Purpose: The introduction of direct-acting antivirals (DAAs) has revolutionized the treatment of chronic hepatitis C viral (HCV) infection. This study aims to establish real-world treatment efficacy of Sofosbuvir-based (SOF-B) and Ombitasvir/Paritaprevir/Ritonavir-based (OPR-B) regimens. Patients and methods: This prospective, non-randomized observational real-life study was conducted in Salmaniya Medical Complex, Bahrain, and included consecutive patients with chronic HCV infection (genotypes 1–4) who were treated with direct-acting antivirals. Sustained virologic response to therapy was assessed at week 12 post end of treatment (SVR12). Results: Of the 167 patients included, 60.5% (n=101) were treated with SOF-B and 39.5% (n=66) with OPR-B regimens for 12 weeks (n=148; 88.6%) or 24 weeks (n=19; 11.4%). SVR12 was achieved in 156 (93.4%) patients, 4 patients failed to achieve SVR despite completion of treatment, and 7 patients discontinued treatment due to non-compliance and were included in the analysis on an intention-to-treat basis. There was no difference between SOF-B and OPR-B regimens (95/101; 94.1%) and (61/66; 92.4%), respectively ( p =0.68). However, SVR12 rates were significantly higher in patients without liver cirrhosis (103/104; 99.0%) compared to patients with cirrhosis (53/63; 84.1%; p <0.001), and in patients who received 12-week-regimen (141/148; 95.3%) compared to those who received 24-week regimen (15/19; 78.9%; p <0.024). However, logistic regression analysis identified cirrhosis at baseline to be the only independent predictor of non-SVR12 (OR: 16.1, 95% confidence interval 1.96–131.91, p =0.01). Apart from Hb, INR, and ALP, all other laboratory parameter improved following treatment ( p <0.05). Conclusion: Both SOF-B and OPR-B regimens achieved high SVR12 rates in this real-life cohort of patients with chronic HCV infection, similar to what is reported in other real-world studies. Cirrhosis was the only independent predictor of poor response.

No abstract

Introduction Sleep associated seizures especially Nocturnal Frontal Lobe Epilepsy (NFLE) represents a spectrum of challenging clinical manifestations presenting as complex nocturnal movements/behaviors, making the diagnosis often difficult. Report of Case A 64 y/o male, with history of ongoing complex movements occurring during his sleep, with no history of strokes or neurological deficits. Had extensive neurologic workup (all negative) including routine electroencephalogram (EEG), prolonged inpatient EEG (12 hours), and MRI of the brain. Home sleep study showing moderate obstructive sleep apnea (OSA) AHI 24/hour successfully treated with CPAP therapy (residual AHI 1.7/hour) with improved nighttime symptoms initially. Wife recalls events as happening only at night while sleep, as patient often confused upon waking up in the morning, at times appear to sit up and smack his lips. No nighttime hallucinations, sleep paralysis, or acting out dreams were reported. Had two episodes associated with tongue biting and loss of bladder control. Another episode happened after a daytime nap, patient went outside and was mowing his lawn, went “completely blank “, appeared confused. No daytime or nighttime seizures were ever noticed. Patient do not recall any of the above events. Repeat EEG was normal. MRI/MRA of the head /neck showed small tiny focus in left frontoparietal lobe, suggesting remote cortical ischemic injury. Polysomnography (PSG) with seizure montage showed Interictal epileptic discharges (IEDs) foci recorded in the frontal/frontopolar leads without accompanying body movements. Interictal spike and wave activity seen during stage N2. Initially treated with carbamazepine (had skin reaction) switched to levetiracetam with complete resolution of his symptoms. Conclusion This case illustrates the importance of reviewing the clinical history, behavior semiology, and diagnostic ancillary testing such as polysomnography with EEG monitoring in distinguishing nocturnal epileptic seizures from other nocturnal complex behavior disorders and parasomnias.

Introduction Hypoglossal Nerve Stimulation (HGNS) has become an alternative therapy for moderate to severe obstructive sleep apnea (OSA) patients intolerant to PAP therapy. HGNS devices typically comprise of implantable pulse generator (IPG) placed surgically in an infraclavicular subcutaneous pocket. An electrode cuff attached to the IPG wraps around the distal portion of the of the hypoglossal nerve. This device has an implantable chest sensor that monitors the respiratory efforts. Report of Case A 76-year-old male with history of severe OSA (AHI 39 /hour) was intolerant to PAP therapy. HGNS was implanted in the right infraclavicular pocket under general anesthesia without any complications. Patient had successful tongue motion to stimulus per protocol intra- operatively in the OR. However, no tongue movement was noted despite maximum stimulation up to 4.5 V at follow up clinic visit. Follow up C spine x ray showed very low-lying HGNS cervical lead cuff, and possible dislodgement. Patient was taken back to the OR. Intraoperatively it was noted that the previously placed cervical lead cuff has folded back and was lying on the surface of the submandibular gland /digastric anchor site. It was dissected free and replaced on the distal inclusion branches of the hypoglossal nerve with loupe magnification and EMG confirmation (tongue deviation at 1.5 volts). Patient developed tongue neuropraxia with difficulty swallowing, difficulty speaking and right sided tongue deviation lasting for months, that gradually improved. Patient had successful HNS activation 6 months later using 2.2 V. Conclusion (HGNS) failure secondary to cervical lead cuff dislodgement is a rare complication and should be taken in consideration. Post-operative imaging and comprehensive clinical examination are crucial in detecting such problems. Temporary tongue neuropraxia post Hypoglossal nerve stimulator placement is another possible complication.