BackgroundAn outcome measure to evaluate the neurological function of cervical myelopathy was proposed by the Japanese Orthopaedic Association in 1975 (JOA score), and has been widely used in Japan. However, the JOA score does not include patients’ satisfaction, disability, handicaps, or general health, which can be affected by cervical myelopathy. The purpose of this study was to develop a new outcome measure for patients with cervical myelopathy.MethodsThis study was conducted in eight university hospitals and their affiliated hospitals from February to May 2002. The questionnaire included 77 items. Forty-one questions, which were originally listed by the authors, were for evaluation of the physical function of the cervical spine and spinal cord. The Medical Outcome Study Short-Form 36-Item Health Survey (SF-36) was used to examine health-related quality of life (QOL). Patients with cervical myelopathy and healthy volunteers were recruited at each institution. After analysis of the answers from patients and volunteers, irrelevant questions using the following criteria were excluded: (1) a question 80% of answers for which were concentrated on one choice, (2) a question whose answer was highly correlated with that of other questions, (3) a question that could be explained by other questions, and (4) a question for which the distribution of the answers obtained from the patients was not different from that obtained from the normal volunteers.ResultsThe patients comprised 164 men and 86 women, and the healthy volunteers 96 men and 120 women. Thirteen items from the questions about the physical functions of the cervical spine and the spinal cord and 11 items from SF-36 remained as candidates that should be included in the final outcome measure questionnaire.ConclusionTwenty-four questions remained as candidates for the final questionnaire. This new self-administered questionnaire might be used to evaluate the outcomes in patients with cervical myelopathy more efficiently.
Hippocampal neurones isolated from rat embryos were maintained on glial monolayers in a medium containing no L-glutamate (Glu). The administration of Glu for a limited period induced a massive death (loss) of neurones. The degree of neuronal loss increased with time after exposure to Glu. The extent of neuronal loss assessed 24 h after exposure to Glu was dependent upon the concentration Glu and on the duration of the exposure. An increase in concentration of external Ca2+ during the exposure to Glu enhanced the extent of loss. By contrast, an increment in concentration of environmental Mg2+ reduced the loss. The inhibitor of spike firing, tetrodotoxin (TTX) and the suppressor of Ca2+ entry, nitrendipine, both decreased the extent of loss, when delivered prior to Glu. The toxicity of Glu became progressively more apparent with further days of culture. The cytosolic concentration of Ca2+ ([Ca2+]i) in single hippocampal neurones was monitored by microscopic fluorometry under conditions equivalent to those in the death assay. The time required for the recovery of [Ca2+]i from the level elevated by exposure to Glu to pre-stimulus levels closely paralleled the degree of neuronal loss; i.e. high doses of Glu, long periods of exposure, high concentrations of external Ca2+, low concentrations of external Mg2+, and extended days of culture all retarded [Ca2+]i recovery, while TTX and nitrendipine accelerated it. These findings show that neuronal death resulting from an extraneous excitation (excitotoxicity) can be analyzed in vitro. Furthermore, substantial support has been provided to the hypothesis that excitotoxicity has an underlying mechanism, an excess loading of Ca2+ in neuronal cytoplasm.
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