Genetic analysis in glioma has been developed recently. Spinal cord glioma is less common than intracranial glioma. Thus, the clinical significance of genetic mutations in spinal cord gliomas remains unclear. Furthermore, because the spinal cord is an important communication channel between the brain and the rest of the body, increased attention should be paid to its functional prognosis. In this study, we investigated the functional prognosis and driver genetic mutations in eight patients with spinal cord gliomas (World Health Organization grade I, three cases; grade II, two cases; grade III/IV, three cases). IDH mutations were detected in all grade II cases and H3F3A mutations were detected in all grade III/IV cases. The functional status of grade I and II gliomas remained unchanged or improved 1 year after surgery, whereas grade III/IV gliomas remained unchanged or deteriorated. Spinal glioma progenitor cells with H3F3A mutations were associated with accelerated tumor-associated spinal cord injury, which led to functional impairment. Conversely, the presence of IDH mutations, which are rarely reported in spinal gliomas, indicated a relatively favorable functional prognosis.

Background: Spinal arachnoid webs (SAW) occur when abnormally thickened bands of arachnoid membranes commonly located dorsal to the thoracic spine cause blockage of normal cerebrospinal fluid (CSF) flow, resulting in focal cord compression and myelopathy. The pathognomonic MR finding for SAW is the “positive scalpel sign” comprised of an enlarged dorsal CSF space with a normal ventral subarachnoid space. The main differential diagnostic consideration for SAW is idiopathic spinal cord herniation (ISCH); however, for ISCH, MR studies classically demonstrate ventral displacement of the spinal cord through an anterior dural defect. Here, we describe a 60-year-old female with an atypical SAW at the T3-T4 level (i.e., the preoperative MR failed to demonstrate the “positive scalpel sign”). Nevertheless, at surgery, intraoperative ultrasonography confirmed that SAW was present and was decompressed/marsupialized/removed. Case Description: A 60-year-old female presented with sensory impairment to both lower extremities. The thoracic MR images showed an enlarged dorsal CSF space at the T3-T4 level but without the “scalpel sign” suggesting “interruption” of CSF flow by thickened bands of focal dorsal arachnoidal tissues. Although the initial preoperative diagnosis was ISCH, intraoperative ultrasound (IOUS) confirmed the presence of a thickened arachnoid band, confirming the diagnosis of a SAW that was appropriately decompressed/resected. Conclusion: Correctly, establishing the preoperative diagnosis of a SAW based on MR imaging may sometimes be difficult as the typical “scalpel sign” may not be present in all patients. Notably, in cases like this one, IOUS may critically confirm the diagnosis of SAW thus leading to appropriate SAW decompression/removal.

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Hereditary neuropathy with liability to pressure palsies is an extremely rare genetic disorder; it is an autosomal dominant disorder with a high incidence of neuropathic and/or musculoskeletal pain. A case of achieving pain relief by spinal cord stimulation using differential target multiplexed stimulation for a 44-year-old female patient with hereditary neuropathy with liability to pressure palsies who was experiencing severe pain in her back, face, and all four limbs is presented. In her early teens, the initial symptoms were numbness and weakness of a limb after movement, which improved spontaneously. Transient pain in her back followed by systemic and persistent muscle weakness and pain developed. Deletion of the gene for peripheral myelin protein 22 was detected by peripheral nerve biopsy. The diagnosis of hereditary neuropathy with liability to pressure palsies was made in her early thirties. A spinal cord stimulation trial was performed because her severe pain continued despite administering many medications. Therefore, two spinal cord stimulation systems were implanted at the C3-5 and Th8-9 levels by two procedures. Pain in her back, arms, and legs decreased from 8 to 1, 5 to 1, and 6 to 2 on the numerical rating scale, respectively. Furthermore, opioid usage was tapered. The pain of hereditary neuropathy with liability to pressure palsies has a complicated pathogenesis and is resistant to pharmacological treatment. Spinal cord stimulation using differential target multiplexed stimulation may be a viable treatment option.

Background: The optimal treatment of lumbar canal stenosis (LCS) associated with osteoporotic vertebral fractures (OVFs) remains unclear. Here, we have combined a minimally invasive unilateral laminotomy for bilateral decompression (ULBD) alone with balloon kyphoplasty (BKP) for LCS aggravated by OVF. Methods: ULBD with BKP was performed in three patients who showed LCS associated with OVFs on MR images with progressive lower extremity neurological deficits. Clinical outcomes were assessed using the numerical rating scale (NRS) and the Japanese Orthopaedic Association (JOA) score. Radiological outcomes were evaluated using multiple parameters (i.e., fractured vertebral body height, lumbar lordosis [LL], and focal angle of the fractured vertebral body). Results: Over 6 postoperative months, the NRS and JOA scores were clearly improved while radiological parameters remained maintained (i.e., loss of fractured vertebral body height was only 0.3–1.4 mm in all cases). Two of the three cases showed restoration of LL and focal angle postoperatively. Conclusion: The combination of ULBD with BKP is an effective option for LCS aggravated by OVF.