Atlantoaxial Subluxation due to Psoriatic Arthritis

Atlantoaxial subluxation causing spinal cord compression at the craniovertebral junction may develop in patients with rheumatoid or psoriatic arthritis. There have been only a few reports of atlantoaxial subluxation in patients with psoriatic arthritis in the world. The authors report a case of psoriatic arthritis with atlantoaxial subluxation accompaning periodontoid pannus formation. This 53-year-old man with a 3-year history of psoriatic skin lesion presented with nuchal pain and myelopathy. We performed decompression by C1 total laminectomy with transarticular screw fixation and obtained remarkable improvement in motor function and immediate postoperative stability.

The Effect of D,L-6,8-Thioctic Acid on the Volume of Cerebral Infarction in Ischemic Rat Model

OBJECTIVE: The authors demonstrate neuroprotective effects of antioxidant in reperfusion injury using ischemic rat model and evaluate the clinical eligibility of this agent to ischemic cerebrovascular diseases. METHODS: Rat model was made according to Longa method. Thirty-six Sprague-Dawley rats were used and were equally divided into three groups;A) treated subcutaneously with D,L-6,8-Thioctic acid 30 minutes before occlusion, B) within one hour after occlusion, and C) with vehicle only. Neurologic examination was performed immediately and 24 hours after reperfusion. Twenty-four hours after reperfusion, brains were extracted and stained with 2% 2,3,5-Triphenyltetrazolim chloride in 2mm-thickness section. Then, fixed sections were digitalized and used for infarct area calculation. RESULTS: There was no significant statistical difference in recorded hemodynamic and physiologic parameters between three groups. The neurologic status taken immediately following reperfusion were A) 2.67+/-0.492, B) 2.75+/-0.452, and C) 2.83+/-0.389, and were improved to A) 1.67+/-0.898, B) 1.92+/-0.900, and C) 2.08+/-0.793 just before sacrificing. However, there was no statistically significant difference between three groups. Mean volume of cerebral infarction was A) 9.5+/-1.67%, B) 10.4+/-1.58%, and C) 11.3+/-1.12% with no significant difference. Any specific correlation between the neurologic status and the mean infarction volume was not observed. CONCLUSION: Any single agent does not seem to reduce the infarction volume holistically, therefore, the incoming therapeutic target should be the development of versatile neuroprotective agents or the selection of preexisting synergistic compounds without compromising patients' safety.