Intravenous Administration of Mesenchymal Stem Cell-Derived Exosome Alleviates Spinal Cord Injury by Regulating Neutrophil Extracellular Trap Formation through Exosomal miR-125a-3p.

Spinal cord injury (SCI) leads to devastating sequelae, demanding effective treatments. Recent advancements have unveiled the role of neutrophil extracellular traps (NETs) produced by infiltrated neutrophils in exacerbating secondary inflammation after SCI, making it a potential target for treatment intervention. Previous research has established that intravenous administration of stem cell-derived exosomes can mitigate injuries. While stem cell-derived exosomes have demonstrated the ability to modulate microglial reactions and enhance blood-brain barrier integrity, their impact on neutrophil deactivation, especially in the context of NETs, remains poorly understood. This study aims to investigate the effects of intravenous administration of MSC-derived exosomes, with a specific focus on NET formation, and to elucidate the associated molecular mechanisms. Exosomes were isolated from the cell supernatants of amnion-derived mesenchymal stem cells using the ultracentrifugation method. Spinal cord injuries were induced in Sprague-Dawley rats (9 weeks old) using a clip injury model, and 100 µg of exosomes in 1 mL of PBS or PBS alone were intravenously administered 24 h post-injury. Motor function was assessed serially for up to 28 days following the injury. On Day 3 and Day 28, spinal cord specimens were analyzed to evaluate the extent of injury and the formation of NETs. Flow cytometry was employed to examine the formation of circulating neutrophil NETs. Exogenous miRNA was electroporated into neutrophil to evaluate the effect of inflammatory NET formation. Finally, the biodistribution of exosomes was assessed using 64Cu-labeled exosomes in animal positron emission tomography (PET). Rats treated with exosomes exhibited a substantial improvement in motor function recovery and a reduction in injury size. Notably, there was a significant decrease in neutrophil infiltration and NET formation within the spinal cord, as well as a reduction in neutrophils forming NETs in the circulation. In vitro investigations indicated that exosomes accumulated in the vicinity of the nuclei of activated neutrophils, and neutrophils electroporated with the miR-125a-3p mimic exhibited a significantly diminished NET formation, while miR-125a-3p inhibitor reversed the effect. PET studies revealed that, although the majority of the transplanted exosomes were sequestered in the liver and spleen, a notably high quantity of exosomes was detected in the damaged spinal cord when compared to normal rats. MSC-derived exosomes play a pivotal role in alleviating spinal cord injury, in part through the deactivation of NET formation via miR-125a-3p.

Preoperative dorsal disc height is a predictor of indirect decompression effect through oblique lateral interbody fusion in lumbar degenerative stenosis.

The extent of indirect decompression after oblique lateral interbody fusion (OLIF) is one of the most important factors in deciding the strategy. To assess the radiographical predictors of the effect of indirect decompression in patients with lumbar degenerative spondylosis by OLIF. Thirty-two consecutive patients who underwent OLIF at 58 lumbar disc levels were enrolled in this study. The radiographic measurements included central disc height (cDH), dorsal disc height (dDH), right/left foraminal height in sagittal plane computed tomography (CT), and cross-sectional dural sac antero-posterior diameter (CDSD) in axial plane CT. All patients were followed up for 1 year after surgery. All CT parameters (cDH, dDH, CDSD, right foraminal height [RFH], and left foraminal height [LFH]) significantly increased after OLIF (P < .0001). The mean raised height difference was 4.3, 3.4, 3.4, and 2.6 mm for cDH, dDH, RFH, and LFH, respectively. The mean CDSD increase was 1.4 mm. The median values of post/pre-operation (change rates) were 1.5 times in cDH, 1.9 times in dDH, and 1.2 times in CDSD, RFH, and LFH. RFH and LFH change rates were related with both cDH and dDH change rates, while the CDSD change rate was only associated with the dDH change rate (P = .0206*) but not with cDH (P = .2061). There was a significant negative relationship between the CDSD change rate and preoperative dDH (P = .0311*, R2 = 0.0817) but not with preoperative cDH (P = .4864). OLIF should be avoided for patients with preserved high dDH.

Intravenous transplantation of amnion-derived mesenchymal stem cells promotes functional recovery and alleviates intestinal dysfunction after spinal cord injury.

Spinal cord injury (SCI) is often accompanied by gastrointestinal dysfunction due to the disconnection of the spinal autonomic nervous system. Gastrointestinal dysfunction reportedly upregulates intestinal permeability, leading to bacterial translocation of the gut microbiome to the systemic circulation, which further activates systemic inflammation, exacerbating neuronal damage. Mesenchymal stem cells (MSC) reportedly ameliorate SCI. Here, we aimed to investigate their effect on the associated gastrointestinal dysfunction. Human amnion-derived MSC (AMSCs) were intravenously transplanted one day after a rat model of midthoracic SCI. Biodistribution of transplanted cells, behavioral assessment, and histological evaluations of the spinal cord and intestine were conducted to elucidate the therapeutic effect of AMSCs. Bacterial translocation of the gut microbiome was examined by in situ hybridization and bacterial culture of the liver. Systemic inflammations were examined by blood cytokines, infiltrating immune cells in the spinal cord, and the size of the peripheral immune tissue. AMSCs released various neurotrophic factors and were mainly distributed in the liver and lung after transplantation. AMSC-transplanted animals showed smaller spinal damage and better neurological recovery with preserved neuronal tract. AMSCs transplantation ameliorated intestinal dysfunction both morphologically and functionally, which prevented translocation of the gut microbiome to the systemic circulation. Systemic inflammations were decreased in animals receiving AMSCs in the chronic phase. Intravenous AMSC administration during the acute phase of SCI rescues both spinal damage and intestinal dysfunction. Reducing bacterial translocation may contribute to decreasing systemic inflammation.

Efficacy of Two-Stage Surgery for Spinal Cord Ependymomas.

STUDY DESIGN: Retrospective cohort study. PURPOSE: This study aimed to elucidate cases for which staged surgeries are effective by a retrospective review of previous operative cases of spinal ependymomas. OVERVIEW OF LITERATURE: Patients with spinal ependymomas are expected to have a good prognosis following total resection. However, forcible dissection of spinal ependymomas will lead to neurological deterioration. Moreover, resection is sometimes difficult when the tumor is large. We have performed two-stage surgeries for large spinal ependymomas, but the indication of staged surgery is unclear. METHODS: We retrospectively reviewed patients diagnosed with spinal ependymomas who underwent tumor resection in our institution. We obtained data regarding patients' clinical characteristics, tumoral radiological characteristics, and surgical factors and compared them to clear prognostic factors. Two-stage surgery was performed in 11 patients (36.7%), and single surgery was performed in 19 patients (63.3%). RESULTS: Thirty patients were included in the analyses and divided into two groups: single surgery and two-stage surgery groups. In the single surgery group, high tumor-cord ratio (TCR) and intraoperative motor evoked potential (MEP) reduction were significantly correlated with unfavorable outcomes, which were defined as deterioration of the modified McCormick scale grades 2 months and 1 year postoperatively. Alternatively, these factors were not significantly correlated with postoperative unfavorable outcomes in the two-stage surgery group. Receiver operating characteristic curves indicated that TCR of 0.866 yielded 85.7% sensitivity and 83.3% specificity 2 months postoperatively. CONCLUSIONS: The results suggested that high TCR might be an indication of two-stage surgery and that its cutoff value is 0.866. Moreover, switching from single surgery to two-stage surgery may prevent postoperative neurological deterioration when intraoperative MEP is decreasing.

Correlation of active contact location with weight gain after subthalamic nucleus deep brain stimulation: a case series.

BACKGROUND: Weight gain (WG) is a frequently reported side effect of subthalamic deep brain stimulation; however, the underlying mechanisms remain unclear. The active contact locations influence the clinical outcomes of subthalamic deep brain stimulation, but it is unclear whether WG is directly associated with the active contact locations. We aimed to determine whether WG is associated with the subthalamic deep brain stimulation active contact locations. METHODS: We enrolled 14 patients with Parkinson's disease who underwent bilateral subthalamic deep brain stimulation between 2013 and 2019. Bodyweight and body mass index were measured before and one year following the surgery. The Lead-DBS Matlab toolbox was used to determine the active contact locations based on magnetic resonance imaging and computed tomography. We also created sweet spot maps for WG using voxel-wise statistics, based on volume of tissue activation and the WG of each patient. Fluorodeoxyglucose-positron emission tomography data were also acquired before and one year following surgery, and statistical parametric mapping was used to evaluate changes in brain metabolism. We examined which brain regions' metabolism fluctuation significantly correlated with increased body mass index scores and positron emission tomography data. RESULTS: One year after surgery, the body mass index increase was 2.03 kg/m2. The sweet spots for WG were bilateral, mainly located dorsally outside of the subthalamic nucleus (STN). Furthermore, WG was correlated with increased metabolism in the left limbic and associative regions, including the middle temporal gyrus, inferior frontal gyrus, and orbital gyrus. CONCLUSIONS: Although the mechanisms underlying WG following subthalamic deep brain stimulation are possibly multifactorial, our findings suggest that dorsal stimulation outside of STN may lead to WG. The metabolic changes in limbic and associative cortical regions after STN-DBS may also be one of the mechanisms underlying WG. Further studies are warranted to confirm whether dorsal stimulation outside of STN changes the activities of these cortical regions.

Mesenchymal Stem Cell Sheet Promotes Functional Recovery and Palliates Neuropathic Pain in a Subacute Spinal Cord Injury Model.

Stem cell therapy has been shown to reverse the sequelae of spinal cord injury (SCI). Although the ideal treatment route remains unknown, providing a large number of stem cells to the injured site using less invasive techniques is critical to achieving maximal recovery. This study was conducted to determine whether administration of bone marrow stem cell (BMSC) sheet made on its own without a scaffold is superior to intramedullary cell transplantation in a rat subacute SCI model. Adult female Sprague-Dawley rats were subjected to SCI by 30 g clip compression at the level of Th6 and Th7 and were administered BMSC cell sheet (7 × 104 cells, subdural), cell suspension (7 × 104 cells, intramedullary), or control seven days after the injury. Motor and sensory assessments, as well as histological evaluation, were performed to determine the efficacy of the different cell transplantation procedures. While both the cell sheet and cell intramedullary injection groups showed significant motor recovery compared to the control group, the cell sheet group showed better results. Furthermore, the cell sheet group displayed a significant sensory recovery compared to the other groups. A histological evaluation revealed that the cell sheet group showed smaller injury lesion volume, less inflammation, and gliosis compared to other groups. Sensory-related fibers of µ-opioid receptors (MOR, interneuron) and hydroxytryptamine transporters (HTT, descending pain inhibitory pathway), located around the dorsal horn of the spinal cord at the caudal side of the SCI, were preserved only in the cell sheet group. Stem cells could also be found inside the peri-injured spinal cord in the cell sheet group. BMSC cell sheets were able to promote functional recovery and palliate neuropathic pain more effectively than intramedullary injections, thus serving as a good treatment option for SCI.

[A Case of Positional Vertebral Artery Occlusion due to Physiological Cervical Extension with Occipital Condylar Spur].

Positional vertebral artery occlusion(PVAO)is a mechanical occlusion of the extracranial vertebral artery(VA)due to physiological movement of the head and neck. However, only a few cases of mechanical VA compression due to routine flexion-extension of the neck have been reported. We present a unique case of PVAO due to neck extension with an occipital condylar spur. A 78-year-old man was admitted to our hospital for sudden onset of right hemiparesis and dysarthria. Magnetic resonance imaging(MRI)revealed bilateral occipital and cerebellar infarctions and vessel occlusion extending from the VA to the basilar artery. Mechanic thrombectomy resulted in partial recanalization. Computed tomography angiography(CTA)performed the next day showed spontaneously recanalized left VA with some wall irregularity. CTA in the neck-extended position revealed a severely compressed left VA in its V3 segment, which was attributed to the left occipital condylar spur with degenerative changes of the condyle-C1 facet. Cervical MRI also showed a pseudotumor from the lower clivus to the odontoid process that indicated mechanical stress on the occipitocervical ligaments. An occiput to C2 fusion was performed to stabilize and avoid dynamic vascular compression. Postoperative CTA revealed no evidence of restricted flow with flexion or extension movements of the neck. It should be noted that physiological head and neck movements accompanied by condylar degenerative changes could be a cause of vertebrobasilar insufficiency.

Prognostic role of H3K27M mutation, histone H3K27 methylation status, and EZH2 expression in diffuse spinal cord gliomas.

The objective of this study is to clarify clinical significance of the H3F3A K27M mutation (H3K27M) and analyze the correlation between H3K27M, H3K27me3 status, and EZH2 expression and prognosis in spinal cord gliomas. Patients with spinal cord diffuse glioma regardless of World Health Organization (WHO) grade underwent genetic analysis for H3F3A, HIST1H3B, TERT promoter, IDH1/2, and BRAF. H3K27me3 status and EZH2 expression were analyzed through immunohistochemistry. Thereafter, the association between H3K27M, H3K27me3 status, and EZH2 expression and prognosis was retrospectively analyzed using the log-rank test. A total of 26 cases, 5 with WHO grade 4, 9 with grade 3, and 12 with grade 2 glioma, were analyzed. Although WHO grade 2 cases tended to present favorable overall survival, the difference was not statistically significant. H3K27M, which was detected in four grade 4 cases (80%) and three grade 3 cases (33%), was not associated with prognosis among grade 3 and 4 cases. Among WHO grade 2-4 cases, the combination of retained H3K27me3 and negative EZH2 expression was correlated with favorable overall survival (p = 0.03). The combination of H3K27me3 status and EZH2 expression was considered as a potential prognostic marker in WHO grade 2-4 diffuse spinal cord gliomas.

Clinical Trials of Stem Cell Treatment for Spinal Cord Injury.

There are more than one million patients worldwide suffering paralysis caused by spinal cord injury (SCI). SCI causes severe socioeconomic problems not only to the patients and their caregivers but also to society; therefore, the development of innovative treatments is crucial. Many pharmacological therapies have been attempted in an effort to reduce SCI-related damage; however, no single therapy that could dramatically improve the serious long-term sequelae of SCI has emerged. Stem cell transplantation therapy, which can ameliorate damage or regenerate neurological networks, has been proposed as a promising candidate for SCI treatment, and many basic and clinical experiments using stem cells for SCI treatment have been launched, with promising results. However, the cell transplantation methods, including cell type, dose, transplantation route, and transplantation timing, vary widely between trials, and there is no consensus regarding the most effective treatment strategy. This study reviews the current knowledge on this issue, with a special focus on the clinical trials that have used stem cells for treating SCI, and highlights the problems that remain to be solved before the widespread clinical use of stem cells can be adopted.

Undiagnosed Peripheral Nerve Disease in Patients with Failed Lumbar Disc Surgery.

STUDY DESIGN: Retrospective study (level of evidence=3). PURPOSE: We examine the relationship between residual symptoms after discectomy for lumbar disc herniation and peripheral nerve (PN) neuropathy. OVERVIEW OF LITERATURE: Patients may report persistent or recurrent symptoms after lumbar disc herniation surgery; others fail to respond to a variety of treatments. Some PN neuropathies elicit symptoms similar to those of lumbar spine disease. METHODS: We retrospectively analyzed data for 13 patients treated for persistent (n=2) or recurrent (n=11) low back pain (LBP) and/or leg pain after primary lumbar discectomy. RESULTS: Lumbar re-operation was required for four patients (three with recurrent lumbar disc herniation and one with lumbar canal stenosis). Superior cluneal nerve (SCN) entrapment neuropathy (EN) was noted in 12 patients; SCN block improved the symptoms for eight of these patients. In total, nine patients underwent PN surgery (SCN-EN, n=4; peroneal nerve EN, n=3; tarsal tunnel syndrome, n=1). Their symptoms improved significantly. CONCLUSIONS: Concomitant PN disease should be considered for patients with failed back surgery syndrome manifesting as persistent or recurrent LBP.

[Treatment Results of Low Back and Leg Pain Considering Para-Lumbar Spine Disease and Peripheral Nerve Neuropathy].

INTRODUCTION: Here we report our treatment results of low back and leg pain(LBLP)considering para-lumbar spine disease(PLSD)and peripheral nerve neuropathy(PNN). MATERIALS AND METHODS: We enrolled 103 patients who were admitted to our institute for LBLP treatment between January and December in 2014. For the treatment, we preferentially performed intensive block therapy for PLSD. RESULT: Among 103 patients, 89 patients had PLSD. In 85 patients, we performed intensive block therapy and 82 patients experienced short-term improvement of symptoms. In 35 of these 82 patients, lumbar spine and/or PNN surgical treatment was required as the effect of block therapy was transient. Intensive block therapy was effective in 47 of 103 patients(45.6%), and the remaining patients required surgical treatment(PLSD and/or PNN:31 cases, lumbar spine:13 cases, both:8 cases). CONCLUSION: Among 103 patients with LBLP, intensive block therapy for PLSD and PNN was useful for short-term symptom improvement in 82 patients(79.6%), and for long-term symptom improvement in 47 patients(45.6%)as evaluated at the final follow-up. Surgical treatment of PLSD and/or PNN was required in 39 patients(37.9%). These results suggested that treatment of PLSD and PNN might yield good results for patients with LBLP.

Clinical Features and Surgical Treatment of Superficial Peroneal Nerve Entrapment Neuropathy.

Superficial peroneal nerve (S-PN) entrapment neuropathy (S-PNEN) is comparatively rare and may be an elusive clinical entity. There is yet no established surgical procedure to treat idiopathic S-PNEN. We report our surgical treatment and clinical outcomes. We surgically treated 5 patients (6 sites) with S-PNEN. The 2 men and 3 women ranged in age from 67 to 91 years; one patient presented with bilateral leg involvement. Mean post-operative follow-up was 25.3 months. We recorded their symptoms before- and at the latest follow-up visit after surgery using a Numerical Rating Scale and the Japan Orthopedic Association score to evaluate the affected area. We microsurgically decompressed the affected S-PN under local anesthesia without a proximal tourniquet. We made a linear skin incision along the S-PN and performed wide S-PN decompression from its insertion point at the peroneal tunnel to the peroneus longus muscle (PLM) to the point where the S-PN penetrated the deep fascia. One patient who had undergone decompression in the area of a Tinel-like sign at the initial surgery suffered symptom recurrence and required re-operation 4 months later. We performed additional extensive decompression to address several sites with a Tinel-like sign. All 5 operated patients reported symptom improvement. In patients with idiopathic S-PNEN, neurolysis under local anesthesia may be curative. Decompression involving only the Tinel area may not be sufficient and it may be necessary to include the area from the PLM to the peroneal nerve exit point along the S-PN.

Impact of Additional Treatment of Paralumbar Spine and Peripheral Nerve Diseases After Lumbar Spine Surgery.

OBJECTIVE: Some patients experience failed back surgery syndrome after lumbar spine surgery. We report the effect of additional treatments for paralumbar spine and peripheral nerve diseases addressing residual symptoms after surgery. METHODS: We enrolled 74 patients (59 men and 15 women; mean age 62.9 years) who had undergone lumbar posterior decompression surgery. Mean follow-up after initial surgery was 26.2 months (range, 13-48 months). We subsequently diagnosed paralumbar spine diseases, including superior cluneal nerve entrapment neuropathy with (n = 3) or without gluteus medius muscle pain (n = 4) and gluteus medius muscle pain alone (n = 5), and peripheral nerve diseases, including peroneal nerve entrapment neuropathy (n = 4) and tarsal tunnel syndrome (n = 1), based on persistent or recurring clinical symptoms and nerve block effects. Treatment outcomes were analyzed by comparing Roland-Morris Disability Questionnaire and Japanese Orthopaedic Association scores. RESULTS: Of 74 patients, 54 (73.0%) improved after initial lumbar surgery (group A), and 20 (27.0%) continued to experience symptoms or experienced symptom recurrence during follow-up (group B). In group B, 4 patients improved with conservative therapy, 11 underwent 1 additional surgical procedure, and 5 underwent >1 additional surgical procedures. After these additional treatments, clinical outcomes were recorded as good. At the last follow-up visit, there was no difference between group A and group B. CONCLUSIONS: Of 74 patients who underwent lumbar spine surgery, 16 (21.6%) required additional surgery. To reduce the incidence of failed back surgery syndrome, concurrent diseases that may be masked by symptoms resulting from severe lumbar spine disease must be ruled out, as these diseases may become apparent after initial lumbar spine surgery.

Intraoperative Visualization of a Spinal Arachnoid Cyst Using Pyoktanin Blue.

BACKGROUND: Spinal arachnoid cysts (SACs) are filled with cerebrospinal fluid, and they include the arachnoid membrane, making it difficult to distinguish the walls of the cyst from the arachnoid membrane and excise the cyst as a lump. Here we report a technique for the intraoperative visualization of SACs, involving the use of pyoktanin blue. METHODS: Four patients with spinal intradural arachnoid cysts underwent total excision of the cysts between October 2016 and April 2017. In 1 case, magnetic resonance imaging revealed the cyst clearly, but in the other cases, the cysts were unclear. All cysts were injected with 1% pyoktanin blue (Wako Pure Chemical Industries, Osaka, Japan) diluted 500 times with physiological saline before excision. When it was difficult to distinguish the cyst from the normal arachnoid membrane, 1% pyoktanin blue diluted 1000 times with physiological saline was injected into both the cyst and the subarachnoid space, and the spread of the stain was observed. RESULTS: The cysts were better visualized after pyoktanin blue injection than before injection. When it was difficult to distinguish the cyst from the normal arachnoid space, pyoktanin blue injection was useful for judging the cyst space. There were no perioperative complications, and the patients' symptoms improved partially or completely after treatment. CONCLUSIONS: Our technique of pyoktanin blue injection into SACs could make their excision easy and safe.

Low back pain due to middle cluneal nerve entrapment neuropathy.

PURPOSE: The etiology of low back pain (LBP) is complicated and the diagnosis can be difficult. Superior cluneal nerve entrapment neuropathy (SCN-EN) is a known cause of LBP, although the middle cluneal nerve (MCN) can be implicated in the elicitation of LBP. METHODS: A 76-year-old woman with a 4-year history of severe LBP was admitted to our department in a wheelchair. She complained of bilateral LBP that was exacerbated by lumbar movement. Her pain was severe on the right side and she also suffered right leg pain and numbness. Based on palpation and nerve blocking findings we diagnosed SCN-EN and MCN entrapment neuropathy (MCN-EN). RESULTS: Her symptoms improved with repeated SCN and MCN blocking; the MCN block was the more effective and her symptoms improved. As her right-side pain around the MCN -EN with severe trigger pain recurred we performed microscopic right MCN neurolysis under local anesthesia. This led to dramatic improvement of her LBP and leg pain and the numbness improved. At the last follow-up, 7 months after surgery, she did not require pain medication. CONCLUSIONS: The MCN consists of sensory branches from the dorsal rami of S1-S4. It sandwiches the sacral ligament between the posterior superior and inferior iliac spine as it courses over the iliac crest. Its entrapment at this hard orifice can lead to severe LBP with leg symptoms. An MCN block effect is diagnostically useful. Less invasive MCN neurolysis under local anesthesia is effective in patients who fail to respond to observation therapy.

The Relationship between Carotid Stump Pressure and Changes in Motor-Evoked Potentials in Carotid Endarterectomy Patients.

Background The threshold of ischemic tolerance has not been completely identified in human clinical studies. Distal carotid artery pressure can be easily measured through the internal shunt tube during carotid endarterectomy (CEA). To confirm the critical threshold of intracranial arterial pressure and its maximum duration, we investigated the distal internal carotid artery (ICA) pressure and motor-evoked potential (MEP) changes during ICA clamping. Material and Methods Between September 2012 and March 2014, 9 patients (10 sides) with carotid stenosis (70-99%) were surgically treated at our hospital. All CEAs were performed under general anesthesia, and we routinely used a carotid shunt with the intraoperative MEP monitors. When the MEP amplitude decreased to < 50% of the control during carotid clamping, the MEP amplitude was defined as significantly reduced. Results The MEP amplitude significantly decreased in 2 of the 10 procedures (20%) during ICA clamping. The mean distal ICA pressure varied widely, ranging from 13 to 48 mm Hg. In seven cases with a mean distal ICA pressure > 20 mm Hg, there were no significant changes in the MEP during ICA clamping. However, there were three cases with a mean distal ICA pressure < 20 mm Hg, and the MEP amplitude significantly decreased in two of those three patients from 4 to 5 minutes after clamping. Conclusions The present study provides considerable information about a higher incidence of MEP amplitude deterioration in CEA patients with a mean distal ICA pressure < 20 mm Hg during ICA clamping.

[Non-Specific Back Pain due to Superior Cluneal Nerve Entrapment Neuropathy Treated with Neurolysis: A Case Report].

A 43-year-old man with a 10-year history of low back pain (LBP) had been conservatively treated elsewhere with medications for non-specific back pain. He presented to our institute with LBP and difficulty in standing up, sitting down, and sitting for prolonged periods. His Numerical Rating Scale score, due to LBP, was 8 out of 10. He had numbness on the lateral aspect of his left thigh. A lumbar radiography and magnetic resonance imaging studies revealed mild degenerative changes and mild canal stenosis in the lumbar spine. Palpation over the left posterior superior iliac crest, 8 cm from the midline over the iliac crest, revealed severe tenderness. A superior cluneal nerve(SCN)block performed at the trigger point in both the buttocks resulted in complete pain abatement and disappearance of the radiating pain. Therefore, we diagnosed SCN entrapment neuropathy(SCNE). However, the pain reappeared a few days later and subsequent treatments failed to relieve it; therefore, we decided to perform surgery. The SCN penetrates the thoracolumbar fascia through an orifice just before crossing over the iliac crest. We opened the orifice with microscissors in a distal to rostral direction along the SCN and released the entrapped nerve. After surgery, the symptoms were relieved and the patient experienced no recurrence in the last 4 years after the treatment. SCNE should be considered as a causative factor of LBP, and its treatment using minimally invasive surgery yields excellent clinical outcome.

Association between intermittent low-back pain and superior cluneal nerve entrapment neuropathy.

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.

Treatment of low back pain in patients with vertebral compression fractures and superior cluneal nerve entrapment neuropathies.

BACKGROUND: Superior cluneal nerve entrapment neuropathy (SCN-EN) may contribute to low back pain (LBP). However, it is often misdiagnosed as lumbar spine disorder and poorly understood. METHODS: Between April 2012 and September 2013, we treated 27 patients (3 men, 24 women; mean age 75.0 years) with LBP due to SCN-EN elicited by vertebral compression fractures. Symptoms were unilateral in 4 patients and bilateral in 23 patients. The interval between symptom onset and treatment averaged 10.8 months; the mean postoperative follow-up period was 19.0 months. The clinical outcomes were assessed utilizing the numeric rating scale (NRS) for LBP, the Japanese Orthopedic Association (JOA) score, and the Roland-Morris Disability Questionnaire (RDQ) before and after treatment (e.g., until the latest follow-up). RESULTS: LBP in 17 patients was immediately improved by SCN block only. The remaining 10 patients required surgery (involving 18 sites) as SCN blocks were only transiently effective. Operative intervention resulted in the immediate and continued improvement of their LBP. Notably, their NRS decreased from 7.4 to 1.5, their RDQ scores from 19.6 to 7.0, and their JOA scores increased from 10.7 to 20.3. CONCLUSIONS: In this series, 27 patients with LBP due to SCN-EN responded either to SCN blocks (17 patients) or surgical release of SCN entrapment (10 patients at 18 sites).

Case Report: Trigeminal Neuralgia Caused by a Minute Meningioma with Hyperostosed Suprameatal Tubercle.

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.