The effect of some immunomodulatory and anti-inflammatory drugs on Li-pilocarpine-induced epileptic disorders in Wistar rats.

Evidence shows that inflammatory and immune processes within the brain might account for the pathophysiology of epilepsy. Therefore, developing new antiepileptic drugs that can modulate seizures through mechanisms other than traditional drugs is required for the treatment of refractory epilepsy. This study aims to determine the relationship between brain inflammation and epilepsy, to examine the contribution of some biochemical parameters involved in brain inflammation, and to address the effect of pharmacological interventions using some anti-inflammatory and immunomodulatory drugs in an experimental epilepsy model. Adult male rats were divided into seven groups of 20. G1 was the normal, non-treated control. G2 was the epileptic, non-treated group. G3-G7 were treated with celecoxib, methotrexate, azathioprine, dexamethasone, and valproate, respectively, for a period of three weeks. Induction of status epilepticus (SE) by Li-pilocarpine was performed on groups G2-G7. EEG tracing was conducted, and inflammatory mediators (brain and serum IL-1ß, IL 6, PGE2, HSP70, TGF-ß2, and IFNγ) were measured. The induction of SE increased the amplitude and frequency of EEG tracing and inflammatory mediators more than in the normal control group. Treatments of epileptic rats reduced the frequency and amplitude of EEG tracing and significantly decreased the levels of inflammatory mediators in some treated rats compared to G2. These findings demonstrate that some anti-inflammatory and immunomodulatory drugs can lower the frequency and amplitude of seizures and reduce some inflammatory mediators in epilepsy treatments, strengthening the possibility that targeting these immunological and inflammatory pathways may represent another effective therapeutic approach to preventing epileptic seizures.

Axonal degeneration of the ulnar nerve secondary to carpal tunnel syndrome: fact or fiction?

The distribution of sensory symptoms in carpal tunnel syndrome is strongly dependent on the degree of electrophysiological dysfunction of the median nerve. The association between carpal tunnel syndrome and ulnar nerve entrapment is still unclear. In this study, we measured ulnar nerve function in 82 patients with carpal tunnel syndrome. The patients were divided into group I with minimal carpal tunnel syndrome (n = 35) and group II with mild to moderate carpal tunnel syndrome (n = 47) according to electrophysiological data. Sixty-one age- and sex-matched subjects without carpal tunnel syndrome were used as a control group. There were no significant differences in ulnar sensory nerve peak latencies or conduction velocities from the 4(th) and 5(th) fingers between patients with carpal tunnel syndrome and the control group. The ulnar sensory nerve action potential amplitudes from the 4(th) and 5(th) fingers were lower in patients with carpal tunnel syndrome than in the control group. The ratios of the ulnar sensory nerve action potential amplitudes from the 4(th) and 5(th) fingers were almost the same in patients with carpal tunnel syndrome as in the control group. These findings indicate that in patients with minimal to moderate carpal tunnel syndrome, there is some electrophysiological evidence of traction on the adjacent ulnar nerve fibers. The findings do not indicate axonal degeneration of the ulnar nerve.

Sleep-related breathing disorders in cerebrovascular stroke and transient ischemic attacks: a comparative study.

Sleep-related breathing disorders are said to be common in patients with established cerebrovascular accidents. The aim of this study was to assess the frequency and characteristics of sleep-related breathing disorders in ischemic stroke and transient ischemic attacks. All patients were subjected to neurologic assessment, Berlin questionnaire (Arabic version), brain computed tomographic scan, and polysomnography along 6 to 8 hours overnight with special emphasis to apnea/hypopnea indices. All assessments were done for 30 patients who had stroke and transient ischemic attacks as well as 20 age- and sex-matched controls. Overall, 13.3% of patients had mild sleep apnea (apnea/hypopnea index, >5), 13.3% had moderate sleep apnea (apnea/hypopnea index, >15), and 34% had severe sleep apnea (apnea/hypopnea index, >30). The sensitivity and specificity of Berlin questionnaire for obstructive sleep apnea diagnosis were 55% and 100%, respectively, for mild sleep apnea, 56.3% and 85.7% for moderate sleep apnea, 66.7% and 83.3% for severe condition. Berlin questionnaire is a moderate sensitive but highly specific screening test for sleep apnea in cerebrovascular diseases. Those who scored high risk should consider polysomnography to specify the type and severity of apnea.