Disease relevance of Spinal Cord Diseases

• Vacuolar myelopathy in transgenic mice expressing human immunodeficiency virus type 1 proteins under the regulation of the myelin basic protein gene promoter [1].
• We have investigated the expression, regulation and possible role of MMPs and TIMPs during infection of glial cells with human T-lymphotropic virus type I (HTLV-I), the causative agent of a progressive chronic myelopathy, TSP/HAM [2].
• The development of MDR phenotypes was found to be independent of disease type or status with significant MDR activities being observed in adult T-cell leukemia (ATL), HTLV-associated myelopathy (HAM)/tropical spastic paraparesis (TSP), and asymptomatic HTLV-infected individuals [3].
• We measured human T-cell lymphotropic virus type I proviral load in cerebrospinal fluid cells from human T-cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis patients using real-time quantitative polymerase chain reaction (TaqMan) [4].
• We evaluated the presence of soluble intercellular adhesion molecule-1 (sICAM-1) antigen in the sera of patients with multiple sclerosis and human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM) using an enzyme-linked immunosorbent assay [5].

Psychiatry related information on Spinal Cord Diseases

• We measured the levels of prostaglandin E2 in the cerebrospinal fluid of HIV-positive individuals with dementia and/or myelopathy and compared these levels with those of HIV-negative patients with other neurological diseases and HIV-positive patients without dementia [6].
• Reports also indicate that neuropsychiatric diseases secondary to folate deficiency might include dementia, schizophrenia-like syndromes, insomnia, irritability, forgetfulness, endogenous depression, organic psychosis, peripheral neuropathy, myelopathy, and restless legs syndrome [7].

High impact information on Spinal Cord Diseases

• The myelopathy associated with human immunodeficiency virus (HIV) infection closely resembles that in subacute combined degeneration, a disorder of vitamin B12 metabolism [8].
• Myelopathy after stopping zidovudine [9].
• Transverse myelopathy in systemic lupus erythematosus. Report of three cases and review of the literature [10].
• Patients who were started on steroid therapy within 24 hours of the onset of myelopathy may have benefited [10].
• Transactivation of interleukin 2 and its receptor induces immune activation in human T-cell lymphotropic virus type I-associated myelopathy: pathogenic implications and a rationale for immunotherapy [11].

Chemical compound and disease context of Spinal Cord Diseases

• Intrathecal (IT) cytarabine may result in myelopathy that is incompletely reversible [12].
• Acute transverse myelopathy successfully treated with plasmapheresis and prednisone in a patient with primary Sjögren's syndrome [13].
• Necrotic myelopathy (myelomalacia) in rats with allergic encephalomyelitis treated with tilorone [14].
• Compressive cervical myelopathy due to calcium pyrophosphate dihydrate deposition disease: report of a case and review of the literature [15].
• Oral methionine may improve neuropsychological function in patients with AIDS myelopathy: results of an open-label trial [16].

Biological context of Spinal Cord Diseases

• Ossification of the posterior longitudinal ligament of the spine (OPLL) is the leading cause of myelopathy in Japan and is diagnosed by ectopic bone formation in the paravertebral ligament [17].
• Longer dinucleotide repeat polymorphism in matrix metalloproteinase-9 (MMP-9) gene promoter which correlates with higher HTLV-I Tax mediated transcriptional activity influences the risk of HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) [18].
• Brain magnetic resonance imaging (MRI), multimodality evoked potentials (EPs) and cerebrospinal fluid examination were performed in 42 patients with myelopathy of undetermined aetiology in order to detect abnormalities usually related to multiple sclerosis (MS) [19].
• Risk factors associated with the evolution of myelopathy included greater than 60% OPLL-induced stenotic compromise of the cervical canal, and increased range of motion of the cervical spine [20].
• Expression of FAP-1 (Fas-associated phosphatase) and resistance to Fas-mediated apoptosis in T cell lines derived from human T cell leukemia virus type 1-associated myelopathy/tropical spastic paraparesis patients [21].

Anatomical context of Spinal Cord Diseases

• In advanced cases of superficial siderosis of the human central nervous system, the clinical triad of hearing loss, cerebellar ataxia, and myelopathy permits the diagnosis at the bedside, and magnetic resonance imaging readily confirms the hemosiderin deposits in brainstem, cerebellum, and spinal cord [22].
• Cervical myelopathy caused by ossification of the posterior longitudinal ligament in ankylosing spondylitis [23].
• A clinical lower limb score correlated with the anterior (P = 0.03) and lateral (P = 0.04) column total scores and with the CTSS (P = 0.04) in the nine patients who had had both myelopathy related disability and all cord levels available [24].
• Activated macrophages positive for IL-1 and TNF-alpha are great increased in the posterior and lateral funiculi of HIV+ individuals with and without vacuolar myelopathy, suggesting they are present prior to the development of vacuoles [25].
• We report an elderly patient with aggressive steroid-refractory giant cell arteritis manifesting as myelopathy and bilateral visual loss while on treatment [26].

Gene context of Spinal Cord Diseases

• We wish to increase awareness of this important cause of myelopathy, and to determine if the clinical characteristics of OPLL are similar in non-Japanese and Japanese patients [27].
• Soluble interleukin 2 receptor and soluble CD8 were greatly elevated in blood and CSF when compared with patients with HIV-related vacuolar myelopathy and seronegative patients with other causes of myelopathy [28].
• In one patient with HIV-associated dementia and myelopathy CSF fractalkine levels decreased on initiation of antiretroviral therapy and subsequent clinical improvement [29].
• Tumor necrosis factor, tumor necrosis factor receptors type 1 and 2, lymphotoxin-alpha, and HLA-DRB1 gene polymorphisms in human T-cell lymphotropic virus type I associated myelopathy [30].
• In this study, we first examined the variable number of tandem repeat (VNTR) polymorphism of the aggrecan gene in 227 HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients, in 217 HTLV-I-infected healthy carriers (HCs), and in 85 normal controls [31].

Analytical, diagnostic and therapeutic context of Spinal Cord Diseases

• METHODS: Data on all patients with RA who were hospitalized with rheumatoid vasculitis or to undergo splenectomy for Felty's syndrome, cervical spine fusion for myelopathy, or total knee arthroplasty at hospitals in California were abstracted from a state hospitalization database [32].
• Remission of HIV-associated myelopathy after initiation of lopinavir in a patient with extensive previous exposure to highly active antiretroviral therapy [33].
• Upper cervical myelopathy associated with low CSF pressure: a complication of ventriculoperitoneal shunt [34].
• Among 22 patients with human T-lymphotropic virus type I (HTLV-I)-associated chronic progressive myelopathy, agarose isoelectric focusing (AIF) revealed oligoclonal IgG bands in 21: in 3 in CSF only; in 11 in CSF and to some extent in serum; and in 7, identical patterns in CSF and serum [35].
• In undiagnosed myelopathy, metrizamide myelography has the potential to detect unsuspected syringomyelia even when the cord is normal-sized or small [36].

References