The Arabic version of the Stroop Test and its equivalency to the English version

The Stroop test is one of the most popular tests frequently used to assess the function of the frontal lobe in neurological and psychiatric patient populations. Performance on the Stroop test is very sensitive to lesions of the frontal lobes and is commonly used in clinical settings. In 1999, we decided to find out if the Stroop test will be as reliable after translation to the Arabic language as the original English version. We completed the work in Riyadh Military Hospital in 2000. A sample of 10 Saudi adult healthy individuals participated in this study. Their mean age was 31.9 and their mean years of education were 17.3. All subjects performed the Arabic and the English versions of Stroop test. Performance showed no differences between the English and the Arabic versions of the Stroop test. Equivalency data between the two versions of Stroop test are provided. The availability of this data will help us to provide a normative data for the Saudi Committee of Health Education, and in carrying out research on frontal lobe function

Normative data for the two equivalent forms of the Arabic verbal fluency test

Performance on verbal fluency (VF) test is sensitive to lesions on the frontal lobes. We earlier developed two equivalent forms of formal VF in the Arabic language for use with healthy Saudi individuals

Protection by 2-Deoxy-D-glucose against b,b8-Iminodipropionitrile-Induced Neurobehavioral Toxicity in Mice

This investigation was undertaken to study the effect of 2-deoxy-D-glucose (2-DG) on b,b8-iminodipropionitrile (IDPN)-induced neurobehavioral toxicity in mice. Animals were divided into five groups of nine animals each. One of the groups served as control and received vehicle only, whereas the remaining four groups were treated with IDPN (250 mg/kg, ip) daily for 11 days. 2-DG was injected intraperitoneally in the doses of 0 (vehicle only), 100, 300, and 600 mg/kg daily 30 min before IDPN administration. The animals were observed for dyskinetic behavior including vertical (retrocollis) and horizontal (laterocollis) head movements and circling. Twenty-four hours after the last dose of IDPN, the animals were sacrificed by decapitation and striata were isolated from the brain for the analysis of serotonin (5-HT). Our results showed that 2-DG significantly and dose dependently attenuated the incidence and severity of IDPN-induced neurobehavioral toxicity. Administration of 2-DG also protected mice against IDPN-induced increase in striatal 5-HT levels. Further studies are warranted to investigate the neuroprotective mechanism of 2-DG against IDPN-induced neurotoxicityAcademic Pres

Establishment of the military neurosurgeons committee within the world federation of neurosurgical societies

In 2009, during the World Congress of Neurological Surgery in Boston, Massachusetts, the World Federation of Neurosurgical Societies (WFNS) Executive Committee decided to establish a Military Neurosurgeons Committee. A separate scientific session on military neurosurgery was held at the next WFNS Interim Meeting in September 2011 in Brazil. A further separate session on military neurosurgery will take place at the next WFNS Meeting in Seoul, South Korea. © 2013 Elsevier Inc. All rights reserved.SCOPUS: re.jinfo:eu-repo/semantics/publishe

Proglumide, a Cholecystokinin Receptor Antagonist, Exacerbates b , b9 -Iminodipropionitrile-Induced Dyskinetic Syndrome in Rats

Proglumide, a cholecystokinin receptor antagonist, exacerbates b, b9 -iminodipropionitrile-induced dyskinetic syndrome in rats.NEUROTOXICOL TERATOL 20 (5) 571–579, 1998.—The present investigation was undertaken to study the effect of proglumide, a cholecystokinin (CCK) receptor antagonist, on iminodipropionitrile (IDPN)-induced excitation, chorea, and circling (ECC) syndrome in rats.The animals were exposed to IDPN in the dose of 100 mg/kg/day IP for 9 days. Proglumide (PG) was administered IP daily 1 h before IDPN in the doses of 250, 500, and 750 mg/kg body weight in three different groups of rats. The animals were observed daily for neurobehavioral abnormalities including dyskinetic head movements, circling, tail hanging, air righting reflex, locomotor activity, and contact inhibition of the righting reflex. After behavioral studies, blood and brain samples were collected for the analysis of malondialdehyde (MDA), conjugated dienes, vitamin E, and glutathione peroxidase (GSH-Px). The temporal bones were also collected for inner ear histopathology. Our results showed that proglumide significantly and dose-dependently exacerbated the incidence and the severity of IDPN-induced ECC syndrome during the treatment period as well as up to 3 weeks of postdosing. Administration of IDPN produced a significant increase in MDA and conjugated dienes and a decrease in vitamin E and GSH-Px, suggesting the role of oxygen-derived free radicals (ODFR) in IDPN-induced neurotoxicity. Concomitant treatment with proglumide potentiated IDPN-induced oxidative stress. The histopathology of the inner ear showed significantly high degeneration of sensory hair cells in the crista ampullaris of the rats treated with IDPN plus proglumide compared to IDPN-alone-treated animals. Further studies are warranted to determine the role of CCK in nitrile toxicity and drug-induced dyskinesia.Neuroscience Research Group, Armed Forces Hospital, Riyadh, Saudi ArabiaCorresponding Author: Dr. Mohammad Tariq Armed Forces Hospital, W-912 P.O. Box 7897, Riyadh 11159, Saudi Arabia Fax:1966-1-462-7556. Email

Protective effect of hydrocortisone on iminodipropionitrile-induced neurotoxicity in rats

Occupational and environmental exposure of synthetic nitriles is of potential relevance to human health. Iminodipropionitrile (IDPN), a prototype nitrile toxin, has been shown to produce dyskinetic syndrome in rodents. This study reports the effect of concomitant exposure of rats to hydrocortisone and IDPN on behavioural abnormalities namely excitation, circling and chorea (ECC) syndrome. Four groups of female Wistar rats were given hydrocortisone (0, 10, 30 and 60 mg/kg, gavage, for 10 days) 30 min. before IDPN (100 mg/kg, intraperitoneally for 8 days). Two additional groups of rats were treated with either saline (control group) or 60 mg/kg of hydrocortisone (drug alone group). The animals were observed for neurobehavioural abnormalities including dyskinetic head movement, circling, tail hanging, air righting reflex and contact inhibition of righting reflex. After behavioural studies, the animals were killed, and the discrete brain regions and temporal bones were collected for biochemistry and inner ear histopathology, respectively. Hydrocortisone significantly and dose dependently attenuated the incidence and severity of IDPN-induced behavioural syndrome. Administration of hydrocortisone (60 mg/kg) alone significantly increased glutathione (GSH) levels in olfactory bulb and striatum, whereas IDPN alone significantly reduced GSH levels in olfactory bulb, striatum and hippocampus. Hydrocortisone (60 mg/kg) significantly compensated IDPN-induced depletions of GSH in different brain regions. Hydrocortisone also protected the animals against IDPN-induced vestibular hair cell degeneration. The protective effect of hydrocortisone may be attributed to its anti-inflammatory and antioxidant properties.Corresponding Author: Mohammad Tariq, Research Center, Armed Forces Hospital, PO Box 7897 (W-912), Riyadh 11159, Saudi Arabia. Email: [email protected]

Neurological recovery in diabetic rats following spinal cord injury

This study was designed to assess the effect of spinal cord injury on neurobehavioral, electrophysiological, structural, and biochemical changes in normal and diabetic rats. Experimental diabetes was induced in Sprague–Dawley male rats (weighing 250–280 g) with streptozotocin (50 mg/kg IP). Eight weeks after the treatment with streptozotocin the animals were anaesthetized with chloral hydrate and laminectomy was performed at T 7–8 level leaving the dura intact. A compression plate (2.2 × 5.0 mm) loaded with a weight of 35 g was placed on the exposed spinal cord for 5 min. Post-operative neurological function was assessed using inclined plane test, modified Tarlov score, and vocal and sensory score daily for 10 days. Electrophysiological changes were assessed using somatosensory and corticomotor evoked-potentials. The animals were sacrificed at different time intervals and injured site of the spinal cord was analyzed for changes in vitamin E and glutathione levels (as markers of oxidative stress). Pathological changes in spinal cord were also studied using light microscopy. The data on neurobehavioral study clearly indicated that the compression of spinal cord produced highly significant neurological deficit and poor recovery in diabetic rats as compared to nondiabetic rats. Our histopathological and electrophysiological results also confirmed that diabetic animals are more susceptible to compressive spinal cord injury as compared to nondiabetic animals. A higher depletion of antioxidant defense markers (vitamin E and glutathione) was observed in diabetic rats as compared to nondiabetic rats. These results point toward the role of free radicals in poor recovery in diabetic rats following neurotrauma. Further studies are warranted to assess the neuroprotective potential of antioxidants to retard the secondary pathophysiological events following neurotrauma and to enhance the recovery

On the initiation of world neurosurgery

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