New additions to the scorpion fauna of Riyadh region, Saudi Arabia

In this work, we present additional morphological data about the scorpion fauna of Saudi Arabia. This investigation was carried out in the central region (Riyadh) of the country and identified existing and newly discovered scorpion species for taxonomic documentation while determining the medically important ones. The survey covered the entire Riyadh region, including all major districts, and collected a total of 4,164 specimens. Morphological identification of collected animals was based on identification keys. There were two species (one with a subspecies) that belonged to the family Scorpionidae, namely Scorpio maurus kruglovi (0.02 percent) and Hemiscorpius arabicus (0.05 percent). The latter, currently, is part of the Hemiscorpiidae family that had been upgraded from a subfamily. Eight more species from the Buthidae family were found: Leiurus quinquestriatus (7.20 percent), Androctonus crassicauda (17.24 percent), Androctonus bicolor (64.60 percent), Compsobuthus arabicus (3.84 percent), Compsobuthus werneri (0.94 percent), Buthacusyotvatensis nigroaculeatus (2.31 percent), Buthacusleptochelys (3.24 percent) and Orthochirus innesi (0.55 percent). The major locations of collection were the outskirts of Riyadh city and the airport vicinity. The specimens were transported from all central region areas in 124 short trips.(AU)

Vagus nerve stimulation: indications and limitations.

Vagus nerve stimulation (VNS) is an established treatment for selected patients with medically refractory seizures. Recent studies suggest that VNS could be potentially useful in the treatment of resistant depressive disorder. Although a surgical procedure is required in order to implant the VNS device, the possibility of a long-term benefit largely free of severe side effects could give VNS a privileged place in the management of resistant depression. In addition, VNS appears to affect pain perception in depressed adults; a possible role of VNS in the treatment of severe refractory headache, intractable chronic migraine and cluster headache has also been suggested. VNS is currently investigated in clinical studies, as a potential treatment for essential tremor, cognitive deficits in Alzheimer's disease, anxiety disorders, and bulimia. Finally, other studies explore the potential use of VNS in the treatment of resistant obesity, addictions, sleep disorders, narcolepsy, coma and memory and learning deficits.

Cerebral palsy: incidence and clinical features in Saudi Arabia.

The purpose of this work is to analyse the cerebral palsy (CP) incidence, aetiology, birthweight, types and/or subdiagnosis and associated impairments, individually or in combination, in children at Riyadh Military Hospital (RMH). The study covered the birth year period 1984 - 2003, during which 99,788 live births were recorded at Riyadh Military Hospital (RMH). Incidence ratio and clinical features of 412 positive cases of cerebral palsied children between 1 - 10 years old were investigated. Medical information was collected from patient files at the medical records department. The incidence of CP was 0.41%. The five intervals of the study period gave a pattern of decreasing percentage incidence. The case distribution according to birth weight, aetiology, duration and subdiagnoses was studied. It could be concluded that livebirth incidence of cerebral palsied patients in Saudi Arabia was relatively high as compared to most other studies. Severe disability due to cerebral palsy was associated with impairments such as mental retardation, epilepsy and visual impairments, often found in combinations.

Operation for delayed symptomatic brain oedema after treatment of an arteriovenous malformation by embolization and radiosurgery.

A patient with a Spetzler-Martin-grade-III AVM, initially embolized and then stereotactically irradiated, who - with a latency of several months - showed progressive neurological deterioration, is reported. Magnetic resonance imaging revealed enormous ipsilateral brain oedema, which did not respond to dexamethasone. Upon further neurological deterioration the former AVM nidus plus an adjacent rim of brain tissue were removed and the patient recovered considerably. It is concluded that embolization in conjunction with irradiation may impair the blood-brain-barrier with resulting long-term oedema in the surrounding brain, and that surgical treatment should be considered in selected cases.

Sodium benzoate attenuates iminodipropionitrile-induced behavioral syndrome in rats.

This study reports the effects of the antioxidant sodium benzoate (SB) on iminodipropionitrile (IDPN)-induced excitation with choreiform and circling (ECC) syndrome in adult female Wistar rats. Rats in four different groups (n=8) received i.p. injections of SB (0, 50, 100 and 200 mg/kg) daily for 10 days. IDPN (100 mg/kg, i.p.) was administered daily 30 min before SB for the first 8 days. Two additional groups served as control (vehicle) and SB alone (200 mg/kg) groups. The animals were observed daily for neurobehavioral abnormalities, including dyskinetic head movements, circling, tail hanging, righting reflex and contact inhibition of the righting reflex, characterized as the ECC syndrome. In the IDPN-alone treated group, the onset of ECC syndrome occurred on day 9 (2 out of 8 rats), whereas none of the animals treated with IDPN plus SB (100 or 200 mg/kg) showed any signs of ECC syndrome on that day. All the animals in the IDPN-alone group developed severe dyskinesia on day 11. Treatment of rats with SB significantly and dose-dependently attenuated IDPN-induced behavioral deficits.

Baclofen attenuates harmaline induced tremors in rats.

Recent experimental and clinical studies clearly suggest the role of gamma-aminobutyric acid (GABA) in the pathogenesis of tremors. The present study was undertaken to investigate the effect of baclofen, a GABA B receptor agonist on harmaline induced tremors. Four groups of female Wistar rats weighing 100+/-15 g were injected with harmaline (10 mg/kg, intraperitoneally) for inducing experimental tremors. The animals in groups 2, 3 and 4 were given baclofen by gavage at doses of 2.5, 5 and 10 mg/kg, respectively, half an hour before harmaline administration, whereas, the rats in group 1 served as control and received water. The latency of onset, intensity and duration of tremor and electromyographic (EMG) responses were recorded. Treatment with baclofen resulted in a dose dependent decrease in the intensity of tremor. Our EMG study also revealed a significant decrease in the amplitude of tremors in baclofen treated rats. A highly significant increase in latency of onset of tremor was observed in the rats treated with high dose (10 mg/kg) of baclofen only. This study clearly suggests beneficial effects of baclofen in harmaline induced tremors.

Dorsal spine injuries in Saudi Arabia--an unusual cause.

BACKGROUND: Motor vehicle accidents are the most common cause of spinal injuries in Saudi Arabia. Camel collisions usually result in cervical spine injuries. Although extremely rare, dorsal spine injuries have also resulted from these accidents. METHOD: Retrospective analysis of the type of accident of all the patients with dorsal spine injuries was conducted at the supra-regional spinal injuries rehabilitation unit in Riyadh. RESULTS: Of all the patients' records reviewed, three patients' injuries to the dorsal spine had resulted from car accidents involving a camel. These patients, during further interviews, described in detail the exact mechanism of their injuries. Protective lateral bending to avoid the direct impact of the animal resulted in their injuries. CONCLUSION: Camel collisions remain a significant cause of mortality and morbidity although they affect the cervical spine most often. Dorsal spine injuries can result from protective lateral bending in unrestrained drivers and passengers.

Protective effect of quinacrine on striatal dopamine levels in 6-OHDA and MPTP models of Parkinsonism in rodents.

Recent studies provide evidence that phospholipase A2 (PLA2) may play a role in the development of experimental parkinsonism. In this investigation an attempt was made to determine a possible protective effect of quinacrine (QNC), a PLA2 inhibitor on MPTP as well as 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rodents. For MPTP studies, adult male mice (C57 BL) were treated with MPTP (30 mg/kg, i.p.) daily for 5 days. QNC was injected i.p. in the doses of 0, 10, 30 and 60 mg/kg daily 30 min before MPTP in four different groups. Two other groups of mice received either vehicle (control) or a high dose of QNC (60 mg/kg). Two hours after the last injection of MPTP, striata were collected for the analysis of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and glutathione (GSH). For the 6-OHDA study, male Wistar rats were infused with 6-OHDA (60 microg) in the right striatum under chloral hydrate anesthesia. The rats in different groups were treated with 0, 5, 15 and 30 mg/kg QNC (i.p.) for 4 days, while first injection was given 30 min before 6-OHDA. On day 5, rats were sacrificed and striata were stored at -80 degrees C. Administration of MPTP or 6-OHDA significantly reduced striatal DA, which was significantly attenuated by QNC. Concomitant treatment with QNC also protected animals against MPTP or 6-OHDA-induced depletion of striatal GSH. Our findings clearly suggest the role of PLA2 in MPTP and 6-OHDA induced neurotoxicity and oxidative stress. However, further studies are warranted to explore the therapeutic potential of PLA2 inhibitors for the treatment of Parkinson's disease.

Vitamin E decreases valproic acid induced neural tube defects in mice.

The present study was undertaken to investigate the effect of vitamin E on valproic acid (VPA) induced teratogenesis. Pregnant Balb mice were divided into six groups of 10-11 animals each. The mice in group 1 served as control and were injected with saline subcutaneously on day 8 of gestation, whereas, animals in group 2 received a single injection of VPA (700 mg/kg (s.c.)). Groups 3 and 4 received an oral administration of vitamin E in the doses of 250 and 500 mg/kg, respectively, 1 h before VPA injection. Group 5 and 6 were given vitamin E only, in the same doses as group 3 and 4. On day 18 of gestation, the mice were killed by cervical dislocation. Embryotoxicity was assessed by counting the number of implants, live and dead fetuses, resorptions, crown rump length and fetal body weight. The fetuses were observed for malformations including neural tube defects (excencephaly), open eye lid and micrognathae. VPA administration resulted in a significant reduction of the average live fetuses/litter, fetal weight and crown rump length and a significant increase in malformations (excencephaly, open eye lid and micrognathae). Concomitant administration of vitamin E significantly attenuated VPA induced decrease in the fetal weight, crown rump length and malformations.

Effect of aluminum on neurological recovery in rats following spinal cord injury.

OBJECT: This investigation was undertaken to study the effect of aluminum on neurobehavioral, electrophysiological, structural, and biochemical changes in rats following spinal cord injury (SCI). METHODS: Adult male Sprague-Dawley rats classified into different groups were given aluminum sulfate-dosed drinking water in the concentrations of 0%, 0.25%, 0.5% and 1%, respectively. After 30 days of aluminum treatment, the animals were subjected to spinal cord trauma. Laminectomy was performed at T7-8 in anesthetized rats, followed by placement of a compression plate (2.2 x 5 mm) loaded with a 35-g weight over the exposed spinal cord for 5 minutes. Control animals underwent the same surgical procedure, but the compression injury was not induced (sham). Postoperative neurological function was assessed using the inclined-plane test and by obtaining a modified Tarlov score and vocal/sensory score daily for 10 days. Electrophysiological changes were assessed using corticomotor evoked potentials, whereas pathological changes were assessed by light microscopy. The level of vitamin E in the spinal cord was measured as an index of antioxidant defense. The behavioral, biochemical, and histological analyses were performed in a blinded fashion. CONCLUSIONS: Analysis of results obtained in the behavioral studies revealed that the compression of spinal cord produced transient paraparesis in which a maximum motor deficit occurred at Day 1 following SCI and resolved over a period of 10 days. Administration of aluminum significantly impaired the recovery following SCI. Analysis of the results of the biochemical, electrophysiological, and histopathological studies also confirmed the deleterious effects of aluminum on recovery from SCI in rats.

Exacerbation of iminodipropionitrile-induced behavioral toxicity, oxidative stress, and vestibular hair cell degeneration by gentamicin in rats.

This study describes the effect of gentamicin, an aminoglycoside antibiotic on iminodipropionitrile (IDPN)-induced abnormal neurobehavioral syndrome in female Sprague-Dawley rats. The animals were exposed to IDPN in the dose of 100 mg/kg/day intraperitoneally for 7 days. Gentamicin (GM) was administered intraperitoneally daily 1 h before IDPN in the doses of 10, 40, and 80 mg/kg body weight in three different groups of rats. One more group of animals received gentamicin alone (80 mg/kg) and served as the gentamicin-alone group. The intensity of IDPN induced characteristic excitation with choreiform, and the circling movement (ECC) syndrome was examined using an observational test battery including dyskinetic head movements, circling, tail hanging, air righting reflex, and contact inhibition of the righting reflex on days 6, 8, 10, 12, 19, 26, and 33. The animals for histopathological observation were sacrificed on day 10, whereas the remaining animals that were used for long-term behavioral studies were sacrificed on day 35 for biochemical observations. The blood and brain samples were collected for the analysis of blood urea nitrogen (BUN), serum creatinine, cerebral malondialdehyde (MDA), conjugated dienes, and lipid hydroperoxides, whereas temporal bones were collected for inner ear histopathology. Our results showed that gentamicin significantly and dose dependently exacerbated the incidence and the severity of the IDPN-induced behavioral syndrome. The histopathology of the inner ear demonstrated more severe loss of sensory hair cells in the crista ampullaris of the rats treated with IDPN plus gentamicin compared to the IDPN-alone treated animals. Concomitant treatment with gentamicin also potentiated IDPN-induced increase in free radical indices, suggesting a possible role of oxidative stress in gentamicin-induced aggravation of IDPN toxicity. Further studies are warranted to determine the role of aminoglycosides in nitrile toxicity and drug-induced movement disorders.

Attenuation of acrylamide-induced neurotoxicity in diabetic rats.

In recent years, an increasing number of cases of neuropathy have been reported as a result of accidental or occupational exposure to chemicals. Acrylamide (Acr), a widely used industrial chemical, is known to produce peripheral neuropathy that resembles diabetic neuropathy in many ways. However, the interaction between diabetes and Acr has not been studied. The present study was undertaken to examine the effect of streptozotocin (STZ)-induced diabetes on Acr-induced neurotoxicity in rats. Male Sprague-Dawley rats weighing 300 +/- 10 g were divided into four groups of 10 animals each. The rats in group 1 served as control, and received normal saline. The animals in group 2 were given Acr dissolved in physiological saline (50 mg/kg IP 3 days/week) for 2 weeks. The rats in group 3 and 4 were made diabetic by administering a single IP injection of STZ (50 mg/kg). The animals in group 3 served as diabetic control, whereas the rats in group 4 received Acr in the same dose regimen as in group 2, a week after induction of diabetes. Neurobehavioral responses including foot print length, hind limb function, landing foot splay, and the ability to stay on an inclined plane were assessed 48 h after the last dose of Acr followed by electrophysiological measurements. The animals were then sacrificed, and sciatic nerves were collected for biochemical analysis. The results of this study clearly showed a significant deterioration of neurobehavioral and electrophysiological responses in Acr-treated rats. Although no significant change in these parameters was observed in the diabetic (only) group, Acr-induced functional deficiency was significantly reduced in diabetic animals. However, the difference in electrophysiological response in Acr-treated diabetic and nondiabetic rats was not found to be statistically significant (p 0.05). The precise mechanism by which Acr induced neurobehavioral toxicity is reduced in diabetic animals warrants further investigations.

Effect of lidocaine on harmaline-induced tremors in the rat.

The present study was undertaken to investigate the effect of lidocaine on harmaline-induced tremors in the rat. Four groups of Wistar rats weighing 45-50 g were injected with harmaline (50 mg/kg i.p.) for inducing experimental tremors. The rats in group 1 served as control, whereas the animals in groups 2, 3, and 4 were also given lidocaine i.p. at doses of 12.5, 25, and 50 mg/kg, respectively, 10 min after the onset of tremors (therapeutic study). In a separate four groups of animals intraperitoneal lidocaine injection was given 10 min before harmaline (prophylactic study) in the same dose regimen as mentioned above. The latency of onset, intensity, and duration of tremor and electromyographic responses were recorded. Lidocaine dose dependently attenuated harmaline-induced tremors in rats. The latency period was increased, and duration and intensity of harmaline-induced tremors was reduced by lidocaine. Our electromyography (EMG) study also revealed a decrease in the amplitude of harmaline-induced tremors in lidocaine-treated rats. In conclusion, the results of this study clearly suggest beneficial effects of lidocaine in harmaline-induced tremors.

Diethyldithiocarbamate (DEDC) impairs neuronal recovery following sciatic nerve injury in rats.

PURPOSE: Diethyldithiocarbamate (DEDC) is a substituted dithiocarbamate that is metabolically interconvertible with disulfiram (Ant-abuse). In recent years DEDC has received considerable attention because of its clinical applications and potential role in mediating both the toxic and therapeutic actions of disulfiram which is frequently used for alcohol aversion therapy. DEDC is known for its multiplicity of action that exerts both pro- and antioxidant effects. In rodents DEDC has been shown to produce neuroprotective as well as neurotoxic effects. The purpose of this study was to examine the effect of DEDC on neurological recovery following sciatic nerve crush injury (SNCI) in rats. METHODS: Adult female Wistar rats were subjected to SNCI with a haemostat under deep anaesthesia. The animals were orally treated with DEDC at the doses of 250 mg/kg, 500 mg/kg and 750 mg/kg body weight 1 hr before SNCI and then once daily for 60 days. The animals were observed for sciatic functional index (walking deficit), electrophysiological and histological changes. Vitamin E level was measured to deter-mine antioxidant status of sciatic nerve. RESULTS: Crush injury to the sciatic nerve resulted in a significant impairment of functional response which gradually recovered over a period of 22 days. Treatment of animals with DEDC caused a significant delay in functional recovery which was accompanied by poor histo-logical and electrophysiological outcome. Prooxidant effect of DEDC is quite evident from a significant decrease in vitamin E levels in both injured and uninjured sciatic nerves. CONCLUSIONS: Our results demonstrate that exposure to DEDC adversely affects recovery from peripheral nerve injury. The delay may to some extent be attributed to DEDC induced oxidative stress.

Nitric oxide synthase inhibitor aminoguanidine potentiates iminodipropionitrile-induced neurotoxicity in rats.

This investigation was undertaken to study the effect of nitric oxide synthase inhibitor, aminoguanidine on iminodipropionitrile (IDPN)-induced neurobehavioral and vestibular toxicity in rats. The dyskinetic syndrome was produced in male Wistar rats by i.p. injections of IDPN (100 mg/kg) for 6 days. Aminoguanidine was administered orally in the doses of 50, 150 and 300 mg/kg, 60 min before IDPN in three different groups. Control rats received vehicle only, whereas another group was treated with 300 mg/kg of aminoguanidine alone (without IDPN). Our results showed that aminoguanidine significantly and dose dependently exacerbated the incidence and intensity of IDPN-induced dyskinetic head movements. Aminoguanidine potentiated IDPN-induced loss of air righting reflex. The histopathological examination of inner ear showed aggravation of IDPN-induced degeneration of sensory hair cells in the crista ampullaris by aminoguanidine. These results suggest the role of nitric oxide in IDPN-induced neurobehavioral and vestibular toxicity.

Effect of acrylamide on neurological recovery following spinal cord injury in rats.

Acrylamide (ACR) is a cumulative neurotoxin which causes axonal degeneration in animals and man. Industrial workers exposed to ACR have been reported to suffer from a variety of central and peripheral neuropathological symptoms including numbness of hands and feet, skin peeling and muscular weakness of legs. These reports suggest that the body burden of ACR may be a risk factor in recovery patterns following neurotrauma. The present study was designed to assess the effect of ACR on neurological recovery following spinal cord injury (SCI) in rats. Male Sprague-Dawley rats weighing 200-230 g were anaesthetised with chloral hydrate and laminectomy was performed at T 7-8 level leaving the dura intact. A compression plate (2.2 x 5.0 mm) loaded with a weight of 35 g was placed on the exposed cord for 5 minutes. Animals were divided into seven groups of eight rats each. The animals in Group 1 served as control whereas rats in Group 2 underwent laminectomy alone (sham). The rats in Group 3 to 6 were subjected to SCI as mentioned above. Animals in Groups 4, 5 and 6 also received ACR in the doses of 10 mg/kg, 20 mg/kg and 40 mg/kg, i.p., respectively in addition to SCI, whereas the rats in Group 7 received ACR alone at a dose of 40 mg/kg body weight. The first dose of ACR was given 30 minutes before SCI, followed by daily administration of drug for 7 days. Post traumatic neurological recovery was recorded daily for 10 days using a modified Tarlov score, inclined plane test and sensory and vocal score. Electrophysiological changes were assessed using somatosensory and corticomotor evoked potentials. The animals were sacrificed at different time intervals and the injured site of the spinal cord was analysed for lipid hydroperoxides (LPH), conjugated dienes (CD) and glutathione (GSH). Neuropathological changes in the spinal cord were assessed using light microscopy. The rats exposed to compression injury alone showed a maximum neurological deficit at 24 hr and then a gradual recovery was observed over a period of 10 days. The rats treated with ACR along with SCI showed poor or no recovery over a period of 10 days. Our electrophysiological and histopathological studies also confirmed that concomitant exposure to ACR produces a significant deleterious effect on the recovery from SCI. SCI induced increase in oxidative stress (increase in LPH and CD and decrease in GSH) is also exacerbated by ACR suggesting a role of free radicals. The results of this study suggest that increased body burden of ACR may retard the recovery from neurotrauma or even lead to permanent disability.

Worldwide ethnic distribution of the G protein beta3 subunit 825T allele and its association with obesity in Caucasian, Chinese, and Black African individuals.

Recently, it was demonstrated that one allele (825T) of the gene encoding the G protein beta3 subunit (GNB3) is associated with hypertension in Germans. This study investigates a possible association with obesity in young male Germans, Chinese, and black South Africans with low, intermediate, and high 825T allele frequencies, respectively. In each of these three distinct cohorts, the 825T allele frequency was increased significantly in overweight (body mass index [BMI] > or =25 kg/m2) and obese individuals (BMI >27 kg/m2) compared to those with normal weight. The 825T allele frequencies in these three BMI groups were, respectively, 29.5, 39.3, and 47.7% in Germans, 46.8, 53.9, and 58.6% in Chinese, and 83.1, 87.7, and 90.9% in South Africans. In each of these three distinct groups, the 825T allele was significantly associated with obesity with odds ratios between 2 and 3. More urban than rural black Africans were overweight despite similar 825T allele frequencies in both populations, which underscores the role of both genetic and environmental factors. BP values in young male whites increased significantly with increasing BMI values but were independent of the C825T polymorphism, suggesting that hypertension associated with the 825T allele could be a consequence of obesity. Genotyping of 5254 individuals from 55 native population samples from Africa, the Americas, Europe, Asia, Australia, and New Guinea demonstrated highest 825T allele frequencies in black Africans (82%) and intermediate values in east Asians (47%). It is anticipated that high frequencies of the 825T allele in Africans and Asians may contribute to an obesity and hypertension epidemic if Westernization of lifestyles continues.

Protection by 2-deoxy-D-glucose against beta,beta'-iminodipropionitrile-induced neurobehavioral toxicity in mice.

This investigation was undertaken to study the effect of 2-deoxy-D-glucose (2-DG) on beta, beta'-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, i.p.) 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 neurotoxicity.

An unusual cause of depressed skull fracture: case report.

BACKGROUND: Camel collision accidents are a common occurrence in Saudi Arabia, with a high rate of mortality and morbidity. Isolated injuries are rare because of the nature of impact sustained by the person. CASE DESCRIPTION: A 4-year-old child with an isolated depressed skull fracture resulting from a camel collision is described. The other occupants of the car were crushed to death. The child sustained only an impact to his head, causing a compound depressed skull fracture with localized cortical damage. CONCLUSIONS: Camel collision accidents are a common cause of mortality and morbidity in Saudi Arabia. Isolated skull injuries are rare and result from a localized impact. This is the first report of a compound depressed skull fracture from such an incident. The extent of the problem and efforts toward prevention are described.