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Toru Hayakawa, Kazuyoshi Morimoto, Yukitaka Ushio, Takesada Mori, Toshiki Yoshimine, Akio Myoga and Heitaro Mogami

✓ Levels of astroprotein (an astrocyte-specific protein found in the cerebrum) were measured by radioimmunoassay in the cerebrospinal fluid (CSF) of 120 patients with intracranial diseases and eight control subjects. The astroprotein level was elevated (above 25 ng/ml) in 13 of 30 cases (43.3%) of glial tumors, nine of 57 cases (15.8%) of nongliomatous intracranial tumors, seven of 33 cases (21.2%) of non-neoplastic intracranial diseases, but in none of the eight control cases. In glioblastoma patients, CSF astroprotein was elevated in eight of 12 cases (66.7%), in three of them to a remarkable degree (above 500 ng/ml). The possible role of this test is briefly discussed, and the mechanism of increase of the astroprotein levels in the CSF considered.

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Toshiki Yoshimine, Kazuyoshi Morimoto, Joan M. Brengman, Henry A. Homburger, Heitaro Mogami and Takehiko Yanagihara

✓ Immunohistochemical methods for the determination of tubulin, creatine kinase BB-isoenzyme, and astroprotein-glial fibrillary acidic protein were used to investigate recovery of the ischemic lesion after temporary occlusion of a common carotid artery in the gerbil and the evolution of the postischemic lesion following reperfusion. One group of gerbils was followed from 15 minutes to one month after an ischemic period of 30 minutes, and another group was examined after 7 days following an ischemic period of 5 to 30 minutes. It was found that the postischemic lesion, visualized as loss of the immunohistochemical reaction for tubulin and creatine kinase BB-isoenzyme, evolved within 60 minutes after reperfusion in the hippocampus and cerebral cortex and within 3 hours in the caudoputamen and thalamus. Resolution of the preexisting ischemic lesion was possible only after an ischemic period of less than 10 minutes in the cerebral cortex and caudoputamen and less than 15 minutes in the thalamus. In the CA1-CA2 region of the hippocampus, the ischemic lesion already existed after an ischemic period of 5 minutes and was mostly irreversible. The immunohistochemical method of testing for different cellular and subcellular components was very useful for investigation of cerebral ischemia and may also be advantageous for investigation of other pathophysiological conditions of the nervous system.

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Kazuyoshi Morimoto and Heitaro Mogami

✓ The authors describe the growth pattern of a subependymal giant-cell astrocytoma associated with tuberous sclerosis, which was documented by sequential computerized tomography scans over 7 years. The diagnosis and treatment of this tumor are discussed, and the pertinent literature is reviewed.

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Mami Yamasaki, Norio Arita, Shoju Hiraga, Shuichi Izumoto, Kazuyoshi Morimoto, Susumu Nakatani, Ken Fujitani, Noriko Sato and Toru Hayakawa

✓ To clarify the clinicopathological features of X-linked hydrocephalus, the authors studied 30 affected males from 15 families. In utero ultrasonography, performed at 21 to 40 weeks of gestation, revealed 18 fetuses with hydrocephalus. Computerized tomography (CT) revealed bilateral enlargement of the lateral ventricle with preponderant dilation of the posterior horn. In five patients with complete magnetic resonance (MR) imaging data, the most specific finding was localized atrophy of the anterior vermian lobe. Other MR imaging findings included a large massa intermedia, flat corpora quadrigemina, a small brainstem, and diffuse hypoplasia of the cerebral white matter. In all cases, the corpus callosum was hypoplastic or aplastic. The aqueduct was patent in four of five cases. Asymmetrical reduction of the ventricular size and a rippled ventricular wall were characteristic postshunt CT findings. Progressive macrocephaly and symptoms due to increased intracranial pressure were ameliorated by the shunt; however, the neurological outcome was not improved by shunting. Of 14 patients who lived to be between 2 and 18 years of age, all are retarded. These results indicate that X-linked hydrocephalus is not a disease of simple ventriculomegaly due to aqueduct stenosis alone but involves other complicated central nervous system anomalies.

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Kazuyoshi Morimoto, Osamu Takemoto and Akatsuki Wakayama

✓ The authors reviewed 63 cases of patients with spinal lipomas who had undergone surgical untethering in childhood and found two infants in whom multiplication of the lipomas occurred within 1 year postoperatively. More importantly, the lipomas dramatically increased in size during infancy. In each case, the pathological findings on reoperation were identical to those in the first surgery. Subsequent imaging revealed no change in size of the lesions by 10 and 7 years after reoperation, respectively. This potential for growth of the lipomas should be kept in mind in infants with spinal lipomas who should undergo follow-up neuroimaging.

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Daijiro Morimoto, Toyohiko Isu, Kyongsong Kim, Tetsuaki Imai, Kazuyoshi Yamazaki, Ryoji Matsumoto and Masanori Isobe


Superior cluneal nerve (SCN) entrapment neuropathy is a poorly understood clinical entity that can produce low-back pain. The authors report a less-invasive surgical treatment for SCN entrapment neuropathy that can be performed with local anesthesia.


From November 2010 through November 2011, the authors performed surgery in 34 patients (age range 18–83 years; mean 64 years) with SCN entrapment neuropathy. The entrapment was unilateral in 13 patients and bilateral in 21. The mean postoperative follow-up period was 10 months (range 6–18 months). After the site was blocked with local anesthesia, the thoracolumbar fascia of the orifice was dissected with microscissors in a distal-to-rostral direction along the SCN to release the entrapped nerve. Results were evaluated according to Japanese Orthopaedic Association (JOA) and Roland-Morris Disability Questionnaire (RMDQ) scores.


In all 34 patients, the SCN penetrated the orifice of the thoracolumbar fascia and could be released by dissection of the fascia. There were no intraoperative surgery-related complications. For all patients, surgery was effective; JOA and RMDQ scores indicated significant improvement (p < 0.05).


For patients with low-back pain, SCN entrapment neuropathy must be considered as a causative factor. Treatment by less-invasive surgery, with local anesthesia, yielded excellent clinical outcomes.

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Yasuhiro Chiba, Toyohiko Isu, Kyongsong Kim, Naotaka Iwamoto, Daijiro Morimoto, Kazuyoshi Yamazaki, Masaaki Hokari, Masanori Isobe and Mitsuo Kusano


Superior cluneal nerve (SCN) entrapment neuropathy (SCNEN) is a cause of low-back pain (LBP) that can be misdiagnosed as a lumbar spine disorder. The clinical features and etiology of LBP remain poorly understood. In this study, 5 patients with intermittent LBP due to SCNEN who had previously received conservative treatment underwent surgery. The findings are reported and the etiology of LBP is discussed to determine whether it is attributable to SCNEN.


Intermittent LBP is defined as a clinical condition in which pain is induced by standing or walking but is absent at rest. Between April 2012 and March 2013, 5 patients in this study who had intermittent LBP due to SCNEN underwent surgery. The patients included 3 men and 2 women, with a mean age of 66 years. The affected side was unilateral in 2 patients and bilateral in 3 (total sites, 8). The interval from symptom onset to treatment averaged 51.4 months; the mean postoperative follow-up period was 17.6 months. The clinical outcomes were assessed using the numerical rating scale (NRS) for LBP, the Japanese Orthopaedic Association (JOA) scale, and the Roland-Morris Disability Questionnaire (RDQ) preoperatively and at the last follow-up; these data were analyzed statistically.


None of the 5 patients reported LBP at rest. Intermittent LBP involving the iliac crest and buttocks was induced by standing or walking an average of 136 m. In 2 patients with unilateral involvement, LBP was improved only by SCN block. Surgeries were performed on 6 sites in 5 patients because the SCN block was only transiently effective. Patients’ SCNs penetrated the orifice of the thoracolumbar fascia. SCN kinking at the orifice was exacerbated at the lumbar-extension provocation posture, and radiating pain increased upon manual intraoperative compression of the SCN in this posture. After releasing the SCN surgically, disappearance of the pain was intraoperatively confirmed by manual compression of the SCN with the patients in the lumbar-extension posture. Surgery was effective in all 5 patients, and all clinical outcome scores indicated significant improvement (p < 0.05).


To the authors’ knowledge, this is the first report of patients with intermittent LBP due to SCNEN. Clinical and surgical evidence presented suggests that their LBP was exacerbated by lumbar extension and that symptom relief was obtained by SCN block or surgical release of the SCN entrapment. These results suggest that SCNEN should be considered as a causal factor in patients for whom walking elicits LBP.