Chimeric Antigen Receptor T-cell (CAR-T) therapy has significantly improved outcomes in hematologic malignancies but may lead to rare and severe neurological complications beyond immune effector cell-associated neurotoxicity syndrome (ICANS), such as acute myelopathy. We report the case of a 59-year-old woman treated with CD19-targeted CAR-T cells for relapsed lymphoma, who developed grade IV ICANS followed by a clinical presentation of myelitis attributed to CAR T-cell therapy after exclusion of alternative diagnoses. Aggressive immunosuppressive treatment and supportive care failed to achieve neurological recovery. The patient remained ventilator-dependent due to cervical spinal cord lesions and ultimately died following transition to palliative care. This case underscores the diagnostic challenges posed by this medical emergency in critically ill patients since numerous confounding factors may obscure early signs of spinal cord involvement in the ICU setting. Early neurologic evaluation and multidisciplinary management are critical. This case aims to raise awareness on this rare yet dramatic complication, in which prompt initiation of treatment may prevent long term sequelae.

Myoclonus-Dystonia (M-D) is a rare autosomal dominant disorder predominantly characterized by myoclonus and focal or segmental dystonia. Symptoms typically onset during childhood and are often triggered by specific postures or actions. SGCE gene mutations are the main cause of M-D. The SGCE gene is located on the chromosomal region 7q21 and encodes the ε-sarcoglycan protein. Inheritance follows a paternal transmission pattern with maternal imprinting. Although studies on M-D have expanded, the pathophysiological mechanisms remain to be fully elucidated. To better understand the comprehensive review of SGCE-related M-D (SGCE-M-D), this article focuses on its the clinical manifestations, molecular genetics, pathophysiological mechanisms, and therapeutic strategies in SGCE-M-D. Additionally, we present a schematic illustrating the distribution of SGCE gene variants at the amino acid level.

Post-traumatic hypopituitarism (PTHP), a condition primarily affecting the anterior pituitary, represents a significant and frequently underdiagnosed consequence of traumatic brain injury (TBI). Its clinical course is dynamic, with deficiencies that can be transient, persistent, or of late onset, profoundly impacting both acute prognosis and long-term cognitive and functional recovery. This review summarizes the complex pathophysiology of PTHP, covering established mechanisms such as mechanical and vascular insults, while also discussing emerging concepts including NLRP3 inflammasome-driven pyroptosis, cellular senescence, and the potential role of pituitary-resident folliculostatellate (FS) cells in the secondary injury cascade. From a clinical perspective, the review emphasizes a longitudinal approach to diagnosis and management that spans the acute to chronic phases, addressing key diagnostic pitfalls and summarizing evidence-based therapeutic strategies. By synthesizing current pathophysiological concepts and clinical practices, this review aims to enhance clinical awareness, bridge the knowledge-translation gap, and provide a resource to help optimize care for this vulnerable patient population.

The escalating global burden of neurodegenerative diseases, coupled with a lack of disease-modifying therapies, has intensified the search for modifiable risk factors. This review aims to synthesize the extensive recent literature to position the brain's waste clearance pathway, the glymphatic system, as a core physiological bridge connecting disordered sleep to the molecular pathogenesis of neurodegeneration, thereby providing a coherent mechanistic framework for clinicians and researchers.

Idiopathic intracranial hypertension (IIH) is marked by elevated intracranial pressure with risk of vision loss. Neurofilament light chain (NfL), a marker of axonal injury, may reflect optic nerve damage in IIH.

The aim was to determine the prevalence and characteristics of pain in people with neuromyelitis optica spectrum disorders (pwNMOSD).

Spinocerebellar ataxia (SCA) is a group of inherited disorders that encompasses different types and presentations. One of its types, SCA31, is a rare ataxia that has a wide spectrum of presentations. Therefore, it may be mistakenly diagnosed with another neurological disorder. Here we describe a 52-year-old woman with progressive imbalance and lower limb weakness who was initially diagnosed with multiple sclerosis (MS) based on periventricular MRI lesions and cerebrospinal fluid oligoclonal bands. She received interferon-beta for four years without improvement. After mistreatment for years, she was reassessed and, due to a strong family history of similar ataxic symptoms, was prompted to undergo genetic testing, which confirmed SCA31. This case highlights the diagnostic challenges associated with SCA31 that can mimic MS because of overlapping clinical and radiological features, potentially leading to misdiagnosis and inappropriate treatment. Therefore, clinicians should exercise caution and consider alternative diagnoses, particularly in the presence of poor response to immunotherapy, a progressive disease course, and a positive family history, all of which may indicate an inherited ataxia.