Zoster Paresis Misconceived as a Radiculopathy due to Herniated Intervertebral Disc

Herpes zoster is a viral disease of the posterior root ganglion and sensory nerve fiber, which presents clinically with vesicular eruption of the skin, radicular pain and sensory changes in the distribution of the affected ganglion. However, involvement of the motor neurons can be seen as well. If classic cutaneous lesions are present, herpes zoster-related motor paresis is easily diagnosed. Otherwise, the diagnosis may be more difficult and suspicious, especially if weakness occurs as a symptom before cutaneous lesions appear, or abnormal findings on the MRI are consistent with the signs. There have been few reports of sciatica with motor loss preceding skin lesions. Here, we report a patient with herpes zoster-related motor paresis preceding skin lesions. In the preliminary diagnosis, the herpes zoster-related motor paresis was confused for some structural disorder.

Contralateral allodynia and central change in the chronic post-ischemic pain model rats / 대한마취과학회지

BACKGROUND: Mirror-image allodynia is a mysterious phenomenon that occurs in association with many clinical pain syndromes including complex regional pain syndromes (CRPS). Underlying mechanisms for the development of such pain are still a matter of investigation. Several studies suggest that activation of the N-methyl-D-aspartate (NMDA) receptor is essential for central sensitization as a base for persistent pain. The aim is to assess whether alteration of NMDA receptor expression correlates with the contralateral allodynia in the chronic post-ischemia pain (CPIP) model rats representing CRPS-Type I. METHODS: Application of a tight-fitting tourniquet for a period of 3 hours before reperfusion produced CPIP in male Sprague-Dawley rats. The mechanical paw withdrawal thresholds to von Frey stimuli (using a dynamic plantar aesthesiometer) were measured as pain indicators in ipsilateral and contralateral hindpaws. Phosphorylation of the NMDA receptor 1 subunit (pNR1), assessed with Western blot, was measured in the contralateral L4-6 spinal cord. RESULTS: Ipsilateral and contralateral mechanical allodynia is present at 4 hours after reperfusion, peaked at 3 days, and continued for 7 days after reperfusion. The relative density of pNR1 of CPIP rats significantly decreased in the contralateral L4-6 spinal cord compared to baseline value (P < 0.05). There was significant correlation between paw withdrawal threshold and the relative density of pNR1 (ipsilateral; R2 = 0.75, P < 0.01, contralateral; R2 = 0.60, P < 0.01). CONCLUSIONS: These data suggest that pNR1 is correlated to the contralateral mechanical allodynia in CPIP rats.