(1) Introduction: Spontaneous spinal epidural hematoma (SSEH) points to hematoma within the epidural space of the spinal cord without traumatic or iatrogenic causes. (2) Case Reports: One patient showed paraplegia, numbness of both legs with acute onset, acute myelopathic signs, subsequent to back pain. Magnetic resonance imaging (MRI) showed hematoma in the posterior part of the thoracic spinal cord. Another patient showed acute numbness in the shoulder, upper part of the back, and the upper extremity on the right side after pain in the back, shoulder, and neck on the right side. Sagittal computed tomography (CT) images of the cervical bone showed a high-density area behind the spinal cord between C4 and C7. MRI analysis showed hematoma in the right diagonally posterior part of the cervical spinal cord. These 2 patients lacked traumatic or iatrogenic events, and their symptoms abated without surgical operation. (3) Conclusions: The location of hematoma correlated with symptoms in each patient. SSEH is rare but should be taken into account in patients with myelopathy or radiculopathy with acute onset subsequent to back pain. The usefulness of emergent CT scans of the spinal cord prior to MRI analysis was shown in the diagnosis of SSEH.

Post COVID-19 condition/long COVID, also called post-acute COVID-19 or long-haul COVID, refers to a variety of symptoms that have persisted since the acute phase of the disease or have newly emerged and persisted during the chronic course of the disease. The most common symptoms are fatigue, shortness of breath, dysosmia, dysgeusia, etc., while psychiatric and neurological symptoms such as memory impairment, poor concentration, and headache are important issues, and brain fog is also a well-known problem. Long COVID is thought to be caused by a combination of factors, including sequelae of COVID-19-induced CNS damage, postintensive care syndrome, chronic inflammatory reactions associated with COVID-19, and autonomic disorders; however, the pathogenesis remains unclear. Since the symptoms of long COVID are diverse, a comprehensive approach and follow-up are necessary.

The pathogenesis of neuronal damage in anti-Hu-antibody-positive paraneoplastic neurologic syndrome (Hu-PNS) is thought to be mediated by cytotoxic T lymphocyte (CTL). However, there is no direct evidence showing that antigen-specific T cells are the effector against neurons. Antigen-specific CTL-mediated cell death has been observed in cancer immunology, but not as a neurological disease model. The CTLmediated etiology in PNS should be confirmed using in vivo model systems in the future. Herein, we present an ex vivo model of antigen-specific CTL against cultured neurons. A previous study showed the CTL activity of CD8 + T cells taken from the peripheral blood of patients with Hu-antibody-positive PNS against Hu-proteinderived-peptide-expressing autologous fibroblasts. Results revealed that the HuD peptide, which can bind to major histocompatibility complex (MHC) class I of Balb/c mice, stimulated CD8 + T cells collected from mice immunized with peptide-bound self-activated dendritic cells with murine CD40 ligand-transduced adenovirus vectors (AdmCD40L). Moreover, CTL activity against autologous neurons in culture was observed. Hence, this result could be used in the development of an in vivo model of CTL-induced neurological disorders, which can help in further understanding the pathogenesis of PNS.cytotoxic T cells, Hu-antibody-positive paraneoplastic neurologic syndrome, induction of CTL in mice, killing of cultured neurons | INTRODUCTIONSeveral characteristic autoantibodies against specific neuronal and tumor tissues have been observed in different types of paraneoplastic neurologic syndrome (PNS). 1-5 Among them, anti-Hu antibodies are detected in patients with limbic encephalitis or subacute sensory neuronopathy or other symptoms associated with small-cell lung cancer. Meanwhile, anti-Yo antibodies is commonly found in women with subacute cerebellar symptoms associated with gynecological or breast cancer. These antibodies are highly characteristic in these groups of patients and are detected at the early stages of neurological disease. Moreover, they bind to relevant tumors and neuronal tissues, which indicate a close relationship with the pathogenesis of paraneoplastic neurologic syndromes. Several studies have assessed the direct role of antibodies in neuronal damage. 6 However, the results were controversial, and whether these antibodies, which recognize intracellular antigens such as anti-Hu and anti-Yo, damage the neurons remains unclear. 7-10 By contrast, there is increasing evidence showing that T lymphocytes are the effector of neuronal damage. [11][12][13][14][15][16] At the early stages of paraneoplastic cerebellar degeneration (PCD) with anti-Yo-or anti-Hu-positive PNS, the CSF contains several mononuclear cells. Inflammatory cells, mainly CD8-positive T lymphocytes, infiltrate the tumor and nervous tissues, thereby causing