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The Neck Disability Index (NDI) is one of the most widely used questionnaires for neck pain. The purpose of this study was to validate the Japanese NDI.We performed two surveys with an 8-week interval in 130 patients with neck pain, radiculopathy and myelopathy. We asked patients to answer two versions of the Japanese NDI: the original NDI, which had been completed by a forward-backward translation procedure, and the modified NDI, which has the phrase "because of neck pain" to the phase "because of neck pain or numbness in the arm." The other parameters examined were the strength of pain and numbness, the Japanese Orthopaedic Association Cervical Myelopathy Evaluation Questionnaire, the Hospital Anxiety and Depression Scale, and Short Form 36. Attending surgeons judged the symptom severity. Patients were asked to report the patient global impression of change (PGIC) at the second survey. The internal consistency, criterion-related and discriminative validity, and reliability were evaluated.The original NDI and the modified NDI were 26.9 ± 17.1 and 29.9 ± 15.5, respectively. The Cronbach α values of the original NDI and the modified NDI were 0.92 and 0.89, respectively. Both versions of the NDI had good to excellent correlative coefficients with the related domains. The modified NDI had a higher validity for numbness and mental health-related QOL. The symptom severity was significantly correlated with the modified NDI. The intraclass correlation coefficients of the two surveys of the modified and original NDI were comparable. The effect sizes of the modified and the original NDI were 0.64 and 0.55, respectively. Spearman's ρ between the change of the NDI and the PGIC was 0.47 in the original NDI and 0.59 in the modified NDI.We demonstrated the validity, reliability and responsiveness of the Japanese NDI. The modified NDI was more strongly correlated with numbness and mental health-related QOL.

Elderly patients with osteoporotic vertebral fractures often experience severe pain that reduces their quality of life (QOL). Calcitonin, a bone resorption inhibitor, has been reported to alleviate pain in such patients; however, few clinical studies have demonstrated this effect. The objective of this study was to compare changes in pain scores, activities of daily living (ADL), QOL, bone resorption, bone mineral density (BMD), and fracture healing among patients with new vertebral fractures who received different treatment modalities. We conducted an open-label, multicenter, randomized, parallel control group study comprising 107 female patients ≥55 years old with acute back pain from vertebral fracture. All subjects received either intramuscular injections of elcatonin, a derivative of calcitonin, or an oral nonsteroidal antiinflammatory drug (NSAID) combined with an active vitamin D3 (VD3) analogue for 6 months. The pain was assessed using a visual analogue scale, and ADL and QOL were assessed using questionnaires. BMD was measured using dual-energy X-ray absorptiometry. A two-tailed significance level of 5% was used. The elcatonin IM group had significantly higher QOL score at 2 weeks and later, and significantly lower VAS and ADL scores than those in the NSAID + VD3 group at 1 month and later. The elcatonin IM group had significantly reduced TRACP-5b levels compared with those in the NSAID + VD3 group at 3 months and later and significantly higher percent changes in BMD than the NSAID + VD3 group. These results suggest that elcatonin significantly alleviated pain, inhibited bone resorption, and improved ADL, QOL, and BMD compared with NSAID + VD3.

Study Design. A retrospective study. Objectives. To evaluate clinical outcomes of palliative spinal reconstruction using cervical pedicle screws in metastatic spine tumors. Summary of Background Data. No study to date has investigated the effectiveness of cervical pedicle screw fixation in metastatic lesions of the spine. Methods. A total of 32 patients with metastatic spine tumors who underwent reconstructive surgery using cervical pedicle screws were reviewed. Four patients presented upper cervical lesions and 28 patients had subaxial lesions. All patients had intractable pain, 29 presented myelopathy, and 18 patients were nonambulatory. Combined anterior column reconstruction was considered in cases of life expectancy more than 2 years and anterior spinal cord compression that could not be solved by posterior decompression and kyphosis correction. Posterior fixation alone was performed in 25 patients, and posterior fixation combined with anterior column reconstruction was performed in 7 patients. Results. The average postoperative survival period was 12.2 months. Neck pain was improved in all cases. Twenty-four (83%) of the 29 patients with spinal cord lesions presented neurologic improvement. Of 18 patients who were not ambulatory, 16 patients (89%) became ambulatory. Pain relief, neurologic function, and spinal stability were maintained throughout the survival period in 30 of 32 patients (94%). Conclusion. Spinal reconstruction using cervical pedicle screws improved spinal stability, pain, and neurologic function. These improvements were maintained throughout the survival period in 94% of the patients. Anterior column reconstruction could be avoided in 78% of the patients in spite of damaged anterior column.

An analysis was made of factors related to death from coronary heart disease (CHD) and cerebrovascular disease (CVD) in diabetic patients. The study included 1, 939 patients (the mean age at entry was 52.8±11.1 years), 1, 200 males and 739 females, with type 2 diabetes mellitus. These patients entered the study between 1960 and 1979 and were followed until the end of 1993. The mean observation perrrriod was 14.9±6.6 years. At the end of the follow-up, 1, 000 patients (51.6%) were alive, 880 (45.4%) had died and 59 (3.0%) had been lost to follow-up. Among the deceased patients, 111 had died of CHD and 128 of CVD. The relationship of risk factors to death from CHD or CVD was analyzed in terms of the mortality rate per 1, 000 person-year and odds ratios (relative risks), as well as multiple logistic regression method. In our univariate analysis, we found that deaths from CHD were related to fasting plasma glucose level, blood pressure, ischemic ECG changes, serum cholesterol level, retinopathy, proteinuria and therapeutic regimen. Deaths from CVD were related to hypertension, proteinuria and therapeutic regimen. However, in subsequent multiple logistic analysis, only systolic blood pressure, ischemic changes in electrocardiogram (ECG) findings, serum cholesterol level and retinopathy remained significant with respect to mortality from CHD, while hypertension and fasting plasma glucose level were significant with respect to CVD, in addition to age. We found a much lower mortality from CHD, even in our diabetic subjects, than has been found in Western countries. Moreover, there seemed to be a substantial difference in terms of risk factors between mortality from CHD and from CVD.

Abstract —Adiponectin is a novel, adipose-specific protein abundantly present in the circulation, and it has antiatherogenic properties. We analyzed the plasma adiponectin concentrations in age- and body mass index (BMI)–matched nondiabetic and type 2 diabetic subjects with and without coronary artery disease (CAD). Plasma levels of adiponectin in the diabetic subjects without CAD were lower than those in nondiabetic subjects (6.6±0.4 versus 7.9±0.5 μg/mL in men, 7.6±0.7 versus 11.7±1.0 μg/mL in women; P P r =−0.18, P r =−0.26, P

Epidural hematoma associated with osteoporotic vertebral collapse has not been reported yet in the literature. We report a case of myelopathy caused by chronic epidural hematoma associated with L1 osteoporotic vertebral collapse and review the relevant literature.

A 15 year follow-up study of diabetic patients was performed in Osaka, Japan. The subjects studied were 1939 patients with non-insulin dependent diabetes mellitus (NIDDM), of whom 1000 (51.5%) were alive, 880 (45.4%) had died and 59 (3.0%) were untraceable at the end of 1993. The mortality rate per 1000 person-years of the subjects increased from 28.94 in 1960-1984 to 35.74 in 1985-1993, but the ratio of numbers of observed to expected deaths (O/E ratio) declined from 1.77 to 1.52 for the corresponding periods, suggesting an improvement in the prognosis for diabetic patients, with the exception of patients 65 years or over at the time of entry. Cerebro-cardiovascular and renal diseases were major causes of death, accounting for 48.4% of all deaths. In particular, disease of the heart was the cause of death in 20.5% of all deaths, cerebrovascular disease in 14.5% and renal disease in 12.0%. The O/E ratio was 11.30 for renal disease, which was remarkably high. The O/E ratios were 1.48 for malignant neoplasms, 3.02 for cancer of the liver and 2.15 for cancer of the pancreas. In the subjects less than 65 years of age at entry, a significant decrease in the O/E ratio for overall deaths, malignant neoplasms, disease of the heart, cerebrovascular disease and renal disease was observed, but no notable difference in the O/E ratio for ischemic heart disease was found between the periods 1960-1984 and 1985-1993. By contrast, in the case of subjects 65 years or more at entry, the O/E ratios for overall deaths, malignant neoplasms, disease of the heart, ischemic heart disease and cerebrovascular disease increased markedly in the later period, while there was a considerable decline in renal disease indicated during this period. The analysis suggested a structural change in causes of death of Japanese diabetic patients in recent years, with a relative increase in ischemic heart disease and a relative decrease in renal disease.

Study design Pathologic features of hemodialysis-associated spinal disorders were evaluated using preoperative radiographic images and histologic findings of the spinal lesions resected during surgery. Objectives To investigate the pathology of hemodialysis-related spinal disorders and to determine the role of amyloidosis in the establishment of severe destruction of the spine. Summary of background data The pathologic events leading to hemodialysis-associated spinal disorders are poorly understood. The distribution of amyloid deposits in the spine also has not been clarified. Methods Twenty patients with hemodialysis-associated spinal disorders were investigated regarding pathologic features of neural compression and spinal destruction. Preoperative radiographic images such as plain radiography, tomography, computed tomography, magnetic resonance imaging, and scintigraphy were assessed for the existence of an intracanal mass, hypertrophy of the ligamentum flavum, and destructive changes of the spinal components. Histologic examination also was conducted by light microscopy and scanning electron microscopy to determine the distribution pattern of amyloid deposits in the spinal components. Results Six patients with no destructive changes in the spine showed spinal canal stenosis. In the cervical spine, a main factor associated with spinal canal stenosis was the presence of intracanal amyloid deposits in three patients. In the lumbar spine, a main factor associated with spinal canal stenosis was hypertrophied ligamentum flavum in three patients. Destructive changes of the facet joints, intervertebral disc, and vertebral body were seen in the other 14 patients. Amyloid deposits were densely distributed at the enthesis of capsular fibers to the bone and in anular tears in the intervertebral discs. Vertebral end plates were destroyed by penetration of amyloid granulation into the vertebral body. Osteoclast activity in the destroyed vertebral bodies was enhanced, with no evidence of new bone formation. Conclusions Amyloid deposits played an important role in the progression of spinal destruction and severe instability.

Risk factors related to the prognosis of diabetic patients were studied in a follow-up study of 1939 patients with non-insulin-dependent diabetes mellitus (NIDDM) for a mean observation period of 15 years at our institute. Age at entry into the study was the most powerful risk factor related to the survival of diabetic patients in this study. Moreover, the risk of death, computed in relation to baseline factors, was significantly increased in male patients; in patients with fasting plasma glucose (FPG) levels greater than 140 mg/dl, with hypertension, with diabetic retinopathy or with proteinuria; and in patients treated with an oral hypoglycemic agent of insulin at baseline, even after correction for age. The baseline factors were compared between the groups of patients who were alive and who had died at the end of the follow-up study. Greater age at onset of NIDDM and at entry into the study, higher FPG level, higher systolic and diastolic blood pressure, as well as an increase in the proportion of male patients and in patients with ischemic ECG changes, with diabetic retinopathy, with proteinuria, and with treatment with an oral hypoglycemic agent of insulin, were observed in the group of deceased patients. Furthermore, multiple logistic analysis indicated a significant relationship of age at entry, FPG, hypertension, retinopathy, proteinuria and therapeutic regimen to prognosis. We also found that the baseline factors predictive of prognosis were very different in each age group.

To determine the accuracy of the stated causes of death in diabetic patients, we analyzed 503 death certificates of diabetic patients who had been followed up for 9.4 years on average at Osaka Medical Center for Adulthood Diseases and had died during the observation period from 1960 to 1984. Of the certificates examined, only 213 (42.4%) mentioned diabetes, either as the underlying cause or as a contributory condition. The proportion of certificates that mentioned diabetes was related to the underlying cause of death; it was 18.7% for malignant neoplasms, 40.5% for cerebrovascular disease and 46.9% for disease of the heart, while it was 81.8% for renal disease. The proportion was higher for females (48.7%) than for males (39.5%), and a significant difference was observed between the sexes in the proportion in the case of disease of the heart. The proportion was not related to any significant extent to the year of death or the age at death. However, it was related to fasting plasma glucose (FPG) level and type of treatment. It was 37.8% and 54.4% for patients with FPG200 mg/dl and FPGor = 200 mg/dl, respectively, 24.1% for those treated with diet, 51.4% for those treated with oral hypoglycemic agent and 80.7% for those treated with insulin. As a result, it was found that the proportion of death certificates that mentioned diabetes was related to the accompanying complications and the severity of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

The clinical and laboratory findings in 76 patients with isolated corticotropin deficiency (10 of our own and 66 from literature) were analyzed with the following observations. With the exceptions of hyperpigmentation and hyperkalemia, the similarity of symptoms and signs to those of Addison's disease and their reversibility by glucocorticoids indicate that most, but not all, manifestation of isolated corticotropin deficiency is caused by glucocorticoid deficiency. Isolated corticotropin deficiency seems to be of pituitary origin in most patients, as shown by lack of corticotropin response to insulin-induced hypoglycemia, vasopressin, or corticotropin-releasing factor. Secretion of other pituitary hormones is frequently abnormal, which is mostly attributable to glucocorticoid deficiency. Although the pathogenesis of isolated corticotropin deficiency is unknown in most patients, association with other autoimmune endocrinopathies, postpartum onset in women, or serum antipituitary antibodies suggests an autoimmune pathogenesis in some patients. In two of our 10 patients, cancer developed during glucocorticoid treatment. More observations of complications and long-term prognosis following glucocorticoid therapy are needed for optimal clinical decision making. (Arch Intern Med. 1992;152:1705-1712)

Six cases of Cushing's syndrome with adrenocortical tumors which showed a variety of responsiveness to ACTH were investigated in relation to their clinical pictures and laboratory findings. Abnormal responses to ACTH in tumors was analyzed by in vitro experiments with surgically obtained tumor tissues, and the ACTH responsive mechanism of the tumors was discussed. An 8 hour intravenous ACTH infusion test showed that three of these patients were ACTH responsive, and the other three unresponsive. Histological observation of the tumors revealed that ACTH responsive tumors were adenomas and that ACTH unresponsive tumors were "black adenomas" in two and a carcinoma in one. To investigate possible factors which might account for these differences in ACTH responsiveness, tumor specimens of each one of the responsive and unresponsive adenomas, and a carcinoma were subjected to in vitro studies. When incubated with ACTH or cyclic AMP, tissue sections of a responsive adenoma enhanced cortisol secretion, while that of a black adenoma failed to show any change. Steroidogenesis by carcinoma sections were significantly suppressed in the presence of ACTH or cyclic AMP. Cycloheximide abolished a stimulatory effect of ACTH and cyclic AMP on steroidogenesis in a responsive adenoma without affecting its basal secretion of cortisol. Steroidogenesis by unresponsive tumors (an adenoma and a carcinoma) were decreased by cycloheximide. Since the conversion of cholesterol to pregnenolone, the rate limiting step in steroidogenesis, takes place in adrenal mitochondria, the effect of cyclic AMP on pregnenolone formation from 14C-cholesterol by mitochondrial fractions of these tumors was examined. Cyclic AMP stimulated pregnenolone formation by mitochondrial fraction of an ACTH responsive adenoma, while with that of an unresponsive adenoma pregnenolone formation was not affected. Pregnenolone formation by cancer mitochondria was significantly suppressed by cyclic AMP. These results suggest that the unresponsiveness to ACTH of these tumors might be explained by the ineffectiveness of cyclic AMP to stimulate pregnenolone formation by tumor mitochondria, and that the steroidogenic pathway in unresponsive tumors are in an enhanced state even without cyclic AMP. It should be mentioned that all unresponsive adenomas gave a characteristic appearance of a "black adenoma". Histologically, tumors were composed of compact cells with abundant lipofuscin granules. The possible relationship between the ACTH responsiveness of adrenocortical tumors and some clinical pictures caused by them was also noticed. ACTH unresponsive adenomas resulted in shorter duration, severer conditions of the disease and higher 17-ketosteroid excretion than responsive adenomas. The growth of unresponsive tumors seemed faster than that of responsive ones.

A follow-up study of 1939 diabetic patients with a mean observation period of 9.4 years was carried out in Osaka, Japan. The mortality rates per 1000 person-years were 31.35 for males and 21.99 for females, and the ratios of observed to expected number of deaths were 1.69 for males and 1.74 for females, indicating an excess mortality for diabetic patients of both sexes and higher mortality in males than in females in Japan. Factors related to the prognosis of the patients were age, elevated fasting glucose level, lower obesity index, hypertension, diabetic retinopathy, and albuminuria at entry to the study. Insulin treatment was also associated with poor prognosis. Cerebro-cardiovascular and renal disease were the major causes of death in diabetic patients; heart disease killed 19.5%, cerebrovascular disease 16.7% and renal disease 13.1%. The relatively high frequency of renal disease as a cause of death in type 2 diabetes, especially in patients with a lower age of onset, was noteworthy, suggesting some difference in the clinical manifestations of diabetes between Japan and Western countries. Malignant neoplasms accounted for 25% of deaths, and cirrhosis of the liver for 6.4%.

Despite the accumulation of a number of studies, the mechanism of action of ACTH remains to be clarified. Although it is now clear that cyclic AMP acts as a intracellular mediator of ACTH action, the mechanism of its action on the stimulation of steroidogenesis is not known. The present studies were carried out to test the hypothesis that cyclic AMP might act directly on adrenal mitochondrial fraction to stimulate the metabolism of cholesterol to pregnenolone and progesterone, and to determine whether Ca++ might modulate the action of cyclic AMP. Adrenal mitochondria were obtained from male Sprague-Dawley rats pretreated with dexamethasone. Steroidogenesis by the mitochondrial fraction from cholesterol-4-14C (0.2-0.25 muCi, 3.6-4.5 mmumole/sample) were measured in a system containing 20 mM tris-HCl buffer (pH 7.4), 11.5 mM NaCl, 15.4 mM KCl, 70 mM sucrose, 10 mM sodium succinate and mitochondrial fraction (0.16-0.22 mg protein/sample). Incubations were performed at 37 degrees C, with shaking, in the presence or absence of cyclic AMP, cyclic GMP and cycloheximide. After incubation, the medium was extracted with chloroform, and the extracts were analyzed by thin-layer chromatography. And the radioactivity of the separated steroids was measured. The products from cholesterol-4-14C were mainly pregnenolone and progesterone, and the other products were almost negligible. Cyclic AMP effected the formation of pregnenolone and progesterone by mitochondria. Cyclic AMP exerted its effect even at low concentrations (5 X 10(-6) approximately 5 X 10(-5)M), which was presumably near the intracellular level. On the other hand, cyclic GMP (5 X 10(-5) M) failed to enhance steroidogenesis. The effect of Ca++ on the action of various concentrations (5 X 10(-6) approximately 3 X 10(-3) M) of cyclic AMP was also clearly demonstrated. Addition of Ca++ (1 mM) to the incubation medium intensified the stimulatory effect of cyclic AMP in each concentration. And in the presence of Ca++, the most effective level of cyclic AMP was shifted from 5 X 10(-4) approximately 3 X 10(-3)M to the lower concentration (5 X 10(-5)M). In addition, cyclic AMP action was modified by the changes in the concentration of Ca++ in the medium. At concentration of 10(-6) M of Ca++, steroid formation of mitochondria was maximally activated by cyclic AMP. These observations suggest that cyclic AMP enhances steroidogenesis by acting directly on adrenal mitochondria to stimulate pregnenolone and progesterone formation from cholesterol, and that Ca++ plays a significant role in its action.