Post Herpetic C8 Myotomal Paresis

Herpes Zoster is a neurocutaneus infection of latent Varicella Zoster Virus. It occurs by the reactivation of virus in the sensory ganglia and causes pain and rash in related dermatome. Although it is a disease of sensory ganglia, myotomal paresis can develop. Motor involvement generally affects cranial nerves, but motor palsies of spinal roots are uncommon. We present a patient with postherpetic spinal segmental paralysis, which is developed after the resolution of the rash on right upper extremity

Isolated abducens nerve palsy due to pituitary apoplexy after mild head trauma

YAVASI, OZCAN/0000-0001-8641-7031WOS: 000361839300056PubMed: 26314216Pituitary apoplexy is a relatively rare condition. Cranial nerve palsies may develop due to compression of the surrounding structures by the rapidly expanding tumor. While the most commonly affected nerve is the oculomotor nerve, abducens nerve palsy may also occur less commonly. A 68-year-old male patient was admitted to the emergency department with complaints of severe headache, nausea, vomiting, and diplopia after head trauma due to falling. His magnetic resonance imaging evaluation demonstrated a large pituitary adenoma and bleeding into the tumor, which was acutely expanding and leading to compression of the abducens nerve laterally. Isolated abducens palsy due to posttraumatic pituitary apoplexy is a rare clinical condition, and as the symptoms and signs are nonspecific, it can commonly remain clinically undiagnosed. in this article, our aim was to draw attention to a clinical condition in which unfavorable complications may develop if the diagnosis is overlooked

Syringic acid protects against thioacetamide-induced hepatic encephalopathy: Behavioral, biochemical, and molecular evidence

The objective of this study was to elucidate the effects of syringic acid on thioacetamide-induced hepatic encephalopathy which is a complex serious syndrome with neuropsychiatric abnormalities related to acute liver dysfunctions like cirrhosis. Rats were treated with syringic acid (50 and 100 mg/kg, p.o.) for 14 days in treatment groups. Hepatic encephalopathy was induced by three doses of (200 mg/kg i.p.) thioacetamide injection. Syringic acid effectively alleviated thioacetamide-induced hepatic injury via reduction in ammonia, AST, ALT, ALP, LDH and decrease in oxidative stress (decreased MDA, ROS and increased SOD and GSH). Syringic acid also attenuated inflammatory injury by suppressing TNF-alpha, IL-1 beta, and NF-kappa B and increasing IL-10. The caspase-3 expression was also down-regulated in both liver and brain tissues. Immunohistochemical results confirmed the recovery with syringic acid by downregulation of iNOS, 8-OHdG and GFAP expression. Syringic acid decreased the deteriorating effects of thioacetamide as seen by reduced ammonia concentration and also preserved astrocyte and hepatocyte structure. The behavioral test results from elevated plus maze test, similar to the open-field locomotor test results, confirmed that syringic acid can reverse behavioral impairments. In conclusion, syringic acid exerted hepatoprotective and neuroprotective effects against hepatic encephalopathy by mitigating hepatotoxicity biomarkers, exerting antioxidant, anti-inflammatory effects in addition to suppressing hyperammonemia