Kazuyoshi Yamazaki

Teine Keijinkai Hospital, Sapporo, Hokkaido, Japan

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Publications (9)8.68 Total impact

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    ABSTRACT: OBJECT 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. METHODS 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. RESULTS 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). CONCLUSIONS 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.
    Journal of neurosurgery. Spine 10/2015; DOI:10.3171/2015.1.SPINE14173 · 2.38 Impact Factor
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    ABSTRACT: Cerebellopontine angle tumors might occasionally provoke trigeminal neuralgia but are usually large enough to be diagnosed radiographically. We present a case of trigeminal neuralgia caused by a very small meningioma covering the suprameatal tubercle that displayed hyperostosis at the entrance of Meckel's cave and was not obvious on routine magnetic resonance (MR) images. A 72-year-old woman with intractable trigeminal neuralgia in the left V3 territory was referred to our institution. Preoperative imaging studies revealed that the left trigeminal nerve was medially distorted at the entrance of Meckel's cave by a laterally seated bone bulge covered by a minute enhanced lesion. Trigeminal nerve decompression surgery was performed via a retrosigmoid intradural suprameatal approach. We found a small meningioma that had compressed and flattened the trigeminal nerve root at the entrance of Meckel's cave, which was grossly and totally removed by suprameatal tubercle resection. There was no vascular compression of the trigeminal nerve root. The trigeminal neuralgia ceased completely after the operation. Accurate preoperative determination of the causative pathologies is essential to achieve adequate surgical results after microvascular decompression for neurovascular compression syndrome. Because conventional MR sequences are inadequate for the precise interpretation of complex neurovascular anatomy in the cerebellopontine angle and such small tumors can be overlooked on routine MR studies, high-resolution thin-slice MR examinations and careful radiological interpretations are required for correct diagnosis and treatment.
    Case Reports in Neurology 08/2015; 7(2):167-172. DOI:10.1159/000438856
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    ABSTRACT: Peroneal nerve entrapment neuropathy (PNEN) is one cause of numbness and pain in the lateral lower thigh and instep, and of motor weakness of the extensors of the toes and ankle. We report a less invasive surgical procedure performed under local anesthesia to treat PNEN and our preliminary outcomes. We treated 22 patients (33 legs), 7 men and 15 women, whose average age was 66 years. The mean postoperative follow-up period was 40 months. All patients complained of pain or paresthesia of the lateral aspect of affected lower thigh and instep; all manifested a Tinel-like sign at the entrapment point. As all had undergone unsuccessful conservative treatment, we performed microsurgical decompression under local anesthesia. Of 19 patients who had undergone lumbar spinal surgery (LSS), 9 suffered residual symptoms attributable to PNEN. While complete symptom abatement was obtained in the other 10 they later developed PNEN-induced new symptoms. Motor weakness of the extensors of the toes and ankle [manual muscle testing (MMT) 4/5] was observed preoperatively in 8 patients; it was relieved by microsurgical decompression. Based on self-assessments, all 22 patients were satisfied with the results of surgery. PNEN should be considered as a possible differential diagnosis in patients with L5 neuropathy due to lumbar degenerative disease, and as a causative factor of residual symptoms after LSS. PNEN can be successfully addressed by less-invasive surgery performed under local anesthesia.
    Neurologia medico-chirurgica 07/2015; 55(8). DOI:10.2176/nmc.oa.2014-0454 · 0.72 Impact Factor
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    ABSTRACT: Noncontrast-enhanced time-resolved four-dimensional magnetic resonance angiography using an arterial spin labeling technique (ASL-4D MRA) is emerging as a next generation angiography for the management of neurovascular diseases. This study evaluated the feasibility of ASL-4D MRA for the diagnosis of Moyamoya disease (MMD) and MMD staging by using digital subtraction angiography (DSA) and time-of-flight MRA (TOF MRA) as current standards. Eleven consecutive non-operated patients who underwent DSA for the diagnosis of MMD were recruited. Two independent observers evaluated the three tests. The data were analyzed for inter-observer and inter-modality agreements on MMD stage. Nine of 22 hemispheres underwent surgical revascularization and ASL-4D MRA was repeated postoperatively. Time-resolved inflow of blood through the cerebral vessels, including moyamoya vessels, was visualized in all the 22 non-operated hemispheres. MMD stages assessed by DSA and ASL-4D MRA were completely matched in 18 hemispheres, with a significant positive correlation between these modalities (r=0.93, P<0.001). Inter-observer agreement with ASL-4D MRA (κ=0.91±0.04, P<0.001) and inter-modality agreement between ASL-4D MRA and DSA (κ=0.93±0.04, P<0.001) were both excellent. MMD stages assessed by ASL-4D MRA have also a significant positive correlation with those assessed by TOF MRA (r=0.68, P=0.004). Repeated ASL-4D MRA clearly demonstrated the bypassed arteries and changes in the dynamic flow patterns of cerebral arteries in all the nine hemispheres after surgical revascularization. Of these, postoperative focal hyperperfusion was detected by single photon emission tomography in 7 hemispheres. In five of the seven hemispheres (71%) with postoperative hyperperfusion, ASL-4D MRA demonstrated focal hyperintense signals in the bypassed arteries, although TOF MRA did not. Noninvasive ASL-4D MRA is feasible for the diagnosis of MMD staging. This next generation angiography may be useful for monitoring disease evolution and treatment response in cerebral arteries after revascularization surgery in MMD. Copyright © 2015 Elsevier B.V. All rights reserved.
    Clinical neurology and neurosurgery 07/2015; 137:105-111. DOI:10.1016/j.clineuro.2015.07.003 · 1.13 Impact Factor
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    ABSTRACT: Peroneal nerve entrapment neuropathy(PEN)is generally known as a drop foot with sensory disturbance. However, some patients experience numbness and pain in the affected area without severe paresis due to PEN. We report the clinical features and our surgical results of PEN cases. We encountered 17 cases of PEN. The patients were 7 females and 10 males and their ages ranged from 30 to 78 years(average 56.1 years). In these cases, conservative therapy was unsuccessful;therefore, we performed surgical treatment for PEN. Among the 17 cases, 4 were of bilateral and 13 were of unilateral PEN. There was no severe paresis, as in drop foot;however, mild paresis(4/5, manual muscle test, MMT)was noted in 15 cases. In all cases, intermittent claudication presented, which ranged from 10 to 800m(average 150m). In 13 cases, radiological abnormality of the lumbar region was noted and 8 cases had a history of lumbar surgery(they had failed back surgery syndrome). In all the cases, we performed neurolysis of the peroneal nerve under local anesthesia;there was no surgical complication. After the surgery, symptoms improved, and the numerical rating of the lower limb improved from 8.6/10 to 0.8/10. Intermittent claudication also improved in all of the cases. We successfully treated 17 cases of PEN, which had lower limb pain without severe paresis, as in drop foot. Our results indicate that PEN should be recognized as a cause of intermittent claudication. Neurolysis for PEN under local anesthesia is less invasive and is useful for the treatment of lower limb pain.
    No shinkei geka. Neurological surgery 04/2015; 43(4):309-316. DOI:10.11477/mf.1436203012 · 0.13 Impact Factor
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    ABSTRACT: The number of patients with a ventricular assist device(VAD)will increase with the spread of heart transplantation in Japan. On the other hand, it is likely that VADs could cause cerebral embolism. However, there are few reports about endovascular therapy for intracranial embolic infarction from VAD. The authors report successful acute endovascular therapy for cerebral embolism. A 19-year-old woman with a VAD who received anti-coagulant treatment by warfarin sodium presented disturbance of consciousness and right hemiparesis. CT scan showed early CT sign in the left middle cerebral artery(MCA)area. 3D-CTA demonstrated occlusion of the left MCA and basilar artery(BA). We first performed endovascular recanalization in the left MCA, because IV tPA was ineligible. The left MCA was recanalized with TICI 2b perfusion and her symptoms were significantly improved. The treatment of the VAD patient reveals important issues. First, the femoral puncture requires ultrasound due to pulseless femoral artery. Second, the access route is an intact artery because of the anatomy of the VAD. Third, even if the patient has a hemorrhagic complication by intervention, the patient must be kept on anti-coagulant treatment because the VAD requires it. Careful consideration should be given to recanalization of occlusive vessels.
    No shinkei geka. Neurological surgery 11/2014; 42(11):1057-62. DOI:10.11477/mf.1436200033 · 0.13 Impact Factor
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    ABSTRACT: Since the introduction of carotid stenting (CAS), a combined treatment for bilateral lesions using carotid endarterectomy (CEA) and CAS has been developed. However, there has been only 1 report about CEA then CAS. Herein we describe 2 patients with bilateral severe carotid stenosis who were treated by CEA for the symptomatic side and CAS for the contralateral asymptomatic side. A 71-year-old man underwent CEA for the symptomatic side. Although the patient suffered hyperperfusion syndrome after CEA, he recovered fully after 3 weeks of rehabilitation. Two months later, CAS was performed for the asymptomatic side, and he was discharged with no deficit. A 67-year-old man underwent CEA for the symptomatic side. The patient developed no postoperative neurologic deficits except for hoarseness. Four weeks later, CAS was performed for the contralateral asymptomatic side. After the procedure, however, severe hypotension occurred, and treatment by continuous injection of catecholamine was necessary to maintain systematic blood pressure. The patient was ultimately discharged with no deficit. The combined therapy of CAS for the asymptomatic side and then CEA for the symptomatic side has been recommended by several authors. However, one of the problems of this strategy is the higher incidence of postprocedural hemodynamic complications, and hypotension after CAS may be dangerous for the symptomatic hemisphere. We suggest a combined therapy using CEA for the symptomatic side and then CAS for the asymptomatic side can be 1 beneficial treatment option for patients with bilateral carotid stenosis without coronary artery disease.
    Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association 09/2014; 23(10). DOI:10.1016/j.jstrokecerebrovasdis.2014.07.014 · 1.67 Impact Factor
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    ABSTRACT: Object: 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. Methods: 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. Results 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). Conclusions: 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.
    Journal of neurosurgery. Spine 04/2013; 19(1). DOI:10.3171/2013.3.SPINE12420 · 2.38 Impact Factor
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    ABSTRACT: A 74-year-old male complained of lower back pain, paresthesia of the bilateral feet and urinary incontinence. Urinary incontinence manifested at rest and worsened with walking. He had a history of surgery for prostatic cancer. Lumbar magnetic resonance imaging (MRI) demonstrated lumbar canal stenosis at the L4/5 level. The investigations including a cystometrogram manifested an overactive bladder caused by lumbar canal stenosis. His clinical symptoms were unresponsive to conservative treatment and posterior decompression at the L4/5 level was performed surgically to treat lumbar canal stenosis. Postoperatively, his symptoms were relieved. Overactive bladder presenting urinary incontinence that deteriorates with walking due to lumbar canal stenosis is suspected of being caused by circulatory disturbance of the cauda equine or conus medullaris. Emergency treatment including surgery is required for urinary retention in patients with lumbar canal stenosis; however, some degree of urinary disturbance may persist even after prompt and adequate surgery. Overactive bladder such as the present case should be considered as a possible symptom of lumbar canal stenosis, and surgical treatment for lumbar canal stenosis may be considered in the 'overactive bladder' stage before urinary retention begins, if the patient does not respond to conservative treatment.
    No shinkei geka. Neurological surgery 10/2011; 39(10):983-8. · 0.13 Impact Factor