Dorsal arachnoid web (AW) is a rare cause of spinal cord compression, which is indicated on MRI by a dorsal indentation of the spinal cord (scalpel-sign). AW can be associated with a myelon lesion as a sign of secondary syringomyelia resulting from alterations of CSF flow-dynamics. The etiology of AW is unclear, and evidence-based treatment recommendations are still lacking. A retrospective chart study was conducted on patients with the scalpel-sign, treated at a tertiary neurospine center between 2016 and 2024. Clinical presentation, imaging, and histopathological findings were evaluated, and treatment outcome was assessed using the thoracic Japanese Orthopedic Association (tJOA) score pre- and postoperatively, and anatomically and pathophysiologically contributing factors are discussed. 17 patients (mean age 55.5 ± 10.3 yrs, 9 males) were identified. Predilection site was the upper half of the thoracic spine, with additional syringomyelia in 9 patients (53 %). 10 patients (65 %) showed sensory deficits, 10 (59 %) motor symptoms, 10 (59 %) ataxia, 9 (53 %) back pain, and 7 (41 %) neuropathic pain. 10 (59 %) patients underwent surgery with web removal/adhesiolysis. Median follow-up was 176 days. Postoperatively, symptoms worsened in one patient, but improved in the majority of cases (mean tJOA pre-/postoperatively: 8 ± 1.1/9.2 ± 1.3; Wilcoxon signed-rank-test p < .02), with postoperative MRI showing regression of AW and syringomyelia. Surgical intervention appeared beneficial in the majority of patients, even in those with longstanding symptoms and resulting in regression of spinal cord lesions. Awareness of AW should be raised, as it identifies a rare but effectively treatable cause of spinal cord compression and syringomyelia.

Nasopharyngeal cancer with central nervous system metastases is rare. True metastasis to the distal regions of the central nervous system, especially the spinal cord, is incredibly uncommon, although tumor invasion to intracranial locations through the skull base can be prevalent. We report on a 45-year-old male who had been suffering from progressive unsteady gait and numbness of lower limbs for 3 weeks. The numbness eventually ascended to the thigh area and the patient required a wheelchair. His muscle power was normal. Magnetic resonance imaging showed multiple enhancing nodular lesions in the thoracolumbar spinal cord with mild mass effect, causing diffuse syringomyelia and cord edema. Metastasis was confirmed by pathology after tumor excision. The patient underwent concurrent radiotherapy and steroid therapy, after which he eventually could walk with crutches. Due to the complexity and rarity of such case, the standard treatment for this type of disease is unclear. Management should be individualized and multidisciplinary.

Spinal adhesive arachnoidopathy (SAA) is a chronic pathology associated with persistent inflammatory responses in the arachnoid. Adhesive arachnoiditis (AA) is one of the major forms of SAA, with accompanying secondary complications. Therefore, we aimed to systematically review both clinical and animal model studies related to SAA to gain a deeper understanding of this unique pathology. A literature search was conducted in PubMed, EMBASE, and Cochrane Library databases to retrieve relevant publications up to October 2022. Clinical manifestations, etiologies, imaging modalities, treatments, and prognosis in patients with SAA were collected. Data from animal experiments related to SAA were also extracted. A total of 176 studies, including 147 clinical and 29 animal model studies, with a total of 510 patients were enrolled in this study. Pain (37.5%), abnormal nerve sensations (39.58%), and abnormal motor function (78.75%) were the top three common symptoms of SAA. Major etiologies included trauma (22.7%), infection (17.73%), surgery (15.37%), and hemorrhage (13.48%). MRI was widely used to confirm the diagnosis. AA could be involved in cervical (96/606, 15.84%), thoracic (297/606, 49.01%), lumbar (174/606, 28.71%), and sacrococcygeal (39/606, 6.44%) vertebral segments. Patients with AA in cervical segments had a higher post-surgery recovery rate (p = 0.016) compared to that of other segments. The common pathological diagnoses of SAA were AA (80.82%), AA combined with arachnoid cyst (12.79%), arachnoid calcification/scars (3.43%), and arachnoid web/fibrosis (2.97%). Patients with AA were more likely to develop syringomyelia, compared with patients with other forms of SAA (p < 0.001). Animal studies mainly focused on new AA therapeutic agents (n = 14), the pathomechanism of AA (n = 14), and the development of new MRI sequences for improved diagnosis (n = 1). The pathological consequences of SAA are more complex than AA and manifest in different forms, such as AA combined with arachnoid cyst, arachnoid calcification/scars, and arachnoid web/fibrosis. In many instances, AA was associated with secondary syringomyelia. Unspecific clinical manifestations of SAA may easily lead to misdiagnosis and missed diagnosis. Although SAA may result from multiple etiologies, including spinal trauma, meningitis, spinal surgery, and hemorrhage, the pathogenesis and treatment of SAA have still not been standardized.

This review aims to enrich our understanding of Chiari-like malformation (CLM) by combining human and veterinary insights, and providing a detailed cross-species overview. CLM is a developmental abnormality characterised by caudal displacement of the hindbrain into the foramen magnum due to an entire brain parenchymal shift caused by insufficient skull volume. This malformation leads to a progressive obstruction at the craniocervical junction, which disrupts the normal cerebrospinal fluid flow, leading to secondary syringomyelia. The clinical signs of CLM and syringomyelia include phantom scratching, head tilt, head tremor, ataxia, tetraparesis, pain, muscle atrophy, and scoliosis or torticollis. Magnetic resonance imaging remains the gold standard for diagnosing CLM, since it allows the visualisation of abnormal findings such as the caudal cerebellar herniation, caudal cerebellar compression from occipital dysplasia, and attenuated cerebrospinal fluid cisternae. Although various medical and surgical interventions, including foramen magnum decompression, can provide temporary symptomatic/clinical sign relief, current literature shows a lack of sustained long-term efficacy. Therefore, additional research is needed to evaluate the long-term effects of existing treatment strategies and to compare different techniques utilised in conjunction with foramen magnum decompression.