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Shunsuke Nomura, Akitsugu Kawashima, Hiroyuki Akagawa, and Takakazu Kawamata

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Kimihiko Sawakami, Kei Watanabe, Kazuhiro Hasegawa, Noriaki Yamamoto, Taketoshi Shimakura, Masayuki Ohashi, Hirokazu Shoji, Tatsuki Mizouchi, Yuki Tanaka, Hiroyuki Segawa, Seiichi Ishikawa, Toru Hirano, Hiroyuki Kawashima, Naoto Endo, and Hideaki E. Takahashi


Teriparatide (TPTD) is a potent promoter of early-stage osteogenesis and may be a useful adjuvant therapy to reduce complications related to bone fragility in spinal surgery patients with osteoporosis. However, effective neoadjuvant TPTD therapy regimens remain poorly understood. This study aimed to examine the effect of preoperative TPTD administration on cancellous bone with bone histomorphometry and to clarify the timing of preoperative TPTD administration for patients with spinal fusion and osteoporosis.


In this longitudinal multicenter study, 57 patients with spinal fusion and osteoporosis, who consented to undergo iliac biopsy, were allocated to the following treatment groups: neoadjuvant TPTD therapy group (n = 42) and no neoadjuvant therapy (NTC) group (n = 15). Patients in the TPTD group were categorized into subgroups on the basis of duration of preoperative TPTD administration, as follows: 1 month (n = 9), 2 months (n = 8), 3 months (n = 9), 4 months (n = 7), and 6 months (n = 9). All patient samples were preoperatively double labeled with tetracycline, and iliac biopsies were performed during spinal fusion surgery. Histomorphometric analyses were performed on nondecalcified, thin-sliced specimens. Specimens were classified on the basis of TPTD administration duration and subsequently compared with those of the NTC group. Postoperative complications and Oswestry Disability Index scores were evaluated at 1 and 2 years after surgery.


There were no demographic differences between groups. Mineralizing surface/bone surface, a key parameter of dynamic bone formation, started to increase after 1 month of TPTD administration; this increase became significant after 3 months of administration and peaked at 4 months, with a 6-fold increase relative to that of the NTC group. The patients who received preoperative TPTD for 3 months or more had superior clinical results in terms of the osteoporotic complication rate and Oswestry Disability Index scores, except for bisphosphonate-pretreated patients.


When considering neoadjuvant TPTD therapy, the authors recommend at least 3 months of preoperative administration to provide a more substantial anabolic effect from the early postoperative stage.

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Takanori Nozawa, Kouichirou Okamoto, Shinji Nakazato, Kunio Motohashi, Tomoaki Suzuki, Kotaro Morita, Hideki Tashi, Kei Watanabe, Hitoshi Hasegawa, Masato Watanabe, Hiroyuki Kawashima, and Yukihiko Fujii


Bow hunter’s syndrome or stroke (BHS) is characterized by rotational vertebrobasilar insufficiency elicited by rotation of the neck. It is caused by dynamic and reversible occlusion of the vertebral artery (VA). Reversible symptoms of rotational vertebrobasilar insufficiency are described as bow hunter’s syndrome, although brain infarction is rarely reported as bow hunter’s stroke.


A 70-year-old man experienced repeated cerebellar infarctions three times in the posterior inferior cerebellar artery (PICA) distribution of the nondominant right VA connecting the basilar artery. The onset of symptoms indicating cerebellar infarcts and the patient’s head position changes were unrelated. Dynamic digital angiography (DA) revealed that the nondominant right VA was occluded by an osteophyte from the C4 vertebral body, and the right PICA branches were shown to be passing through the distal right VA from the left VA. These findings were observed when the patient’s head was tilted to the right. An arterio-arterial embolic mechanism was suggested as the cause of repeated cerebellar infarctions.


Transient nondominant VA occlusion has been rarely reported as a cause of BHS when the head is tilted. To confirm the diagnosis of BHS, additional head tilt is recommended when performing dynamic DA in patients with a cervical osteophyte.

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Atsushi Ogata, Masatou Kawashima, Tomihiro Wakamiya, Masashi Nishihara, Jun Masuoka, Yukiko Nakahara, Ryo Ebashi, Kohei Inoue, Yukinori Takase, Hiroyuki Irie, and Tatsuya Abe


Hypoxia induces angiogenesis and plays a major role in the progression of carotid plaques. During carotid intervention, plaques with high-intensity signals on time-of-flight (TOF) magnetic resonance angiography (MRA) often cause ischemic stroke and embolic complications. However, the role of intraplaque hypoxia before carotid endarterectomy (CEA) and carotid artery stenting is not presently understood. In this study the authors aimed to investigate the relationship between intraplaque hypoxia and MRA findings.


Nineteen consecutive patients with 20 carotid artery stenoses who underwent CEA at Saga University Hospital between August 2008 and December 2014 were enrolled in the study. The expressions of hypoxia-inducible transcription factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) were analyzed by immunohistochemical analysis. In addition, the relationship between the findings on TOF MRA and pathology for the carotid plaques was analyzed.


High-intensity plaques on TOF MRA showed higher expression levels of HIF-1α (p = 0.015) and VEGF (p = 0.007) compared with isointensity plaques. The rate of intraplaque hemorrhage (IPH) on TOF MRA was also significantly higher in the high-intensity plaques than in the isointensity plaques (p = 0.024). Finally, the mean number of neovessels was significantly higher in those without plaque hemorrhage than in those with plaque hemorrhage (p = 0.010).


Plaques with high-intensity signals on TOF MRA were associated with IPH and evidence of intraplaque hypoxia. This fact may represent an opportunity to establish novel therapeutic agents targeting intraplaque hypoxia.