Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus

Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice (iNOS-/-) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.

Celecoxib Attenuates Kainic Acid-induced Neuronal Cell Death Through Suppression of Microglial c-Jun N-terminal Kinase Phosphorylation

In the present study, neuroprotective property of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, and its underlying mechanism were examined in the animal model of kainic acid (KA)-induced excitotoxicity. KA, administered intracerebroventricularly (i.c.v.), induced marked neuronal cell death with concurrent microglial activation and subsequent induction of inducible nitric oxide synthase (iNOS) in the hippocampus. Histopathological analysis demonstrated that celecoxib (100 mg/kg), pre-treated 1 hr before or post-treated 2 hr after KA i.c.v. injection, significantly attenuated KA-induced death of pyramidal neurons in CA3 region. Celecoxib obviously suppressed KA-induced microglial activation and subsequent iNOS expression. KA- induced phosphorylation of c-Jun N-terminal kinases (JNK) was attenuated with celecoxib treatments. The results of the present study demonstrate that suppression of JNK phosphorylation by celecoxib contributes to its neuroprotective action against KA-induced excitotoxicity suggesting that celecoxib may be a potentially valuable in the treatment of acute brain pathologies associated with excitotoxic neuronal damage such as epilepsy, stroke, and traumatic brain injury.

Eikenella Corrodens Cervical Spinal Epidural Abscess Induced by a Fish Bone

Cervical spinal epidural abscess, caused by fish bone injury and a secondary infection by Eikenella corrodens which is part of the normal flora, has not been reported. A 72-yr-old man came to the hospital with pain in his posterior neck and both shoulders for 2 months. He also was experiencing weakness on his right side for 3 days. A fish bone had been stuck in his throat for about 2 months. Neurological examination revealed right hemiparesis, hypesthesia on the left extremities and neck stiffness. Laboratory findings showed an elevated ESR/CRP and leukocytosis, and magnetic resonance imaging revealed a retropharyngeal abscess and cervical myelitis. The patient was treated with emergency surgical decompression and antibiotics. A fish bone was removed from the C3-C4 intervertebral disc space. In the culture of chocolate blood agar and 5% sheep blood agar plate, E. corrodens was detected as a causative organism.

A case of Mobius Syndrome with Duane's Retraction Syndrome

No abstract available.

Bilateral Posterior Ischemic Optic Neuropathy associated with Hemodialysis in a patient with Chronic Renal Failure

Bilateral posterior ischemic optic neuropathy (PION) has rarely been documented in chronic renal failure (CRF). A 78-year-old woman with CRF, who had undergone hemodialysis for 14 years, was admitted due to rapidly progressive visual loss. Her pupils were unreactive to light, but ocular motility and fundoscopic examinations were normal. A brain MRI with angiogram revealed no abnormality and a VEP showed no wave formation bilaterally. Intravenous corticosteroid therapy was conducted without improvement. We report a case of bilateral PION associated with CRF, presumably due to chronic hypotension and anemia occurring during hemodialysis.

Toxocariasis: An Unusual Cause of Cerebral Infarction

Human toxocariasis is a zoonotic parasitic disease caused by Toxocara canis or Toxocara cati larvae. Human infection is usually an outcome of accidental ingestion of the embryonated eggs, and the involvement of central nervous system is rare. We report a case of cerebral infarction which was caused by toxocariasis in adult, who had headache, abdominal pain and right side weakness. He had only a history of ingestion of raw liver of deer.