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Hidenori Inoue, Kazuo Ohmori, Yoshihiro Ishida, Kazuhiro Suzuki, and Tetsuro Takatsu

This study compared the long-term outcome of cervical spondylotic myelopathy (CSM) with that of the ossification of the posterior longitudinal ligament of the cervical spine (OPLL) after suspension laminotomy, which was developed in the authors' clinic. Seventy-six patients who received follow-up care for more than 5 years were available for analysis. The duration of the follow-up period averaged 97.8 months (range 61–160 months). Radiological and neurological analyses were performed in these 76 patients (50 with CSM and 26 with OPLL). There were no differences in sex, age, follow-up period, and preoperative neurological status between the two groups.

In the quantitative study of the dural configuration, 43 patients (86%) with CSM and 17 patients (65.4%) with OPLL attained complete decompression 1 month after surgery. At long-term follow-up review, complete decompression was maintained in 42 patients (84%) with CSM but in only seven patients (26.9%) with OPLL. The neurological evaluation improved markedly at early follow up in both groups but declined insignificantly at the last follow-up review, particularly in the OPLL group. Of 12 patients (24%) with CSM and 10 patients (38.5%) with OPLL whose neurological recovery grades later deteriorated, four (8%) with CSM and nine (34.6%) with OPLL demonstrated reconstriction causing spinal cord compression at long-term follow-up review. For the remaining eight patients (16%) with CSM, who were older than 70 years on average at last follow-up review, no radiological explanation was found. These long-term results indicate that OPLL does not resolve as well as CSM after suspension laminotomy; they both may have late deterioration due to reconstriction that occurs occasionally in CSM and frequently in OPLL.

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Masahiro Funaba, Yasuaki Imajo, Hidenori Suzuki, Norihiro Nishida, Yuji Nagao, Takuya Sakamoto, Kazuhiro Fujimoto, and Takashi Sakai

OBJECTIVE

Neurological and imaging findings play significant roles in the diagnosis of degenerative cervical myelopathy (DCM). Consistency between neurological and imaging findings is important for diagnosing DCM. The reasons why neurological findings exhibit varying sensitivity for DCM and their associations with radiological findings are unclear. This study aimed to identify associations between radiological parameters and neurological findings in DCM and elucidate the utility of concordance between imaging and neurological findings for diagnosing DCM.

METHODS

One hundred twenty-one patients with DCM were enrolled. The Japanese Orthopaedic Association (JOA) score, radiological parameters, MRI and kinematic CT myelography (CTM) parameters, and the affected spinal level (according to multimodal spinal cord evoked potential examinations) were assessed. Kinematic CTM was conducted with neutral positioning or at maximal extension or flexion of the cervical spine. The cross-sectional area (CSA) of the spinal cord, dynamic change in the CSA, C2–7 range of motion, and C2–7 angle were measured. The associations between radiological parameters and hyperreflexia, the Hoffmann reflex, the Babinski sign, and positional sense were analyzed via multiple logistic regression analysis.

RESULTS

In univariate analyses, the upper- and lower-limb JOA scores were found to be significantly associated with a positive Hoffmann reflex and a positive Babinski sign, respectively. In the multivariate analysis, a positive Hoffmann reflex was associated with a higher MRI grade (p = 0.026, OR 2.23) and a responsible level other than C6–7 (p = 0.0017, OR 0.061). A small CSA during flexion was found to be significantly associated with a positive Babinski sign (p = 0.021, OR 0.90). The presence of ossification of the posterior longitudinal ligament (p = 0.0045, OR 0.31) and a larger C2–7 angle during flexion (p = 0.01, OR 0.89) were significantly associated with abnormal great toe proprioception (GTP).

CONCLUSIONS

This study found that the Hoffmann reflex is associated with chronic and severe spinal cord compression but not the dynamic factors. The Babinski sign is associated with severe spinal cord compression during neck flexion. The GTP is associated with large cervical lordosis. These imaging features can help us understand the characteristics of the neurological findings.

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Yoshinari Nakatsuka, Fumihiro Kawakita, Ryuta Yasuda, Yasuyuki Umeda, Naoki Toma, Hiroshi Sakaida, and Hidenori Suzuki

OBJECTIVE

Chronic hydrocephalus develops in association with the induction of tenascin-C (TNC), a matricellular protein, after aneurysmal subarachnoid hemorrhage (SAH). The aim of this study was to examine if cilostazol, a selective inhibitor of phosphodiesterase Type III, suppresses the development of chronic hydrocephalus by inhibiting TNC induction in aneurysmal SAH patients.

METHODS

The authors retrospectively reviewed the factors influencing the development of chronic shunt-dependent hydrocephalus in 87 patients with Fisher Grade 3 SAH using multivariate logistic regression analyses. Cilostazol (50 or 100 mg administered 2 or 3 times per day) was administered from the day following aneurysmal obliteration according to the preference of the attending neurosurgeon. As a separate study, the effects of different dosages of cilostazol on the serum TNC levels were chronologically examined from Days 1 to 12 in 38 SAH patients with Fisher Grade 3 SAH.

RESULTS

Chronic hydrocephalus occurred in 12 of 36 (33.3%), 5 of 39 (12.8%), and 1 of 12 (8.3%) patients in the 0 mg/day, 100 to 200 mg/day, and 300 mg/day cilostazol groups, respectively. The multivariate analyses showed that older age (OR 1.10, 95% CI 1.13–1.24; p = 0.012), acute hydrocephalus (OR 23.28, 95% CI 1.75–729.83; p = 0.016), and cilostazol (OR 0.23, 95% CI 0.05–0.93; p = 0.038) independently affected the development of chronic hydrocephalus. Higher dosages of cilostazol more effectively suppressed the serum TNC levels through Days 1 to 12 post-SAH.

CONCLUSIONS

Cilostazol may prevent the development of chronic hydrocephalus and reduce shunt surgery, possibly by the inhibition of TNC induction after SAH.

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Tim Lekic, William Rolland, Anatol Manaenko, Paul R. Krafft, Joel E. Kamper, Hidenori Suzuki, Richard E. Hartman, Jiping Tang, and John H. Zhang

Object

Primary pontine hemorrhage (PPH) represents approximately 7% of all intracerebral hemorrhages (ICHs) and is a clinical condition of which little is known. The aim of this study was to characterize the early brain injury, neurobehavioral outcome, and long-term histopathology in a novel preclinical rat model of PPH.

Methods

The authors stereotactically infused collagenase (Type VII) into the ventral pontine tegmentum of the rats, in accordance with the most commonly affected clinical region. Measures of cerebrovascular permeability (brain water content, hemoglobin assay, Evans blue, collagen Type IV, ZO-1, and MMP-2 and MMP-9) and neurological deficit were quantified at 24 hours postinfusion (Experiment 1). Functional outcome was measured over a 30-day period using a vertebrobasilar scale (the modified Voetsch score), open field, wire suspension, beam balance, and inclined-plane tests (Experiment 2). Neurocognitive ability was determined at Week 3 using the rotarod (motor learning), T-maze (working memory), and water maze (spatial learning and memory) (Experiment 3), followed by histopathological analysis 1 week later (Experiment 4).

Results

Stereotactic collagenase infusion caused dose-dependent elevations in hematoma volume, brain edema, neurological deficit, and blood-brain barrier rupture, while physiological variables remained stable. Functional outcomes mostly normalized by Week 3, whereas neurocognitive deficits paralleled the cystic cavitary lesion at 30 days. Obstructive hydrocephalus did not develop despite a clinically relevant 30-day mortality rate (approximately 54%).

Conclusions

These results suggest that the model can mimic several translational aspects of pontine hemorrhage in humans and can be used in the evaluation of potential preclinical therapeutic interventions.

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Masanori Tsuji, Tatsuya Ishikawa, Fujimaro Ishida, Kazuhiro Furukawa, Yoichi Miura, Masato Shiba, Takanori Sano, Hiroshi Tanemura, Yasuyuki Umeda, Shinichi Shimosaka, and Hidenori Suzuki

OBJECT

Histopathological examination has revealed that ruptured cerebral aneurysms have different hemostatic patterns depending on the location of the clot formation. In this study, the authors investigated whether the hemostatic patterns had specific hemodynamic features using computational fluid dynamics (CFD) analysis.

METHODS

Twenty-six ruptured middle cerebral artery aneurysms were evaluated by 3D CT angiography and harvested at the time of clipping. The hemostatic patterns at the rupture points were assessed by means of histopathological examination, and morphological parameters were obtained. Transient analysis was performed, and wall shear stress–related hemodynamic parameters and invariant Q (vortex core region) were calculated. The morphological and hemodynamic parameters were compared among the hemostatic patterns.

RESULTS

Hematoxylin and eosin staining of the aneurysm wall showed 13 inside-pattern, 9 outside-pattern, and 4 other-pattern aneurysms. Three of the 26 aneurysms were excluded from further analysis, because their geometry models could not be generated due to low vascular CT values. Mann-Whitney U-tests showed that lower dome volume (0.04 cm3 vs 0.12 cm3, p = 0.014), gradient oscillatory number (0.0234 vs 0.0289, p = 0.023), invariant Q (−0.801 10−2/sec2 vs −0.124 10−2/sec2, p = 0.045) and higher aneurysm formation indicator (0.986 vs 0.963, p = 0.041) were significantly related to inside-pattern aneurysms when compared with outside-pattern aneurysms.

CONCLUSIONS

Inside-pattern aneurysms may have simpler flow patterns and less flow stagnation than outside-pattern aneurysms. CFD may be useful to characterize the hemostatic pattern of ruptured cerebral aneurysms.

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Masashi Fujimoto, Masato Shiba, Fumihiro Kawakita, Lei Liu, Naoshi Shimojo, Kyoko Imanaka-Yoshida, Toshimichi Yoshida, and Hidenori Suzuki

OBJECT

Tenascin-C (TNC), a matricellular protein, is induced in the brain following subarachnoid hemorrhage (SAH). The authors investigated if TNC causes brain edema and blood-brain barrier (BBB) disruption following experimental SAH.

METHODS

C57BL/6 wild-type (WT) or TNC knockout (TNKO) mice were subjected to SAH by endovascular puncture. Ninety-seven mice were randomly allocated to WT sham-operated (n = 16), TNKO sham-operated (n = 16), WT SAH (n = 34), and TNKO SAH (n = 31) groups. Mice were examined by means of neuroscore and brain water content 24–48 hours post-SAH; and Evans blue dye extravasation and Western blotting of TNC, matrix metalloproteinase (MMP)-9, and zona occludens (ZO)-1 at 24 hours post-SAH. As a separate study, 16 mice were randomized to WT sham-operated, TNKO sham-operated, WT SAH, and TNKO SAH groups (n = 4 in each group), and activation of mitogen-activated protein kinases (MAPKs) was immunohistochemically evaluated at 24 hours post-SAH. Moreover, 40 TNKO mice randomly received an intracerebroventricular injection of TNC or phosphate-buffered saline, and effects of exogenous TNC on brain edema and BBB disruption following SAH were studied.

RESULTS

Deficiency of endogenous TNC prevented neurological impairments, brain edema formation, and BBB disruption following SAH; it was also associated with the inhibition of both MMP-9 induction and ZO-1 degradation. Endogenous TNC deficiency also inhibited post-SAH MAPK activation in brain capillary endothelial cells. Exogenous TNC treatment abolished the neuroprotective effects shown in TNKO mice with SAH.

CONCLUSIONS

Tenascin-C may be an important mediator in the development of brain edema and BBB disruption following SAH, mechanisms for which may involve MAPK-mediated MMP-9 induction and ZO-1 degradation. TNC could be a molecular target against which to develop new therapies for SAH-induced brain injuries.

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Yu-Chi Tsai, Fang-Chen Liu, Chao-Ming Chang, Che-Hsien Chang, Yin-Hsien Liao, Tse-Bing Yang, and Dueng-Yuan Hueng