Activated spinal astrocytes are involved in the maintenance of chronic widespread mechanical hyperalgesia after cast immobilization.

BACKGROUND: In the present study, we examined spinal glial cell activation as a central nervous system mechanism of widespread mechanical hyperalgesia in rats that experienced chronic post-cast pain (CPCP) 2 weeks after cast immobilization. Activated spinal microglia and astrocytes were investigated immunohistologically in lumbar and coccygeal spinal cord segments 1 day, 5 weeks, and 13 weeks following cast removal. RESULTS: In the lumbar cord, astrocytes were activated after microglia. Astrocytes also were activated after microglia in the coccygeal cord, but with a delay that was longer than that observed in the lumbar cord. This activation pattern paralleled the observation that mechanical hyperalgesia occurred in the hindleg or the hindpaw before the tail. The activating transcription factor 3 (ATF3) immune response in dorsal root ganglia (DRG) on the last day of cast immobilization suggested that nerve damage might not occur in CPCP rats. The neural activation assessed by the phosphorylated extracellular signal-regulated kinase (pERK) immune response in DRG arose 1 day after cast removal. In addition, L-α-aminoadipate (L-α-AA), an inhibitor of astrocyte activation administered intrathecally 5 weeks after cast removal, inhibited mechanical hyperalgesia in several body parts including the lower leg skin and muscles bilaterally, hindpaws, and tail. CONCLUSIONS: These findings suggest that activation of lumbar cord astrocytes is an important factor in widespread mechanical hyperalgesia in CPCP.

Early dynamic 201Tl SPECT in the evaluation of brain tumours.

OBJECTIVE: To estimate the usefulness of early dynamic 201Tl single photon emission computed tomography (SPECT) studies in distinguishing the histological malignancy of brain tumours. METHODS: Dynamic 201Tl SPECT was performed for 3 min per scan for 15 min immediately after the administration of 201TlCl in 110 patients with brain tumours (111 lesions). The data obtained each 3 min were used for dynamic SPECT, and the five sets of data obtained were added to acquire static SPECT data. For static SPECT, the static thallium index (STI) was calculated as the ratio of 201Tl uptake in the tumour to that of the contralateral normal brain. The ratio of the 201Tl uptake for each 3 min was defined as the dynamic thallium index (DTI). The dynamic thallium rate (DTR), as a per cent, was calculated as DTR=(DTI for every 3 min)/STI H 100. The five values were approximated as a linear function and the slope (%/min) was calculated. RESULTS: In static SPECT, there was no significant difference between the STI of malignant tumours (glioblastoma and anaplastic astrocytoma) and that of benign tumours (low-grade glioma, meningioma, pituitary adenoma, neurinoma and haemangioblastoma) (3.7+/-1.5, 5.0+/-3.5, respectively). On dynamic SPECT, DTI increased markedly over 15 min for malignant tumours. In contrast, the DTI of benign tumours increased slightly, steadily or decreased. The slope of the linear functions calculated from the DTRs was much higher in the malignant tumour group than in the benign tumour group (P<0.001). CONCLUSIONS: We suggest that the performance of 201Tl dynamic SPECT for 15 min is useful for distinguishing malignant brain tumours from benign brain tumours and reduces the examination stress of patients.