Jianxiong Li, Bin Li, Yujie Bu, Hailin Zhang, Jia Guo, Jianping Hu, and Yanfang Zhang. Mol. Cells 2022;45:216-30. https://doi.org/10.14348/molcells.2021.0071

Background: In this study, we report a case of a young female who was hospitalized for seizures and diagnosed with anti–N-methyl-D-aspartate receptor (NMDAR) encephalitis. Case presentation: The main feature of this patient was bilateral temporal calcifications detected by routine head computed tomography (CT). The co-existence of anti-NMDAR encephalitis and cerebral calcifications has not been reported. We supposed that the patient had an incomplete form of celiac disease (CD), epilepsy and cerebral calcifications syndrome (CEC). The patient's symptoms were alleviated by a series of treatments, and she remained stable during the follow-ups. Conclusions: Our findings confirm the rarity co-existing anti-NMDAR encephalitis and cerebral calcifications. In future clinical work, we need to elucidate the relationship between anti-NMDAR encephalitis and cerebral calcifications, and the association between anti-NMDAR encephalitis and other co-existing autoimmune disorders.

Introduction: Spinal cord infarction secondary to ankylosing spondylitis is a rare but severe disorder.Case presentation: Here we present a case of acute spinal cord infarction in a 54 years-old man with a medical history of ankylosing spondylitis, scoliosis, and hypotension. The patient complained of a sudden onset of lower limb weakness. A physical examination showed that he suffered from a dissociative sensory disorder, paralysis, and concomitant sphincter disturbances. After undergoing a whole-spine MRI, he was diagnosed with an acute ischemic injury from T2 to T5. As he did not treat his ankylosing spondylitis, it later caused a spinal deformity, making the lumbar puncture technically challenging. However, using Taylor’s approach, a CSF sample was successfully obtained. A CSF biochemical test ruled out myelitis, NMOSD, and MS. After receiving treatment with low-molecular-weight heparin, atorvastatin calcium, and methylprednisolone, his sphincter function gradually recovered, but his strength was only partially restored.Conclusion: Although this is a rare entity, it is necessary for physicians to consider it when evaluating patients with a sudden loss of sensation and strength in their lower limbs.

Background: Overlap between aquaporin-4 immunoglobulin G (AQP4-IgG)-positive neuromyelitis optica spectrum disorder (NMOSD) and anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is uncommon and may be difficult to recognize, especially when NMOSD initially presents with brain-predominant lesions and nonspecific symptoms. Case presentation: A 47-year-old woman initially presented with anorexia, dizziness, nausea, and intractable vomiting. Brain MRI showed a non-enhancing lesion along the anterior wall of the third ventricle involving the hypothalamic region and adjacent periependymal diencephalon, and she was initially treated for possible Wernicke encephalopathy with only partial transient improvement. Seven months later, she developed bilateral blurred vision, and repeat MRI showed persistent diencephalic involvement together with a new lesion in the left cerebellar hemisphere. Over the following three months, she developed progressive cognitive decline and neuropsychiatric symptoms. Neuro-ophthalmologic assessment supported bilateral optic neuritis. Brain MRI later revealed bilateral thalamic and mesial temporal abnormalities, while cervical MRI disclosed a subtle dorsal medullary lesion corresponding to the area postrema. Cerebrospinal fluid (CSF) showed no pleocytosis or protein elevation, but serum and CSF were positive for AQP4-IgG, and CSF anti-NMDAR1 IgG was positive at a low titer (1:10). The patient was treated with high-dose intravenous methylprednisolone followed by oral prednisone taper and maintenance inebilizumab. During follow-up, cognition, mood, and visual acuity improved substantially, and serial MRI showed no new lesions. Conclusion: This case highlights that persistent vomiting with a periependymal diencephalic or area postrema-region lesion may indicate brain-predominant AQP4-IgG-positive NMOSD rather than nutritional encephalopathy alone. In patients with AQP4-IgG-positive NMOSD who later develop prominent psychiatric or cognitive deterioration with mesial temporal-thalamic abnormalities, CSF anti-NMDAR1 IgG positivity with encephalitic features should be interpreted carefully as a possible overlap rather than definite anti-NMDAR encephalitis. Correlation of the clinical course, serial MRI findings, and CSF and serum antibody results may help support earlier diagnosis and treatment in autoimmune overlap syndromes.

Background: We report a rare case of a previously healthy female who presented with acute onset of back pain and lower limb weakness. She was ultimately diagnosed with spinal cord infarction (SCI) as the initial manifestation of acute lymphoblastic leukemia (ALL). Findings: The diagnosis of SCI was based on the sudden clinical onset, neurological examination, and characteristic spinal cord changes on magnetic resonance imaging (MRI). Initial complete blood pictures were unremarkable. However, MRI also revealed additional abnormal signals outside the spinal cord. 18F-FDG-positron emission tomography-computed tomography (18F-FDG-PET/CT) suggested possible extramedullary hematopoiesis. Subsequent peripheral blood analysis showed abnormal circulating cells, and bone marrow examination confirmed the diagnosis of ALL. Conclusions: This case highlights the diagnostic challenges of SCI as an initial and atypical presentation of acute leukemia, particularly in the absence of hematologic abnormalities at onset. Clinicians should remain alert to rare underlying causes of acute myelopathy, especially when imaging reveals extramedullary involvement.

Neuroinflammation is a common pathological feature of diverse brain diseases, but inflammatory activity is rarely distributed uniformly across diseased tissue. Instead, microglia, astrocytes, infiltrating immune cells and inflammatory mediators are often organized around specific pathological structures, including amyloid plaques, demyelinated lesion rims, ischemic borders, necrotic tumor regions and perivascular white matter compartments. Although bulk and dissociation-based single-cell approaches have defined many inflammatory cell states, they cannot determine where these states reside, how they relate to local pathology, or whether inferred cell–cell interactions occur within plausible spatial neighborhoods. Spatial omics addresses this limitation by preserving molecular information within intact tissue architecture. In this review, we summarize major spatial transcriptomic, proteomic, metabolomic and same-section multi-omic technologies, with emphasis on the types of neuroinflammatory questions each platform can answer. We then examine how spatial omics has reshaped the understanding of neuroinflammation across Alzheimer’s disease and tauopathies, multiple sclerosis, ischemic stroke, glioma, infection-related neuroinflammation and aging. Across these settings, spatial studies have revealed plaque-associated glial niches, lipid- and iron-enriched lesion rims, core–penumbra inflammatory zonation, and hypoxic or perivascular immune microenvironments. These findings suggest that neuroinflammation should be understood not only as a set of molecular or cellular states, but also as a spatially organized tissue process shaped by local pathology, cellular adjacency and microenvironmental gradients and spatial compartments. Finally, we discuss the limitations of current spatial maps, including resolution, human tissue constraints and insufficient functional validation, and outline future directions toward integrated, temporal and clinically translatable spatial atlases.