[Monitoring for Spine and Spinal Cord Surgery].

Injuries of the spine and nerve root may occur during spine or spinal cord surgery, which can induce serious neurological deficits. Intraoperative monitoring plays important roles in monitoring the nerve function in various surgical manipulations, such as surgical positioning, mechanical compression, and tumor removal. This monitoring issues a warning to neuronal injuries at an early stage, and surgeons are able to prevent postoperative complications. The appropriate monitoring systems should be chosen with compatibility to the disease, surgical procedure, and lesion localization. The team should share the significance of monitoring and understand the timing of stimulation to perform a safe surgery. In this paper, we overview various intraoperative monitoring techniques and pitfalls in spine and spinal cord surgeries based on cases from our hospital.

[Attainment of the Lessinvasive Neurospinal Surgery: Full Endoscopic Spinal Surgery].

Full endoscopic spinal surgery(FESS)is the the least invasive surgery among the current spinal surgeries. FESS approach can be used to perform discectomy, decompression for stenosis, posterolateral fusion, etc. with little destruction of the spinal structure and posterior supporting elements, under local or general anesthesia. A major difference from conventional spinal surgeries is "underwater surgery," in which surgery is performed under continuous saline irrigation. In addition, for neurosurgeons, there is a steep learning curve to becoming proficient in using a small diameter endoscope for full-endoscopic surgery as well as performing treatment with the surgical field completely. We would like to explain the indication and surgical procedure of the transforaminal approach, then introduce decompression by FESS at the cervical spine level as well as full endoscopic lateral lumbar interbody fusion(ELIF).

E8002 Inhibits Peripheral Nerve Adhesion by Enhancing Fibrinolysis of l-Ascorbic Acid in a Rat Sciatic Nerve Model.

Perineural adhesions leading to neuropathy are one of the most undesirable consequences of peripheral nerve surgery. However, there are currently no widely used compounds with anti-adhesive effects in the field of peripheral nerve surgery. E8002 is a novel, anti-adhesive, multi-layer membrane that contains L-ascorbic acid (AA). Here, we investigated the effect and mechanism of E8002 in a rat sciatic nerve adhesion model. A total of 21 rats were used. Six weeks after surgery, macroscopic adhesion scores were significantly lower in the E8002 group (adhesion procedure followed by nerve wrapping with E8002) compared to the E8002 AA(-) group (adhesion procedure followed by nerve wrapping with the E8002 membrane excluding AA) and adhesion group (adhesion procedure but no treatment). Correspondingly, a microscopic examination revealed prominent scar tissue in the E8002 AA(-) and adhesion groups. Furthermore, an in vitro study using human blood samples showed that AA enhanced tissue-type, plasminogen activator-mediated fibrinolysis. Altogether, these results suggest that E8002 may exert an anti-adhesive action via AA and the regulation of fibrinolysis.

Application of a Novel Anti-Adhesive Membrane, E8002, in a Rat Laminectomy Model.

Neuropathic pain after spinal surgery, so-called failed back surgery syndrome, is a frequently observed common complication. One cause of the pain is scar tissue formation, observed as post-surgical epidural adhesions. These adhesions may compress surrounding spinal nerves, resulting in pain, even after successful spinal surgery. E8002 is an anti-adhesive membrane. In Japan, a clinical trial of E8002 is currently ongoing in patients undergoing abdominal surgery. However, animal experiments have not been performed for E8002 in spinal surgery. We assessed the anti-adhesive effect of E8002 in a rat laminectomy model. The dura matter was covered with an E8002 membrane or left uncovered as a control. Neurological evaluations and histopathological findings were compared at six weeks postoperatively. Histopathological analyses were performed by hematoxylin⁻eosin and aldehyde fuchsin-Masson Goldner staining. Three assessment areas were selected at the middle and margins of the laminectomy sites, and the numbers of fibroblasts and inflammatory cells were counted. Blinded histopathological evaluation revealed that adhesions and scar formation were reduced in the E8002 group compared with the control group. The E8002 group had significantly lower numbers of fibroblasts and inflammatory cells than the control group. The present results indicate that E8002 can prevent epidural scar adhesions after laminectomy.

Acquired Simple Bone Cyst Associated With Lumbar Spinal Canal Stenosis Progression: A Case Report.

A simple bone cyst (SBC) in the posterior lumbar bone structure is very rare. Here, we report a case of SBC at the L5 lumbar lamina with venous obstruction associated with ligamentum flavum thickening. A 59-year-old woman presented with intermittent claudication due to low back pain and bilateral sciatica. A lumbar MRI showed L4-5 lumbar spinal canal stenosis and a T2-weighted image hyperintense lesion in the L5 lamina. Imaging four years earlier showed no lesions in the L5 lamina. Her symptoms improved after lumbar decompression surgery. The L5 lamina lesion was SBC, leading to a diagnosis of venous infarction. The involvement of neovascularization in the mechanism of degenerative hypertrophy in the ligamentum flavum was suggested. In this case, increased venous perfusion and venous obstruction were involved in the formation of the bone cyst.

Oleic Acid-Containing Phosphatidylinositol Is a Blood Biomarker Candidate for SPG28.

Hereditary spastic paraplegia is a genetic neurological disorder characterized by spasticity of the lower limbs, and spastic paraplegia type 28 is one of its subtypes. Spastic paraplegia type 28 is a hereditary neurogenerative disorder with an autosomal recessive inheritance caused by loss of function of DDHD1. DDHD1 encodes phospholipase A1, which catalyzes phospholipids to lysophospholipids such as phosphatidic acids and phosphatidylinositols to lysophosphatidic acids and lysophoshatidylinositols. Quantitative changes in these phospholipids can be key to the pathogenesis of SPG28, even at subclinical levels. By lipidome analysis using plasma from mice, we globally examined phospholipids to identify molecules showing significant quantitative changes in Ddhd1 knockout mice. We then examined reproducibility of the quantitative changes in human sera including SPG28 patients. We identified nine kinds of phosphatidylinositols that show significant increases in Ddhd1 knockout mice. Of these, four kinds of phosphatidylinositols replicated the highest level in the SPG28 patient serum. All four kinds of phosphatidylinositols contained oleic acid. This observation suggests that the amount of oleic acid-containing PI was affected by loss of function of DDHD1. Our results also propose the possibility of using oleic acid-containing PI as a blood biomarker for SPG28.

A case of mid-thoracic osteoporotic vertebral fracture with the inability to belch syndrome.

Background: Osteoporotic vertebral fractures (OVF) commonly occur at the thoracolumbar junction, but are less frequently encountered in the mid-thoracic region. Here, a 69-year-old female presented with back pain and the new onset of symptoms characterized by the inability to belch. Case Description: A 69-year-old female presented with back pain. 2 months later, she developed anorexia and difficulty belching. The thoracic magnetic resonance (MR) demonstrated a T7 OVF. As she ultimately underwent a balloon kyphoplasty (BKP), as conservative treatment was unsuccessful. Conclusion: OVF should be suspected in elderly females with the inability to belch accompanied by chest and back pain. The diagnosis is best established with a spinal MR imaging and should be followed by BKP.

Cerebrospinal fluid shunt for normal pressure hydrocephalus patient exacerbates cord symptoms due to spinal tumor.

Background: Normal-pressure hydrocephalus (NPH) and spinal intradural extramedullary benign tumors rarely exist together. Here, a 72-year-old female who presented with NPH symptoms (i.e., gait disturbance and dementia) newly developed symptoms of spinal cord compression attributed to a previously undiagnosed schwannoma. Case Description: A 72-year-old female was diagnosed with NPH without disproportionately enlarged subarachnoid space hydrocephalus. The lumbar puncture revealed an elevated cerebrospinal fluid (CSF) protein level of 0.141 g/dl, but with normal pressure. The patient's NPH symptoms improved after lumbar-peritoneal shunt placement. However, a year later, she subacutely developed a progressive Brown-Sequard syndrome. On the cervical magnetic resonance (MR), an intradural extramedullary lesion was found at the C5-C6 level which at surgery, proved to be a schwannoma. A review of this patient and three others with NPH and intradural extramedullary benign tumors revealed that 4.3 months following CSF shunting for NPH, they developed rapidly progressive cord deficits, attributed to their benign spinal tumors. Conclusion: Before the placement of shunts for NPH, patients should undergo holospinal MR imaging studies to rule out attendant spinal intradural extramedullary tumors.

Factors Associated with Rapidly Deteriorating Myelopathy in Patients with Spinal Arteriovenous Shunts.

Spinal arteriovenous (AV) shunts are rare conditions that sometimes present with myelopathy symptoms. The progression of the symptoms is usually gradual; however, some cases show rapid deterioration. We retrospectively investigated the factors that induced the rapid deterioration of myelopathy symptoms in patients with spinal AV shunts. We treated 33 patients with myelopathy with spinal AV shunts at our institutions, eight of whom experienced rapid deterioration (within 24 hours: 24.2%). Of these, three were related to the body movement or particular postures associated with playing golf, 30 minutes of Japanese straight sitting, and massage care. One patient showed deterioration after embolization for a tracheal aneurysm. The remaining four patients received steroid pulse therapy (high-dose steroid infusion) shortly before the rapid deterioration. These symptoms stopped progressing after cessation of steroid use. While positional or physical factors contributing to myelopathy deterioration might exist, we could not identify specific factors in this study. Nevertheless, rapid deterioration was frequently observed after high-dose steroid use. We must take care not to administer high-dose steroids for myelopathy caused by spinal AV shunt disease.

"Motion-specific Headache": A Predictor for Diagnosis and Favorable Prognosis after Surgery in Young Patients with Chiari Malformation Type 1.

As headache is known as one of the most common symptoms in the patients with Chiari malformation type 1 (CM1), it is difficult to find out CM1-related headache among the symptoms because headache itself is commonly seen. Herein, we retrospectively review the cases of six CM1 patients complaining only of headache by which they complained of deterioration in daily life activities. The symptom of headache worsened during anteflexion (n = 2; 33%), retroflexion (n = 1; 17%), jumping (n = 3; 50%), going up the stairs (n = 1; 17%), and running (n = 1; 17%). Mean age at the onset was 15.7 years old (ranging 11-18) and four out of six were female. These inductive factors were clearly different from "Valsalva-like maneuvers," although the mechanism might originate from dynamic tonsil changes. We named these headaches as "motion-specific." These headaches radiated to the posterior side. MRI revealed that the extent of tonsillar ectopia was 11.3 mm, while syringomyelia was observed in three out of six patients (50%). All patients underwent surgical treatment, with the "motion-specific headache" completely disappearing 12.5 days thereafter. Although headaches are common, "motion-specific headache" may be a good candidate symptom to distinguish CM1 patients, especially among teenagers with headaches, and a good predictor for favorable outcomes after surgical treatment.

The eagle jugular syndrome as the cause of delayed intracranial hemorrhage after microvascular decompression for hemifacial spasm: A case report.

BACKGROUND: Eagle syndrome is a rare disorder whereby an elongated styloid process (ESP) causes not only some otolaryngological symptoms, but also cerebrovascular events caused by compression of the carotid artery. In recent years a syndrome, denominated as Eagle jugular syndrome, involving internal jugular vein (IJV) compression caused by an ESP has been proposed as a variation of Eagle syndrome. Clinical impact of the Eagle jugular syndrome on neurosurgical procedures has not been reported yet. CASE DESCRIPTION: We present a case of a 68-year-old woman who underwent microvascular decompression for hemifacial spasm of the left side and developed delayed intracranial hemorrhage on postoperative day 3. We also demonstrate that this patient developed ipsilateral IJV stenosis between an ESP and the muscle bundle of the rectus capitis lateralis with antero-flexion neck position, which would induce venous congestion in addition to surgical disruption of emissary vein. CONCLUSION: This case is the first report demonstrating the association of an ESP with postoperative delayed intracranial hemorrhage. Our report elucidates the importance of the awareness among neurosurgeons of considering the ESP as an important bony anomaly, especially when planning for posterior fossa surgery.

Micro-anatomical structures of the lumbar intervertebral foramen for full-endoscopic spine surgery: review of the literatures.

Percutaneous endoscopic lumbar discectomy (PELD) is a minimally invasive spinal surgical technique. PELD can be performed via 2 routes, transforaminal (TF) or interlaminar. The TF approach is a well-established modality in the treatment of patients with herniated lumbar discs. This technique makes the most of the space within the intervertebral foramen where, as Kambin claimed, the safe approach to the lesion is possible. Knowledge of the lumbar artery with its branches and various ligaments of anatomies of the intervertebral foramen are needed to perform successful surgeries and to reduce complications.

Neurosurgical versus endovascular treatment of spinal dural arteriovenous fistulas: a multicenter study of 195 patients.

OBJECTIVE: The purpose of the present study was to compare the treatment success rates of primary neurosurgical and endovascular treatments in patients with spinal dural arteriovenous fistulas (dAVFs). METHODS: Data from 199 consecutive patients with thoracic and lumbosacral spinal dAVFs were collected from 18 centers. Angiographic and clinical findings, the rate of initial treatment failure or recurrence by procedures, risk factors for treatment failure, complications, and neurological outcomes were statistically analyzed. RESULTS: Spinal dAVFs were frequently detected in the thoracic region (81%), fed by a single feeder (86%), and shunted into an intradural vein via the dura mater. The fistulous connection between the feeder(s) and intradural vein was located at a single spinal level in 195 patients (98%) and at 2 independent levels in 4 patients (2%). Among the neurosurgical (n = 145), and endovascular (n = 50) treatment groups of single dAVFs (n = 195), the rate of initial treatment failure or recurrence was significantly higher in the index endovascular treatment group (0.68% and 36%). A multivariate analysis identified endovascular treatment as an independent risk factor with significantly higher odds of initial treatment failure or recurrence (OR 69; 95% CI 8.7-546). The rate of complications did not significantly differ between the two treatment groups (4.1% for neurosurgical vs 4.0% for endovascular treatment). With a median follow-up of 26 months, improvements of ≥ 1 point in the modified Rankin Scale (mRS) score and Aminoff-Logue gait and Aminoff-Logue micturition grades were observed in 111 (56%), 121 (61%), and 79 (40%) patients, respectively. Independent risk factors for lack of improvement in the Aminoff-Logue gait grades were multiple treatments due to initial treatment failure or recurrence (OR 3.1) and symptom duration (OR 1.02). CONCLUSIONS: Based on data obtained from the largest and most recently assessed multicenter cohort, the present study shows that primary neurosurgery is superior to endovascular treatment for the complete obliteration of spinal dAVFs by a single procedure.

Microsurgical versus endovascular treatment of spinal epidural arteriovenous fistulas with intradural venous drainage: a multicenter study of 81 patients.

OBJECTIVE: Spinal arteriovenous shunts are rare vascular lesions and are classified into 4 types (types I-IV). Due to rapid advances in neuroimaging, spinal epidural AVFs (edAVFs), which are similar to type I spinal dural AVFs (dAVFs), have recently been increasingly reported. These 2 entities have several important differences that influence the treatment strategy selected. The purposes of the present study were to compare angiographic and clinical differences between edAVFs and dAVFs and to provide treatment strategies for edAVFs based on a multicenter cohort. METHODS: A total of 280 consecutive patients with thoracic and lumbosacral spinal dural arteriovenous fistulas (dAVFs) and edAVFs with intradural venous drainage were collected from 19 centers. After angiographic and clinical comparisons, the treatment failure rate by procedure, risk factors for treatment failure, and neurological outcomes were statistically analyzed in edAVF cases. RESULTS: Final diagnoses after an angiographic review included 199 dAVFs and 81 edAVFs. At individual centers, 29 patients (36%) with edAVFs were misdiagnosed with dAVFs. Spinal edAVFs were commonly fed by multiple feeding arteries (54%) shunted into a single or multiple intradural vein(s) (91% and 9%) through a dilated epidural venous plexus. Preoperative modified Rankin Scale (mRS) and Aminoff-Logue gait and micturition grades were worse in patients with edAVFs than in those with dAVFs. Among the microsurgical (n = 42), endovascular (n = 36), and combined (n = 3) treatment groups of edAVFs, the treatment failure rate was significantly higher in the index endovascular treatment group (7.5%, 31%, and 0%, respectively). Endovascular treatment was found to be associated with significantly higher odds of initial treatment failure (OR 5.72, 95% CI 1.45-22.6). In edAVFs, the independent risk factor for treatment failure after microsurgery was the number of intradural draining veins (OR 17.9, 95% CI 1.56-207), while that for treatment failure after the endovascular treatment was the number of feeders (OR 4.11, 95% CI 1.23-13.8). Postoperatively, mRS score and Aminoff-Logue gait and micturition grades significantly improved in edAVFs with a median follow-up of 31 months. CONCLUSIONS: Spinal epidural AVFs with intradural venous drainage are a distinct entity and may be classified as type V spinal vascular malformations. Based on the largest multicenter cohort, this study showed that primary microsurgery was superior to endovascular treatment for initial treatment success in patients with spinal edAVFs.

Deep Cervical Artery as a Source of Bleeding in Postoperative Spinal Epidural Hematoma: A Case Report.

The source of bleeding in postoperative spinal epidural hematoma (pSEH) is often unclear. We describe a surgical case of pSEH in which the source of bleeding was thought to be the deep cervical artery (DCA). A 67-year-old man underwent C3 laminectomy, C4-6 unilateral open door laminoplasty, and C7 partial laminotomy for cervical spondylotic myelopathy. Intraoperatively, arterial hemorrhage from a distal branch of the right DCA was observed while drilling the lateral end of the C3 lamina, so electrocoagulation hemostasis was performed. A suction drain was used to obliterate the epidural space, and it was removed 22 h postoperatively. The patient suddenly felt posterior cervical pain 26 h postoperatively. Computed tomography demonstrated a huge epidural hematoma at the C3-6 level. The hematoma was evacuated 4 h after the onset of symptoms. Active bleeding was not seen intraoperatively. The patient was discharged on postoperative day 13, and no symptoms caused by the epidural hematoma remained. Considering the findings of the first operation, we concluded that a branch of the DCA might have been the source of bleeding in pSEH, and the site of the drain and removal procedure might have been one of the causes of bleeding. It is important to be aware of the DCA as a blood vessel because it requires careful attention when dissecting the semispinalis cervicis or performing operations for hemostasis before wound closure.

Predictive Value of Leakage Signs for Pure Brain Contusional Hematoma Expansion.

Hematoma expansion is an important consideration in patients with traumatic brain injury (TBI). No precise methods are available, however, for predicting the expansion of TBI-related hematoma. We aimed to establish a more sensitive predictor for contusional hematoma expansion based on the presence of leakage signs on computed tomography angiography (CTA). Thirty-three patients with pure contusion were included in the analysis (age: 64.1 ± 20.6 years; 24 men and 7 women). We compared Hounsfield unit (HU) values within set regions of interest (diameter, 10 mm) between serial CTA phase and delayed-phase CT images (5 min after CTA phase). Positive leakage signs were defined as >10% increases in HU value. Hematoma expansion was determined using plain CT at 24 h in patients who did not undergo emergent surgery. Glasgow Coma Scale (GCS) scores measured at admission and 24 h after admission were also compared. Leakage signs predicted hematoma expansion with high specificity (100%) and sensitivity (92.8%). Patients with positive leakage signs had significant decreases in GCS scores 24 h after the scan (GCS change: positive group, -0.92 ± 0.59; negative group, 1.14 ± 0.82). Positive leakage signs were clearly associated with surgical hematoma removal. Five patients without hematoma who had positive leakage signs at admission exhibited significant expansion of hematomas 24 h later. Our results indicate that leakage signs had high sensitivity in the prediction of contusional hematoma expansion and were significantly associated with delayed neurological deterioration and the necessity of surgical removal.

A novel frameshift mutation of DDHD1 in a Japanese patient with autosomal recessive spastic paraplegia.

Spastic paraplegia (SPG) type 28 is an autosomal recessive SPG caused by mutations in the DDHD1 gene. We examined a Japanese 54-years-old male patient with autosomal recessive SPG. His parents were consanguineous. He needed a wheelchair for transfer due to spastic paraplegia. There was a history of operations for bilateral hallux valgus, thoracic ossification of the yellow ligament, bilateral carpal tunnel syndrome, bilateral ankle contracture, and lumbar spinal canal stenosis. He noticed gait disturbance at age 14. He used a cane for walking in his 40s. On neurological examination, he showed hyperreflexia, spasticity, and weakness in the lower extremities and bilateral Babinski reflexes. Urinary dysfunctions and impaired vibration sense in the lower limbs were observed. By exome sequencing analysis using Agilent SureSelect and Illumina MiSeq, we identified 17,248 homozygous nucleotide variants in the patient. Through the examination of 48 candidate genes known to be responsible for autosomal recessive SPG, we identified a novel homozygous 4-bp deletion, c.914_917delGTAA, p.Ser305Ilefs*2 in exon2 of the DDHD1 gene encoding phosphatidic acid-preferring phospholipase A1 (PA-PLA1). The mutation is expected to cause a frameshift generating a premature stop codon 3-bp downstream from the deletion. In consequence, the DDHD domain that is known to be critical for PLA1 activity is completely depleted in the mutated DDHD1 protein, predicted to be a functionally null mutation of the DDHD1 gene. By Sanger sequencing, we confirmed that both parents are heterozygous for the mutation. This variation was not detected in 474 Japanese control subjects as well as the data of the 1,000G Project. We conclude that the novel mutation in DDHD1 is the causative variant for the SPG28 patient that is the first record of the disease in Japanese population.

Endoscopic biopsy for the diagnosis of neurosarcoidosis at the fourth ventricle outlet with hydrocephalus.

BACKGROUND: Fourth ventricle mass lesion in neurosarcoidosis is very rare and difficult to be diagnosed pathologically. We report a rare case of progressive hydrocephalus associated with neurosarcoidosis mass lesion located at the fourth ventricle outlet and suprasellar region. CASE DESCRIPTION: A 23-year-old man had a disturbance of consciousness and neck stiffness with fever. Magnetic resonance imaging revealed diffuse leptomeningeal enhancement, and the obstructive mass lesions at the outlet of the fourth ventricle. We performed an endoscopic biopsy of the enhanced lesion at the foramen Magendie, via foramen Monro and the aqueduct of the midbrain. Pathologically, the diagnosis of neurosarcoidosis was confirmed, and we started treatment with prednisolone. His neurological symptoms disappeared after ventriculo-peritoneal shunt and steroid therapy, and he was discharged without deficit 40 days after emergent admission. CONCLUSION: Endoscopic procedure is less invasive and more effective for biopsy of neurosarcoidosis with hydrocephalus, even if the lesion is located at the fourth ventricle outlet.