Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two hundred and twelve patients with clinically evidenced encephalomyelitis disseminata (ED), hospitalized in a neurological hospital, were observed with regard to psychopathological characteristics and cognitive changes in conformity with ICD-10 diagnostic criteria. The basis of this investigation was a standardized psychiatric interview. The age of the patients averaged 47 years whereas the duration of the disease averaged 14.3 years. 83.5% of the patients had a disease history of more than 6 years. The medium range of EDSS scores was 5.95%, the BPRS 36.7%. In 5.2% of the patients the course of ED was primarily chronic-progressive while 48% suffered from the intermittent, incomplete-reversible form: 47.6% developed secondary chronic-progressive symptoms. 18 psychopathological symptoms could be identified, the main symptom was depressive mood (49%), followed by impairment of affective sensitivity (34.9%) and affective instability/incontinence (31.1%). The most prevalent diagnoses were dementia (23.1%), organic personality disorder (18.5%), mild cognitive impairment (9%), and depressive disorder (7.6%) Only 33.5% were psychopathologically unaffected. The duration of the disease in all demented patients exceeded 6 years. Patients with an organic personality disorder showed a marked increase in the later stages of their illness in contrast to patients suffering from depressive disorder. At the beginning of ED, a highly significant (p < 0.0001) impairment of vision was found in all psychiatric patients. Dementia patients and organic personality patients, on the other hand, showed an advanced degree of ataxia. Actually, there was a considerably lesser incidence of pareses in the non-psychopathological group whereas ataxia was significantly more prevalent in the three cognitively impaired ED-subgroups than in the control group. These findings set the stage for constructive discussions, taking due consideration of existing research results on ED with particular reference to the implications regarding future research as well as the clinical therapy of patients.
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PMID:Psychopathological changes and cognitive impairment in encephalomyelitis disseminata. 1036 56

Cognitive dysfunction has been demonstrated in multiple sclerosis but has not been extensively studied after acute disseminated encephalomyelitis (ADEM). Because ADEM often presents with widespread demyelination, which may not completely resolve, these patients may be at risk for persistent cognitive dysfunction. The study objective was to explore the profile and severity of neurocognitive sequelae in pediatric ADEM. Children aged 6-15 years diagnosed with ADEM were invited to participate in a structured neurologic assessment, neuropsychological evaluation, and a follow-up magnetic resonance imaging. Nine of 15 children diagnosed with ADEM met the age criteria and six participated in the study. The mean age at presentation was 7.7 years; the mean duration of follow-up was 3.5 years. As a group, these children with prior ADEM performed within the average range on cognitive testing. However, a variety of mild cognitive deficits were demonstrated in each of the children, even in those whose magnetic resonance imaging studies had completely normalized. Four children demonstrated a cognitive profile of relatively poorer visuospatial/visuomotor function. The cognitive deficits observed in these children are similar but less severe than those previously reported in adults and children with multiple sclerosis, which may reflect the monophasic nature of ADEM, compared with the chronic, recurrent demyelination characteristic of multiple sclerosis.
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PMID:Neurocognitive outcome after acute disseminated encephalomyelitis. 1458 Jun 54

Clinical symptoms in multiple sclerosis include cognitive dysfunction. Difficulties in learning and remembering new information represent the most common cognitive deficit and are associated with a general and progressive brain pathology. Possible pathogenetic mechanisms for neuronal damage such as neuroprotective strategies are under active investigation also in experimental allergic encephalomyelitis, the most widely used experimental model for multiple sclerosis. In this paper we demonstrate that a selective deficit in learning and memory performance, as investigated by the Morris water maze test, is a consistent feature in rat encephalomyelitis, which correlates with a decline in choline acetyltransferase activity and nerve growth factor mRNA level in cerebral cortex, hippocampus, and basal forebrain. Treatment aimed to restore acetylcholine content through chronic administration of selective acetylcholinesterase inhibitors (rivastigmine and donepezil) restores cognitive performance, choline acetyltransferase activity, and nerve growth factor mRNA expression.
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PMID:Cognitive deficit associated with cholinergic and nerve growth factor down-regulation in experimental allergic encephalomyelitis in rats. 1571 Aug 75

Recombinant human erythropoietin (epoetin) has become the standard of care in the treatment of anaemia resulting from cancer and its treatment, and chronic kidney disease. The discovery that erythropoietin and its receptor are located in regions outside the erythropoietic system has led to interest in the potential role of epoetin in other tissues, such as the central nervous system. Animal studies have shown that systemically applied epoetin can cross the blood-brain barrier, where it reduces tissue injury associated with stroke, blunt trauma and experimental autoimmune encephalomyelitis. Pilot studies in humans have shown that epoetin treatment given within 8 h of stroke reduces infarct size and results in a significantly better outcome when compared with placebo treatment. Studies also suggest that epoetin has the potential to improve cognitive impairment associated with adjuvant chemotherapy in patients with cancer. Anaemia is a major factor causing tumour hypoxia, a condition that can promote changes within neoplastic cells that further tumour survival and malignant progression and also reduces the effectiveness of several anticancer therapies including radiotherapy and oxygen-dependent cytotoxic agents. Use of epoetin to prevent or correct anaemia has the potential to reduce tumour hypoxia and improve treatment outcome. Several therapeutic studies in anaemic animals with experimental tumours have shown a beneficial effect of epoetin on delaying tumour growth. Furthermore, clinical observations in patients with multiple myeloma and animal studies have suggested that epoetin has an antimyeloma effect, mediated via the immune system through activation of CD8+ T cells. Therefore, the role of epoetin may go well beyond that of increasing haemoglobin levels in anaemic patients, although additional studies are required to confirm these promising results.
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PMID:Beyond anaemia management: evolving role of erythropoietin therapy in neurological disorders, multiple myeloma and tumour hypoxia models. 1624 7

We report the case of paraneoplastic vasculitis of the central nervous system associated with breast cancer. A 54-year old woman had a complete workup because of recidive seizures. Magnetic resonance imaging (MRI) showed cerebral and medullary cryptogenic lesions, and a diagnosis of encephalomyelitis of unknown origin was made. She was treated with corticosteroids, but because of cognitive impairment and recurrence of epileptic seizures, she was finally transferred to our Neurology Department. The previous diagnosis was then changed, because a poorly differentiated invasive lobular breast cancer was discovered. Thoracic and abdominal computed tomography (CT) scans diagnosed pulmonary, pericardial, adrenal, and renal metastases. Because MRI findings did not fit with the diagnosis of brain metastases, a CT-guided cerebral biopsy was performed, and she was eventually diagnosed with paraneoplastic vasculitis of the central nervous system.
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PMID:Paraneoplastic vasculitis of central nervous system presenting as recurrent cryptogenic stroke. 1744 85

Multiple Sclerosis (MS) is an autoimmune inflammatory disease that presents clinically with a range of symptoms including motor, sensory, and cognitive dysfunction as well as demyelination and lesion formation in brain and spinal cord. A variety of animal models of MS have been developed that share many of the pathological hallmarks of MS including motor deficits (ascending paralysis), demyelination and axonal damage of central nervous system (CNS) tissue. In recent years, neuropathic pain has been recognized as a prevalent symptom of MS in a majority of patients. To date, there have been very few investigations into sensory disturbances in animal models of MS. The current work contains the first assessment of hind paw mechanical allodynia (von Frey test) over the course of a relapsing-remitting myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE) rat model of MS and establishes the utility of this model in examining autoimmune induced sensory dysfunction. We demonstrate periods of both decreased responsiveness to touch that precedes the onset of hind limb paralysis, and increased responsiveness (allodynia) that occurs during the period of motor deficit amelioration traditionally referred to as symptom remission. Furthermore, we tested the ability of our recently characterized anti-inflammatory IL-10 gene therapy to treat the autoimmune inflammation induced behavioral symptoms and tissue histopathological changes. This therapy is shown here to reverse inflammation induced paralysis, to reduce disease associated reduction in sensitivity to touch, to prevent the onset of allodynia, to reverse disease associated loss of body weight, and to suppress CNS glial activation associated with disease progression in this model.
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PMID:Anti-inflammatory cytokine gene therapy decreases sensory and motor dysfunction in experimental Multiple Sclerosis: MOG-EAE behavioral and anatomical symptom treatment with cytokine gene therapy. 1883 35

It has been reported that autoimmune inflammatory processes in human multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), may induce an alteration in neurogenesis. Studies with transgenic EAE mice have demonstrated an enhancement of neurogenesis in the subventricular zone (SVZ). In contrast, a reduction of stem cell proliferation in the same region has been observed by Pluchino et al. [Brain 2008;131:2564-2578] in myelin oligodendrocyte glycoprotein (MOG)-induced EAE mice. We immunized female C57BL/6 mice with MOG 35-55 peptide and successfully developed chronic/nonremitting EAE, which is believed to be analogous to the progressive form of MS. On day 21 postimmunization, coronal brain sections were collected and stained with anti-5-bromo-2'-deoxyuridine (BrdU) antibody. By counting the number of BrdU-labeled cells, we demonstrated that the neural stem/progenitor cell (NSC/NPC) proliferation decreased in the SVZ, which basically confirms the study of Pluchino et al. on the changes in the SVZ. A reduction of NSC/NPC proliferation also occurred in the hippocampal subgranular zone of the dentate gyrus. The hippocampus is well known to be an important region involved in learning and memory; thus, our finding may offer a possible explanation for the cognitive impairment in human chronic MS.
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PMID:Decreased neural stem/progenitor cell proliferation in mice with chronic/nonremitting experimental autoimmune encephalomyelitis. 1978 10

Over half of multiple sclerosis (MS) patients experience cognitive deficits, including learning and memory dysfunction, and the mechanisms underlying these deficits remain poorly understood. Neuronal injury and synaptic loss have been shown to occur within the hippocampus in other neurodegenerative disease models, and these pathologies have been correlated with cognitive impairment. Whether hippocampal abnormalities occur in MS models is unknown. Using experimental autoimmune encephalomyelitis (EAE), we evaluated hippocampal neurodegeneration and inflammation during disease. Hippocampal pathology began early in EAE disease course, and included decreases in CA1 pyramidal layer volume, loss of inhibitory interneurons and increased cell death of neurons and glia. It is interesting to note that these effects occurred in the presence of chronic microglial activation, with a relative paucity of infiltrating blood-borne immune cells. Widespread diffuse demyelination occurred in the hippocampus, but there was no significant decrease in axonal density. Furthermore, there was a significant reduction in pre-synaptic puncta and synaptic protein expression within the hippocampus, as well as impaired performance on a hippocampal-dependent spatial learning task. Our results demonstrate that neurodegenerative changes occur in the hippocampus during autoimmune-mediated demyelinating disease. This work establishes a preclinical model for assessing treatments targeted toward preventing hippocampal neuropathology and dysfunction in MS.
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PMID:Hippocampal CA1 atrophy and synaptic loss during experimental autoimmune encephalomyelitis, EAE. 2015 91

Primary diffuse meningeal melanomatosis can clinically mimic a wide variety of other conditions, including lymphoma, leukemia, neurosarcoidosis, metastatic carcinoma, acute disseminated encephalomyelitis, subacute meningitis, viral encephalitis, and idiopathic hypertrophic cranial pachymeningitis. We report on a young patient with primary diffuse meningeal melanomatosis who presented with papilledema, flaccid paraparesis, and cognitive impairment. The importance of imaging of the whole central nervous system, cerebrospinal fluid analysis, and pathohistological examination is emphasized in making the appropriate diagnosis.
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PMID:Primary diffuse meningeal melanomatosis. 2022 Apr 48

Limbic encephalitis is a paraneoplastic syndrome that is often associated with small cell lung cancer (SCLC), breast cancer, testicular tumors, teratoma, Hodgkin's lymphoma and thymoma. The common clinical manifestations of limbic encephalitis are subacute onset, cognitive dysfunction, seizures and psychiatric symptoms. Paraneoplastic neurological disorders are considered to occur because of cytotoxic T cell responses and antibodies against target neuronal proteins that are usually expressed by an underlying tumor. The main intracellular antigens related to limbic encephalitis are Hu, Ma2, and less frequently CV2/CRMP5 and amphiphysin. The anti-Hu antibody, which is involved in cerebellar degeneration and extensive or multifocal encephalomyelitis such as limbic encephalitis is closely associated with a history of smoking and SCLC. The anti-Ma2 antibody is associated with encephalitis of the limbic system, hypothalamus and brain-stem. For this reason, some patients with limbic encephalitis have sleep disorders (including REM sleep abnormalities), severe hypokinesis and gaze palsy in addition to limbic dysfunction. In men aged less than 50 years, anti-Ma2 antibody encephalitis is almost always associated with testicular germ-cell tumors that are occasionally difficult to detect. In older men and women, the most common tumors are non-SCLC and breast cancer. Limbic encephalitis associated with cell-surface antigens (e.g., voltage-gated potassium channels, NMDA receptors) is mediated by antibodies and often improves after a reduction in the antibody titer and after tumor resection. Patients with antibodies against intracellular antigens, except for those with anti-Ma2 antibodies and testicular tumors, are less responsive. Early diagnosis and treatment with immunotherapy, tumor resection or both are important for improving or stabilizing the condition of limbic encephalitis.
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PMID:[Limbic encephalitis with antibodies against intracellular antigens]. 2042 Jan 74


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