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Kenichi Sato, Karel G. TerBrugge and Timo Krings

Object

Spinal dural arteriovenous fistulas (SDAVFs) consist of a shunt with converging feeding vessels arising from radiculomeningeal arteries and draining retrogradely via a radicular vein into the perimedullary veins, thereby causing progressive myelopathy due to venous hypertension in the spinal cord. The purpose of this study was to evaluate the hypothesis that the obstruction of radicular venous outlets could be an additional factor inducing symptomatic venous hypertension due to a decreased outflow in SDAVFs.

Methods

The authors compared the clinical and imaging findings in patients with asymptomatic SDAVFs identified incidentally at the upper thoracic region with the findings in symptomatic patients who harbored SDAVFs at the same level.

Results

All symptomatic patients presented with medullary dysfunction. The mean age of patients with asymptomatic SDAVF was 51.5 years, approximately 10 years younger than the patients with symptomatic SDAVF (64.1 years old). Despite the existence of dilated perimedullary vessels in the dorsal side of the spinal cord in all patients, the spinal cord edema seen in symptomatic patients was not detected on the MR images obtained in patients with asymptomatic SDAVF. The spinal angiograms of the asymptomatic patients distinctively demonstrated early radicular venous outflow from affected perimedullary veins to the extradural venous plexus as a potential alternate route for the venous hypertension to be released.

Conclusions

Obstruction of the radicular venous outflow could be an important factor in inducing spinal congestive edema due to venous hypertension, as well as subsequent clinical symptoms of SDAVFs.

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Mitsuo Kaneko, Keisei Tanaka, Tsutomu Shimada, Kengo Sato and Kenichi Uemura

✓ In the past 10 years, the authors performed microsurgical evacuation of hypertensive intracerebral hematoma in 100 cases during the ultra-early stage (within 7 hours) after the apoplectic attack. Operative indications were the presence of obvious hemiplegia and disturbed consciousness (from stupor to semicoma). Functional outcomes at 6 months postoperatively were as follows: 15 patients had returned to a full social life, 35 were capable of self-care at home, 33 required partial care at home, two were bedridden and in a vegetative state, and seven had died.

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Kazuhiko Nishino, Hitoshi Hasegawa, Kenichi Morita, Masafumi Fukuda, Yasushi Ito, Yukihiko Fujii and Mitsuya Sato

OBJECTIVE

Arteriovenous malformations (AVMs) in the cerebellopontine angle cistern (CPAC) are specific lesions that can cause neurovascular compression syndromes as well as intracranial hemorrhage. Although case reports describing the CPAC AVMs, especially those presenting with trigeminal neuralgia (TN), have been accumulating by degrees, the pathophysiology of CPAC AVMs remains obscure. The authors' purpose in the present study was to evaluate the clinical and radiographic features of CPAC AVMs as well as the treatment options.

METHODS

This study defined a CPAC AVM as a small AVM predominantly located in the CPAC with minimal extension into the pial surface of the brainstem and closely associated with cranial nerves. All patients with CPAC AVMs treated in the authors' affiliated hospitals over a 16-year period were retrospectively identified. Clinical charts, imaging studies, and treatment options were evaluated.

RESULTS

Ten patients (6 men and 4 women), ranging in age from 56 to 77 years (mean 65.6 years), were diagnosed with CPAC AVMs according to the authors' definition. Six patients presented with hemorrhage, 3 with TN, and the remaining patient developed a hemorrhage subsequent to TN. Seven AVMs were associated with the trigeminal nerve (Group V), and 3 with the facial-vestibulocochlear nerve complex (Group VII–VIII). All patients in Group VII–VIII presented with the hemorrhage instead of hemifacial spasm. Regarding angioarchitecture, the intrinsic pontine arteries provided the blood supply for all CPAC AVMs in Group V. In addition, 5 of 7 AVMs with hemorrhagic episodes accompanied flow-related aneurysms, although no aneurysm was detected in patients with TN alone. With respect to treatment, all patients with hemorrhagic presentation underwent Gamma Knife surgery (GKS), resulting in favorable outcomes except for 1 patient who experienced rebleeding after GKS, which was caused by the repeated rupture of a feeder aneurysm. The AVMs causing TN were managed with surgery, GKS, or a combination, according to the nidus-nerve relationship. All patients eventually obtained pain relief.

CONCLUSIONS

Clinical symptoms caused by CPAC AVMs occur at an older age compared with AVMs in other locations; CPAC AVMs also have distinctive angioarchitectures according to their location in the CPAC. Although GKS is likely to be an effective treatment option for the CPAC AVMs with hemorrhagic presentations, it seems ideal to obliterate the flow-related aneurysms before performing GKS, although this is frequently challenging. For CPAC AVMs with TN, it is important to evaluate the nidus-nerve relationship before treatment, and GKS is especially useful for patients who do not require urgent pain relief.

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Kenichi Sato, Hidefumi Jokura, Reizo Shirane, Tetsuya Akabane, Hiroshi Karibe and Takashi Yoshimoto

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Ahmed Mansour, Toshiki Endo, Tomoo Inoue, Kenichi Sato, Hidenori Endo, Miki Fujimura and Teiji Tominaga

The authors report the case of a 78-year-old man with a craniocervical junction epidural arteriovenous fistula who presented with subarachnoid hemorrhage from a ruptured anterior spinal artery (ASA) aneurysm. Because endovascular embolization was difficult, a posterolateral approach was chosen and a novel endoscopic fluorescence imaging system was utilized to clip the aneurysm. The fluorescence imaging system provided clear and magnified views of the ventral spinal cord simultaneously with the endoscope-integrated indocyanine green videoangiography, which helped safely obliterate the ASA aneurysm. With the aid of this novel imaging system, surgeons can appreciate and manipulate complex vascular pathologies of the ventral spinal cord through a posterolateral approach, even when the lesion is closely related to the ASA.

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Takumi Kajitani, Toshiki Endo, Tomoo Inoue, Kenichi Sato, Yasushi Matsumoto and Teiji Tominaga

The authors report the case of a 70-year-old woman with lumbar spinal epidural arteriovenous fistula (SEDAVF) who experienced subarachnoid hemorrhage (SAH) after a diagnostic lumbar puncture. According to the literature, perimedullary spinal vein enlargement is a hallmark of spinal vascular diseases; however, there are certain cases in which routine sagittal MRI fails to disclose signal flow voids. In such cases, patients may undergo a lumbar tap to investigate the possible causes of spinal inflammatory or demyelinating disease. Recognizing this phenomenon is essential because lumbar puncture of the epidural venous pouch or an enlarged intradural vein in SEDAVF may induce severe SAH. A high clinical index of suspicion can prevent similar cases in lumbar SEDAVF.

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Susumu Ito, Ken'ichi Sekido, Hiroshi Kanno, Hironobu Sato, Masaaki Tanaka, Kazuo Yamaguchi and Isao Yamamoto

Object. The goal of this study was to elucidate the genotype—phenotype relationship in syndromic craniosynostoses by analyzing the mutations of the fibroblast growth factor receptor (FGFR) gene and its clinical manifestations in patients, particularly those in atypical cases.

Methods. Twenty patients with craniosynostoses unrelated to Apert syndrome were enrolled in this study. The phenotypes indicated the following syndromes: 12 patients with unrelated Crouzon syndrome, including nine sporadic and three familial cases; two with sporadic Pfeiffer syndrome; and one with Antley—Bixler syndrome. The Crouzon phenotype was subdivided into three clinical forms: regular, top, and bottom ones. Two patients who demonstrated craniofacial anomalies and bilateral elbow joint contractures were categorized as having an unspecified craniosynostosis. Three cases of unclassifiable cloverleaf skull malformation were also analyzed.

Methods. Fourteen mutations of the FGFR2 gene were identified in these patients; seven of the 10 cysteine-related mutations were substitutions of codon 342 in the third immunoglobulin-like domain of this gene. The phenotypes of these seven cases were three of regular Crouzon, two of unspecified craniosynostosis, and one each of top Crouzon and unclassifiable cloverleaf skull malformation. In addition, four of the seven patients were found to have the same genotype (Cys342Arg). The phenotypes of these patients, however, were quite variable, ranging from regular Crouzon to unclassifiable cloverleaf skull malformation.

Conclusions. The phenotypes of patients with craniosynostoses unrelated to Apert syndrome proved quite variable, even in cases in which patients demonstrated the same genotype. In view of the phenotypic diversity evident in cases in which the same mutation in the FGFR2 gene is present, it is possible that other disease-modifying genetic factors exist to control the abnormal gain-of-function that accompanies FGFR signaling.

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Lei Zhang, Eiji Sato, Kenichi Amagasaki, Atsuhito Nakao and Hirofumi Naganuma

Object

Malignant glioma cells secrete and activate transforming growth factor–β (TGFβ) and are resistant to growth inhibition by that factor. Nevertheless, the mechanism underlying this effect remains poorly understood. In this study, the mechanism of the resistance to growth inhibition induced by TGFβ was investigated.

Methods

The authors examined the expression of downstream components of the TGFβ receptor, including Smad2, Smad3, Smad4, and Smad7, and the effect of TGFβ1 treatment on the phosphorylation of Smad2 and the nuclear translocation of Smad2 and Smad3 by using 10 glioma cell lines and the A549 cell line, which is sensitive to TGFβ-mediated growth inhibition. The expression of two transcriptional corepressor proteins, SnoN and Ski, and the effect of TGFβ1 treatment on the expression of the SnoN protein and the cell cycle regulators p21, p15, cyclin-dependent kinase–4 (CDK4), and cyclin D1 were also examined.

Expression of the Smad2 and Smad3 proteins was lower in the glioma cell lines than in the A549 cell line and in normal astrocytes. In particular, Smad3 expression was low or very low in nine of the 10 malignant glioma cell lines. Expression of Smad4 was low in four glioma cell lines, and expression of the Smad7 protein was similar when compared with protein expression in the A549 cell line and in normal astrocytes. The levels of Smad2 phosphorylation after TGFβ1 treatment were lower in glioma cell lines than in the A549 cell line, except for one glioma cell line. Seven of the 10 glioma cell lines exhibited lower levels of nuclear translocation of Smad2 and Smad3, and two cell lines that expressed very low levels of Smad3 protein showed no nuclear translocation. All glioma cell lines expressed the SnoN protein and its expression was unaltered by treatment with TGFβ1. Three glioma cell lines expressed high levels of the Ski protein. The expression of the p21cip1, p15INK4B, CDK4, and cyclin D1 proteins was not altered by TGFβ1 treatment, except in one cell line that displayed a slight increase in p21 protein. Overall, the expression of the Smad2 and Smad3 proteins was low in the glioma cell lines, the phosphorylation and nuclear translocation of Smad2 and Smad3 were impaired, and the TGFβ receptor signal did not affect the expression of the SnoN, p21, p15, cyclin D1, and CDK4 proteins.

Conclusions

These results suggest that the ability to resist TGFβ-mediated growth inhibition in malignant glioma cells is due to abnormalities in the TGFβ signaling pathway.

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Masafumi Hiramatsu, Kenji Sugiu, Tomoya Ishiguro, Hiro Kiyosue, Kenichi Sato, Keisuke Takai, Yasunari Niimi and Yuji Matsumaru

OBJECTIVE

The aim of this retrospective multicenter cohort study was to assess the details of the angioarchitecture of arteriovenous fistulas (AVFs) at the craniocervical junction (CCJ) and to determine the associations between the angiographic characteristics and the clinical presentations and outcomes.

METHODS

The authors analyzed angiographic and clinical data for patients with CCJ AVFs from 20 participating centers that are members of the Japanese Society for Neuroendovascular Therapy (JSNET). Angiographic findings (feeding artery, location of AV shunt, draining vein) and patient data (age, sex, presentation, treatment modality, outcome) were tabulated and stratified based on the angiographic types of the lesions, as diagnosed by a member of the CCJ AVF study group, which consisted of a panel of 6 neurointerventionalists and 1 spine neurosurgeon.

RESULTS

The study included 54 patients (median age 65 years, interquartile range 61–75 years) with a total of 59 lesions. Five angiographic types were found among the 59 lesions: Type 1, dural AVF (22 [37%] of 59); Type 2, radicular AVF (17 [29%] of 59); Type 3, epidural AVF (EDAVF) with pial feeders (8 [14%] of 59); Type 4, EDAVF (6 [10%] of 59); and Type 5, perimedullary AVF (6 [10%] of 59). In almost all lesions (98%), AV shunts were fed by radiculomeningeal arteries from the vertebral artery that drained into intradural or epidural veins through AV shunts on the dura mater, on the spinal nerves, in the epidural space, or on the spinal cord. In more than half of the lesions (63%), the AV shunts were also fed by a spinal pial artery from the anterior spinal artery (ASA) and/or the lateral spinal artery. The data also showed that the angiographic characteristics associated with hemorrhagic presentations—the most common presentation of the lesions (73%)—were the inclusion of the ASA as a feeder, the presence of aneurysmal dilatation on the feeder, and CCJ AVF Type 2 (radicular AVF). Treatment outcomes differed among the angiographic types of the lesions.

CONCLUSIONS

Craniocervical junction AVFs commonly present with hemorrhage and are frequently fed by both radiculomeningeal and spinal pial arteries. The AV shunt develops along the C-1 or C-2 nerve roots and can be located on the spinal cord, on the spinal nerves, and/or on the inner or outer surface of the dura mater.

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Shunsuke Omodaka, Hidenori Endo, Kuniyasu Niizuma, Miki Fujimura, Takashi Inoue, Toshiki Endo, Kenichi Sato, Shin-ichiro Sugiyama and Teiji Tominaga

OBJECTIVE

Recent MR vessel wall imaging studies have indicated intracranial aneurysms in the active state could show circumferential enhancement along the aneurysm wall (CEAW). While ruptured aneurysms frequently show CEAW, CEAW in unruptured aneurysms at the evolving state (i.e., growing or symptomatic) has not been studied in detail. The authors quantitatively assessed the degree of CEAW in evolving unruptured aneurysms by comparing it separately to that in stable unruptured and ruptured aneurysms.

METHODS

A quantitative analysis of CEAW was performed in 26 consecutive evolving aneurysms using MR vessel wall imaging. Three-dimensional T1-weighted fast spin echo sequences were obtained before and after contrast media injection, and the contrast ratio of the aneurysm wall against the pituitary stalk (CRstalk) was calculated as the indicator of CEAW. Aneurysm characteristics of evolving aneurysms were compared with those of 69 stable unruptured and 67 ruptured aneurysms.

RESULTS

The CRstalk values in evolving aneurysms were significantly higher than those in stable aneurysms (0.54 vs 0.34, p < 0.0001), and lower than those in ruptured aneurysms (0.54 vs 0.83, p < 0.0002). In multivariable analysis, CRstalk remained significant when comparing evolving with stable aneurysms (odds ratio [OR] 12.23, 95% confidence interval [CI] 3.53–42.41), and with ruptured aneurysms (OR 0.083, 95% CI 0.022–0.310).

CONCLUSIONS

The CEAW in evolving aneurysms was higher than those in stable aneurysms, and lower than those in ruptured aneurysms. The degree of CEAW may indicate the process leading to rupture of intracranial aneurysms, which can be useful additional information to determine an indication for surgical treatment of unruptured aneurysms.