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.

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Background: High-resolution ultrasonography (US) is a non-invasive, readily applicable imaging modality capable of depicting real-time static and dynamic information concerning the peripheral nerves and their surrounding tissues. Although electrophysiological studies are the gold standard in the evaluation of nerve injuries, US can be used also to evaluate the morphological changes of nerve injuries. Objectives: To evaluate the role of the high-resolution US in the assessment of nerve injuries and to compare it to the role of electrodiagnostic studies. Subjects and methods: A total of 30 nerves from 22 consecutive patients with clinically definite nerve injury were considered. Two independent and blinded clinicians perform electrodiagnosis and US. The clinical, neurophysiological, and US findings were collected, and the contribution of US was then classified as " contributive" or "non-contributive", according to whether US confirmed the clinical and neurophysiological diagnosis or not. Results: US was "contributive" (confirming the electrophysiological diagnosis) in 66.67% of cases (n = 20), providing information about continuity of the nerve, morphological changes after injury as swelling, scar tissue formation, or neuroma formation with sensitivity of 75% compared to the electrodiagnostic studies and accuracy of 66.67%. Conclusion: Ultrasound can be used, when available, as a complementary tool for electrodiagnostic studies to provide anatomical information about the injured nerves in case of complete axonal lesion.

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-β2, 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.

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