Reliability Test of Korean Version of Berg Balance Scale

OBJECTIVE: The purpose of this study is to translate the Berg Balance Scale (BBS) to the Korean version (K-BBS) and to evaluate its reliability. METHOD: With the agreement of Katherine Berg, the original editor of the BBS, two physiatrists and three physical therapists had translated the English version of BBS into Korean (K-BBS). This was back-translated into English by a Korean-American physiatrist fluent in English. After a 2- hour K-BBS education course, the video recorded K-BBS of 18 stroke patients were reviewed by nine examiners (four physiatrists and five physical therapists) to assess the inter- rater and the intra-rater reliability. Kendall's correlation coefficient and Pearson's correlation coefficient were computed to assess the intra-rater and test-retest reliability, respectively. RESULTS: The inter-rater reliability was 0.97 at 2 separate evaluations with an interval of 10 days (p<0.05). The intra- rater reliability was 0.95 (p<0.05) in the physiatrist group and 0.97 (p<0.05) in the physical therapist group. CONCLUSION: We recommend that the Korean version of the Berg balance scale is a reliable instrument to be used in balance assessment of stroke patients.

Upregulation of Glutamate Receptors in Rat Cerebral Cortex with Neuronal Migration Disorders

Neuronal migration disorders (NMDs) constitute the main pathologic substrate of medically intractable epilepsy in human. This study is designed to investigate the changes in expression of glutamate receptor subtypes on radiation-induced NMD in rats. The lesion was produced by intrauterine irradiation (240 cGy) on E17 rats, and then 10 weeks old rats were used for the study. The pathologic and immunohistochemical findings for glutamate receptor subunit proteins on NMD cortex were correlated with development of behavioral seizures and EEG abnormality. Spontaneous seizures uncommonly occurred in NMD rats (5%); however, clinical stages of seizures were significantly increased in NMD rats by an administration of kainic acid. Brains taken from irradiated rats revealed gross and histopathologic features of NMD. Focal cortical dysplasia was identified by histopathology and immunohistochemistry with neurofilament protein (NF-M/H). Significantly strong NR1 and NR2A/B immunoreactivities were demonstrated in cytomegalic and heterotopic neurons of NMD rats. The results of the present study indicate that epileptogenesis of NMD might be caused by upregulation of glutamate receptor expression in dysplastic neurons of the rat cerebral cortex with NMDs.

Statistical Analysis for Prognosis of CNS Tumor According to the New WHO Classification

The authors have reviewed and followed up 664 operated patients at the Department of Neurosurgery, Chonnam University Hospital from January 1984 to December 1993 according to the new WHO classification of CNS neoplasms. The sex ratio(M:F) was 1:1.1 and the age distribution showed a peak between 51 to 60 years. Common tumors were glioma(28%), meningioma(21%), pituitary adenoma(15%), schwannoma(9%), metastatic tumor(8%) in the decreasing order of frequency. The most common tumor was glioblastoma(33%) within the category of gliomas. Incidence of pediatric brain tumors was about 12% among the all intracranial tumors. Survival curves for astrocytomas, pilocytic astrocytomas, anaplastic astrocytomas, glioblastoma and metastatic tumors were obtained from follow-up studies of the brain tumor patients regardless of therapeutic mode.

Effects of Experimental Ischemia on Expression of Protein Kinase C Isozyme in Rat Neocortex

Ischemia leads to a complex sequence of events culmination in the loss of functional integrity of the nervous system and, ultimately, in neuronal cell death. Intracellular accumulation of calcium ions following ischemia may alter protein kinase C(PKC) activity. But nature of change of the PKC activity depending on duration and degree of ischemia is not well understood. To understand the effect of the experimental focal ischemia on expression of PKC isozyme, we investigated the expression of PKC gamma, beta, alpha immunocytochemically and activities of cytochrome oxidase(CO) histochemically in focal ischemic brain of the rat. Two groups of focal ischemic infarction were produced in two groups of Sprague Dawley rats(200-300 gm) : Group I, Clip compression of left middle cerebral artery(MCA) for 10min and releases and sacrificed 48 hr later ; Group II, Electric coagulation of left MCA and killed 2-24 hr later. In the group I, CO activity and immunoreactivity(IR) for PKC gamma and beta were decreased generally in the left MCA territory, especially in layers II through IV of ischemic cortex. In the group II, decrease of CO activities and marked increase of three PKC isozyme IRs were noted in the layers I through IV. The isozymes displayed different localization in the control cortex, but the IRs of three isozymes markedly increased in the ischmic region, so that the difference among IR patterns disappeared. Although vacuolation and decrease of number of IR neuron were noted, there were remaining IR pyramidal neurons arounf vacuole in layers IV/V showing dense immuostaining in the cell body and apical dendrite. These results indicate that 10min acute ischemia inhibits activity of PKC gamma and beta and that prolonged ischemia longer than 2hr induces the expression of three PKC isozymes. Inhibition and possible induction of PKC are proposed to represent a critical step during ischemic neuronal injury.