attenuation on DECT and signal on MRI by five experienced radiologists. The specificity, sensitivity, predictive values and intraobserver and interobserver agreements were calculated. RESULTS MRI revealed a total of 47 vertebrae (22.4% of all vertebrae) and DECT revealed 44 vertebrae (21.0% of all vertebrae) with oedema. Using MRI as the reference standard, DECT had sensitivity, specificity, positive-predictive value, negative-predictive value and accuracy of 89.3, 98.7, 95.4, 96.9 and 96.6%, respectively. With respect to establishing the presence of oedema, the interobserver agreement was almost perfect (k = 0.82), and the intraobserver agreement was substantial (k = 0.80). CONCLUSION Compared with MRI, DECT can provide an accurate demonstration of acute vertebral fractures and can be used as an alternative imaging modality for the assessment of vertebral fractures in patients with contraindications for MRI. ADVANCES IN KNOWLEDGE Distinguishing of acute and chronic vertebral compression fracture is important for treatment choices. DECT is very fast compared with MRI and is an alternative imaging modality for the assessment of vertebral fractures in patients with contraindications for MRI.

The role of ischemic neurodegeneration of the nodose ganglia on cardiac arrest after subarachnoid hemorrhage: an experimental study.

BACKGROUND The heart is innervated by several systems that contribute to the control of the hearts rhythm. The cardiac fibers of the vagus nerve have an important role in the regulation of heart rhythm under many emotional and physical conditions. Severe electrocardiographic disturbances have been reported following subarachnoid hemorrhage (SAH), but ischemic neuronal degeneration of the nodose ganglion of the vagus nerve has not been previously investigated. We examined if there is a relationship between ischemic injury of the nodose ganglion of the vagus nerve and the severity of heart rhythm disorders after subarachnoid hemorrhage. METHODS This study was conducted on 20 rabbits. Four rabbits were used as a baseline group. Experimental subarachnoid hemorrhage was applied to half of the remaining animals (n = 8) by injecting homologous blood into the cisterna magna, and the others (SHAM group, n = 8) were injected with isotonic saline solution in the same manner. For 20 days after the injection, heart rhythm changes were observed daily. After the experiment, normal and ischemic neuron densities in the nodose ganglia of the vagus nerves were examined stereologically. The number of heart rhythm irregularities and the number of degenerated neurons in the nodose ganglia were compared statistically. RESULTS The normal heart rhythm rate was 280 ± 45/min. At the beginning of the SAH, the average heart rate was 220 ± 30/min; about 10 hours later, it decreased to 189 ± 30/min, indicating severe bradycardia. However, after 7 days, the average heart rate had increased to 350 ± 30/min. Six animals died due to irregularities in cardiac function and respiration. Histopathological examinations showed that the average density of normal neurons in the nodose ganglion was 10,500 ± 2500 in the baseline animals and the SHAM group, but the normal neuron density was 8250 ± 1500 in survivors and 6450 ± 1330 in dead animals. The ischemic neuronal degeneration in the nodose ganglia was more severe in the dead animals than in the survivors (p < 0.0001). CONCLUSION Afferent vagus nerves originating from the nodose ganglia have an important role in regulating heart rhythm via their afferent fibers and efferent connections. If neurons of the nodose ganglia are lesioned due to ischemic insult during subarachnoid hemorrhage, heart rhythm regulation by vagus afferent reflexes is disturbed. Vagus pathway paralysis may result in indirect sympathetic overactivity. The development of tachycardia causes depletion of the hearts reserves, and cardiac arrest may be inevitable following extensive subarachnoid hemorrhage.

Neuroprotective effect of ACE inhibitors in glutamate - induced neurotoxicity: rat neuron culture study.

AIM Glutamate is known to be neurotoxic at concentrations of 10-6M and 10-7M. Angiotensin converting enzyme (ACE) inhibitors can be assumed to be neuroprotective as they open the mitochondrial adenosine triphosphate-sensitive potassium channels by inhibiting the degradation of bradykinin. In this study, we investigated whether the ACE inhibitors captopril, ramipril and perindopril have protective effects in glutamate-induced neurotoxicity in newborn rat cerebral cortex cell cultures. MATERIAL AND METHODS Viability tests were performed among ACE inhibitors by constituting groups of control and 10-7M and 10-6M glutamate doses in newborn rat cortex cultures. RESULTS While the mean viable cell number was 0.47±0.06 in the control group, it was 0.37±0.03 in the group exposed to 10-7M glutamate (p < 0.05) and 0.37±0.01 in the group exposed to 10-6M glutamate (p < 0.05). Captopril was used at a dose of 10 μM, perindopril was used at a dose of 1 μM, and ramipril was used at a dose of 30 μM against 10-7M and 10-6M glutamate. Ramipril and perindopril reversed the toxicity against 10-6M glutamate (p < 0.05). The neuroprotective properties of captopril, perindopril and ramipril were not found to be statistically significant against 10-7M glutamate at the doses mentioned above. CONCLUSION Data obtained from this study indicate that ramipril and perindopril can prevent 10-6M glutamate-induced neurotoxicity.

Investigation of the effect of telmisartan on experimentally induced peripheral nerve injury in rats

Aim: The aim of this study was to investigate the effects of telmisartan on nerve healing in a rat peripheral nerve injury model. Material and method: Thirty adult male Wistar albino rats were divided into five groups: healthy, axonotmesis, anastomosis, axonotmesis+10 mg/kg telmisartan and anastomosis+10 mg/kg telmisartan. Walking track analyses were performed 4 weeks after the surgery. The right sciatic nerves of all the animals were examined histopathologically, stereologically and molecularly. Results: Many badly damaged axons were detected in the axonotmesis group, in addition to enlarged spaces between the axons. In the anastomosis group, both ir-regular and degenerated axons at different severities were observed. The sections of the telmisartan group after the axonotmesis were similar to those of the healthy group. The sections of the telmisartan group after the anastomosis were similar to those of the healthy group and the telmisartan group after the axonotmesis. Interleukin-1 beta (IL-1β) gene expression increased in both the axonotmesis and the anastomosis groups when compared with the healthy group. Telmisartan had a significant down-regulatory effect on IL-1β expression. Caspase-3 mRNA expression was significantly increased in the anastomosis group, and the administration of telmisartan in this group significantly decreased this rise in caspase-3 mRNA expression. As a functional outcome, telmisartan also increased the walking distance of the rats after axonotmesis and anastomosis. Conclusion: The histopathological, stereological, functional and molecular data suggest that telmisartan improves nerve regeneration in peripheral nerve injuries by inhibiting inflammatory cytokine IL-1β and apoptotic caspase-3.

Effect of Pregabalin in Preventing Secondary Damage in Traumatic Brain Injury: An Experimental Study

Background In this study we aimed to explore the effects of pregabalin on a traumatic brain injury model in rats. Material/Methods This study included 40 adult male Sprague-Dawley rats randomized into 4 groups, each of which contained equal numbers of animals. The control group had no head trauma and thus was not treated. The trauma group had head trauma but was not treated. The pregabalin group had no head trauma but was treated by pregabalin. The trauma + pregabalin group had head trauma treated with pregabalin. The biopsy samples taken from the study animals were histopathologically examined for the presence of edema, inflammation, and neuronal damage. Results All animals in the trauma group had edema, inflammation, and neuronal damage. Four subjects in the control group, 6 in the pregabalin group, and 4 in the trauma + pregabalin group had edema; inflammation was present in 1 subject in the control group, 3 subjects in the pregabalin group, and 3 subjects in the trauma + pregabalin group; neuronal damage existed in 1 subject in the control group, 1 subject in the pregabalin group, and 6 subjects in the trauma + pregabalin group. The trauma group had significantly higher edema and neuronal damage scores than the other groups. Similarly, inflammation was significantly more prevalent in the trauma group than the control and trauma + pregabalin groups. Conclusions The results of the present study indicated anti-edema, anti-inflammatory, and neuroprotective effects of pregabalin in an experimental head trauma model in rats. Pregabalin may thus be beneficial in humans with acute TBI by relieving concomitant edema and inflammation.

Neuroendoscopic approach to quadrigeminal cistern arachnoid cysts.

OBJECTIVE The introduction of neuroendoscopy has provided a minimally invasive modality for the surgical treatment of quadrigeminal arachnoid cysts. Three pediatric patients with arachnoid cyst of the quadrigeminal cistern treated by endoscopic fenestration are reported. MATERIALS AND METHODS The hospital records of patients were retrospectively rewieved. All patients had hydrocephalus. A lateral ventricle-cystostomy and endoscopic third ventriculostomy were performed by using rigid neuroendoscopes. RESULTS There were one boy and two girls with ages 7 months, 9 months and 14 years, respectively. One patient had undergone shunting prior to neuroendoscopic surgery. The postoperative course was uneventful in all cases, with no complications. They showed disappearance of intracranial hypertension symptoms and significant reduction of the cyst size. CONCLUSION Neuroendoscopic technique is an effective and suitable method for the treatment of quadrigeminal cistern arachnoid cysts and accompanying hydrocephalus.

Serum nesfatin-1 levels: a potential new biomarker in patients with subarachnoid hemorrhage*

Background: Acute subarachnoid hemorrhage (SAH) is a neurological emergency with significant potential for long-term morbidity and mortality. Nesfatin-1 is a polypeptide which is found in various regions of the brain that play role in the feeding and metabolic regulation. Objective: So this study aimed to investigate if nesfatin-1 levels in patients with SAH, could be used as a marker for the severity and prognosis. Method: Forty-eight consecutive patients (except those excluded) admitted to the emergency service of our hospital and hospitalized at our clinic with the diagnosis of aneurysmal SAH between 2011 and 2013 were included in the study and followed up for six months for outcome. The control group consisted of 48 healthy individuals of similar age and gender. Results: During the 6-month follow-up, 7 of 48 patients died and 16 (33.3%) patients had poor Glasgow Outcome Score (GOS) scores. In the study group, the mean nesfatin-1 level was significantly higher than the control group (7.36 ± 2.5 pg/ml and 4.29 ± 2.02 pg/ml, respectively; p < 0.01). The mean nesfatin-1 level was 11.58 ± 0.87 pg/ml in the non-survival group and 6.64 ± 1.89 pg/ml in the survival group. Furthermore, it was 10.22 ± 1.42 pg/ml in patients with poor outcome in terms of GOS and 5.93 ± 1.46 pg/ml in those with good outcome. The nesfatin-1 levels significantly increased with worsening of GOS, the World Federation of Neurological Surgeons grading system, and Fisher scores and increasing plasma C-reactive protein levels (p < 0.01 for all). Conclusion: The present study is the first that shows the mortality/poor outcome of the SAH with assessing serum nesfatin-1 levels. So levels of nesfatin-1 might be useful in SAH management.

Preventive Role of Hilar Parasympathetic Ganglia on Pulmonary Artery Vasospasm in Subarachnoid Hemorrhage: An Experimental Study.

AIM Pulmonary arteries are mainly innervated by sympathetic vasoconstrictor and parasympathetic vasodilatory fibers. We examined whether there is a relationship between the neuron densities of hilar parasympathetic ganglia and pulmonary vasospasm in subarachnoid hemorrhage (SAH). MATERIAL AND METHODS Twenty-four rabbits were divided into two groups: control (n=8) and SAH (n=16). The animals were observed for 20 days following experimental SAH. The number of hilar parasympathetic ganglia and their neuron densities were determined. Proportion of pulmonary artery ring surface to lumen surface values was accepted as vasospasm index (VSI). Neuron densities of the hilar ganglia and VSI values were compared statistically. RESULTS Animals in the SAH group experienced either mild (n=6) or severe (n=10) pulmonary artery vasospasm. In the control group, the mean VSI of pulmonary arteries was 0.777±0.048 and the hilar ganglion neuron density was estimated as 12.100±2.010/mm < sup > 3 < /sup > . In SAH animals with mild vasospasm, VSI=1.148±0.090 and neuron density was estimated as 10.110±1.430/mm < sup > 3 < /sup > ; in animals with severe vasospasm, VSI=1.500±0.120 and neuron density was estimated as 7.340±990/mm < sup > 3 < /sup > . CONCLUSION There was an inverse correlation between quantity and neuron density of hilar ganglia and vasospasm index value. The low numbers and low density of hilar parasympathetic ganglia may be responsible for the more severe artery vasospasm in SAH.

Primary extraosseous Ewing sarcoma of the lumbar spine presenting with left leg weakness

A 7-year-old boy presented to the neurosurgery clinic with left leg weakness. Enhanced multidetector computed tomography and magnetic resonance imaging were performed. Multidetector computed tomography images revealed a mass with minimal contrast enhancement that extended into the left L3–L4 foramen and psoas muscle (Fig. 1). Magnetic resonance images revealed a mass that was isointense on T1-weighted images and hyperintense on T2-weighted images comparedwithmuscle (Figs. 2 and 3), with homogenous enhancement after contrast administration (Figs. 2 and 3), consistent with nerve sheath tumors. Pathologic specimens obtained at surgery showed Ewing sarcoma that has imaging features similar to nerve sheath tumors. Extraskeletal Ewing sarcoma is rare but has been reported [1,2].

Neuroprotective effects of agmatine in experimental peripheral nerve injury in rats: a prospective randomized and placebo-controlled trial.

AIM The purpose of this study was to demonstrate the activity of agmatine, an inducible nitric oxide synthase (iNOS) inhibitor and selective N-methyl-D-aspartate receptor (NMDAR) antagonist, on reducing tissue damage in distal part of traumatic nerve in an experimental rat peripheral nerve injury model. MATERIAL AND METHODS Sciatic nerves of 30 Sprague Dawley male rats were used. Rats were divided into 5 groups; group 1 (n=6), control group; group 2 (n=6), axonotmesis + placebo group; group 3 (n=6), axonotmesis + 50 mg/kg agmatine treatment group; group 4 (n=6), neurotmesis + placebo group; group 5 (n=6), neurotmesis + 50 mg/kg agmatine treatment group. Axonolysis, axon degeneration, edema, hemorrhage, and inflammation were evaluated in histopathologic examinations of all the groups. RESULTS When group 2 was compared with group 3 in histopathologic sections, axonolysis was less in group 3 (p=0.007), as was axon degeneration (p=0.022) and edema (p=0.018). When group 4 was compared with group 5, axonolysis was less in group 5 (p=0.009), as was axon degeneration (p=0.006) and edema (p=0.021). CONCLUSION This study demonstrated agmatine to have antioxidant and antineurotoxic effects in an experimental rat peripheral nerve injury model.