Double traumatic non-contiguous lesions of the subaxial cervical region are a rare event mostly caused by multiple, simultaneous or rapidly consecutive high-energy-impact traumas. The modality of treatment chosen for these lesions must be related to local lower cervical spine biomechanics. We present the case of a 59 year-old patient who suffered a subaxial cervical spine double fracture-dislocation following a complex-dynamic trauma. Radiological imaging displayed a C4-C5 and C7-T1 fracture-dislocation with cord signal intensity abnormalities. This patient showed a complete neurological deficit (ASIA A; mJOA 0) with a C4 sensory-motor level. He was urgently operated upon through an anterior approach, reduction of both dislocations and positioning of intervertebral cages and anterior plates at C4-C5 and C7-T1. At a 16-month follow-up he displays neurological improvement, moving his upper extremities at the C7-C8 motor level and a T5 sensory level (mJOA 3; Odom’s Criteria 3). The check-CT scan at 24-month shows the correct positioning of the stabilization system and a complete bone fusion. Double traumatic lesions of the subaxial cervical spine, when interposed by healthy functional segments can be treated as two single independent lesions in order to allow a better outcome.

A collision tumor is one where two neoplasms of differing type occur at the same anatomical site. We present a patient suffering from non Hodgkin small cell lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) and complaining intense lumbar back pain refractory to medical treatment. Lumbosacral MRI showed an intradural extramedullary lesion in the left L2-L3 foramen with extracanalar development and compression of psoas muscle. CT showed intralesional calcification. The patient underwent resection of the lesion through a paraspinal posterolateral approach (Wiltse approach). The histology was of schwannoma with intralesional calcifications and lymphocitic infiltrates compatible with B-lineage SLL/CLL. After the operation the patient suffer from left psoas muscle motor weakness (3/5 MRC). Because of hematological disease progression, she underwent 6 cycles of chemioterapy (Fludarabine, Cyclophosphamide, Rituximab). At a six-month follow-up no recurrence or residual tumor upon lumbosacral MR imaging was detectable and the left thigh flexion returned normal. To our knowledge, this is the first described case in the literature of collision tumor between a solitary spinal Schwannoma and SLL/CLL.

We investigate the possibility to disrupt motor activity via premotor and parietal cortex stimulation, by inducing cortical silent periods (SPs) in the voluntarily activated upper limb. We analyzed data from 17 subjects with normal brain function, using navigated TMS (nTMS) on individual MR anatomies. We applied single-pulse biphasic stimulation at 120% of resting motor threshold (rMT) in blocks of 30 stimulations on each spot of a 10-16 point grid covering the inferior parietal and frontal lobes in the dominant hemisphere while participants performed voluntary submaximal contraction. Electromyography (EMG) was recorded bilaterally from intrinsic hand muscles. We observed SPs not preceded by a MEP in the contralateral hand in 16/17 participants. The maximum overlap, of individual areas where such MEP-independent SPs could be evoked, corresponded to the ventral precentral gyrus (MNI coordinates: [x=-57, y=7, z=33]). In a subset of stimulus sites, MEP-independent SPs were bilateral, with contralateral predominance. Canonical early-onset MEPs were observed in all patients, with maximum overlap over the primary motor cortex. We also observed rare contralateral late-onset (> 23 ms) MEP-like responses from peri-Rolandic TMS. MEP-independent SPs are systematically elicitable in healthy participants They likely reflect interference with premotor representations of ongoing movements. They offer a novel possibility to investigate higher-order motor functions in the experimental and clinical neurosciences.

Dural-based lymphomas are rare extranodal non-Hodgkin lymphomas that span from indolent primary dural entities, most commonly the extranodal marginal zone (mucosa-associated lymphoid tissue) lymphoma, to aggressive variants that are primary or represent secondary involvement from systemic lymphoma. They overlap radiologically with benign meningiomas, dural metastases, and immune-mediated pachymeningitis, creating a risk of anchoring bias, delayed diagnosis, and unnecessarily extensive resections when limited tissue sampling would be sufficient for diagnosis. We conducted a structured narrative review to synthesize the epidemiology, clinico-pathological classification, imaging phenotypes, and management principles of dural lymphomatous disease. This study will especially focus on primary dural lymphoma (PDL) with additional discussion of secondary dural involvement. Emphasis is placed on the clinical value of a multiparametric diagnostic approach that integrates computed tomography contrast-enhanced magnetic resonance imaging with functional techniques, and fluorodeoxyglucose positron emission tomography/computed tomography for systemic staging and for distinguishing truly localized primary dural lymphoma from secondary involvement. Potential diagnostic pitfalls related to somatostatin receptor–based tracer uptake will also be discussed. We introduced a pragmatic operational framework based on four clinico-biological clusters, translated into a step-by-step decision algorithm that prioritizes timely biopsy and comprehensive hematologic staging to guide surgical strategy. Given the absence of dedicated, multidisciplinary guidance for dural-based lymphomas, this algorithm is intended as a reproducible foundation for consensus recommendations and future multicenter validation.