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)

A chronic, progressive form of experimental allergic encephalomyelitis was produced by immunization of rabbits with bovine brain white matter proteolipid apoprotein. Clinical signs appeared 4 to 13 months after sensitization, and were characterized by ataxia and limb paresis which progressed to flaccid paralysis and incontinence. Light and electron microscopic observations showed both acute and chronic nonsuppurative myelitis or encephalomyelitis accompanied by primary demyelination. Myelin damage was most evident in the spinal cord but was also present in the optic nerve and brain. The neuropathology was consistent with lesions of chronic experimental allergic encephalomyelitis produced by central nervous system tissue, and resembled lesions of multiple sclerosis as well. These observations suggest that protein may be involved in the pathophysiology of demyelinating diseases. A mechanism for the chronic course of the disease is discussed.
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PMID:Chronic experimental allergic encephalomyelitis induced in rabbits with bovine white matter proteolipid apoprotein. 710 65

To assess the distribution of insulin-like growth-factor-related proteins during autoimmune CNS demyelination and remyelination, experimental autoimmune encephalomyelitis was produced by injecting Lewis rats with an emulsion containing guinea pig spinal cord and complete Freund's adjuvant. Tail weakness appeared at 10-12 days and was followed by hind and forelimb weakness. Paraplegia and incontinence were observed in some animals. From 8-40 days postinoculation (dpi), spinal cord sections were used to correlate lesion location and severity with mRNA distributions of insulin-like growth factor I (IGF-I), IGF-binding protein 2 (IGFBP-2), IGF-I-receptor (IGFR-I), glial fibrillary acidic protein (GFAP), and myelin basic protein (MBP). These were determined semiquantitatively by in situ hybridization. Fourteen dpi, there were inflammatory infiltrates and demyelination in both white matter (WM) and grey matter (GM). IGF-I and GFAP mRNAs were increased in these lesions and transcripts encoding myelin basic protein (MBP) were greatly reduced. Large lesions with extensive demyelination were evident in both WM and GM when mRNA levels of GFAP and IGF-I peaked 26 dpi. MBP mRNA levels began increasing 21 dpi and peaked 26 dpi, when a few thin regenerating myelin sheaths were found morphologically. Astrocytes, identified by their morphology and GFAP immunoreactivity, expressed very low levels of IGFBP-2 mRNA and peptide in normal controls; their levels were significantly higher 14 dpi, peaked 26 dpi, and then gradually decreased. Some neurons, as well as oligodendroglia in areas undergoing remyelination, expressed IGFR-I. Although levels of IGF-I, IGFBP-2, and GFAP mRNAs were highest in lesion areas, levels were also elevated around lesions and in some normal-appearing areas of WM and GM 14-40 dpi. The gene expression of both IGF-I and IGFBP-2 by hypertrophic GFAP-positive astrocytes was demonstrated 14-40 dpi by combined in situ hybridization and immunocytochemistry as well as by double immunostaining. Coexpression of IGF-I and IGFBP-2 in the same astrocyte was a frequent finding. Relative increases in both IGF-I, GFAP, IGFBP-2, IGFR-I, and MBP mRNAs peaked at about the same time. This suggests that during lesion progression and recovery, astrocytic expression of IGF-I-related peptides may reduce immune-mediated myelin injury. We also suggest that astrocytic IGFBP-2 in lesions may help target IGF-I to IGFR-I-expressing oligodendrocytes and promote remyelination of demyelinated axons.
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PMID:Astrocytes express insulin-like growth factor-I (IGF-I) and its binding protein, IGFBP-2, during demyelination induced by experimental autoimmune encephalomyelitis. 752 31

Chronic relapsing experimental allergic encephalomyelitis (Cr-EAE) was induced in Lewis rats with an emulsion of guinea pig spinal cord tissue in complete Freund's adjuvant enriched with Mycobacterium tuberculosis H37 RA. The sensitized rats developed Cr-EAE showing two to three relapses during the first 40 days. In vitro transverse T2-weighted spin echo images of the spinal cord of Cr-EAE rats, sacrificed at the clinical height (hind leg paralysis and urinary incontinence) of the third bout and their controls, were compared with the corresponding histopathology. Lesions extended over the entire spinal cord, however, the larger lesions were predominantly present in the cervical and upper thoracic regions. In the white matter only areas of demyelination and large perivascular demyelination were discernable on the MR images. Size and shape of these lesions correlated well with the morphological characteristics revealed by histopathology. Plaques in the ventrolateral funiculus were generally located peripherally, while plaques in the dorsal funiculus were mainly present in the medial part. The NMR images, however, could not distinguish between demyelination, remyelination, inflammation, and oedema. Also lesions in the gray matter could not be distinguished with MR imaging techniques. However, if lesions were localized at the interface of the gray and white matter the boundary between the gray and white matter was less well defined.
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PMID:In vitro NMR micro imaging of the spinal cord of chronic relapsing EAE rats. 800 77

Patients with disseminated encephalomyelitis have various urological presentations, ranging from pollakisuria to urge incontinence. After detailed evaluation (neuro-urological examination, urodynamic investigation) drug therapy and various interventional methods must be adapted to the individual manifestations. Patients with detrusor hyperreflexia are treated with oral anticholinergic agents (oxybutynin, trospium chloride, propiverine). Patients with urinary retention are recommended to be managed with clean intermittent (self)-catheterisation. The various interventional therapeutic options (bladder denervation, electrostimulation, local treatment with botulinum toxin) and the surgical therapy (sacral deafferentation and anterior root stimulation, bladder neck closure and cystostomy, sphincterotomy or augmentation cystoplasty) must be reserved for special cases.
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PMID:[Bladder dysfunctions in encephalomyelitis disseminata--drug and interventional therapeutic options]. 858 53

In eleven patients with acute disseminated encephalomyelitis (ADEM), micturitional histories taken during the acute stage revealed that nine were in a state of urinary retention, and the other two had urinary frequency and urge incontinence together with difficulty in voiding. After the follow-up period of 3 to 38 months seven of nine patients with retention became able to urinate, but five of them had difficulty in voiding and four of them developed urinary frequency or urge incontinence. Two patients had urinary retention even after 26 and 38 months from the onset. Ten patients underwent urodynamic studies and disclosed detrusor hyperreflexia in six, low compliance bladder in two, atonic cystometrogram in one and detrusor-sphincter dyssynergia in two patients. Motor unit analysis of the external sphincter revealed polyphasic neurogenic changes is one of four patients. The results were compared with our previous findings in multiple sclerosis (MS), and we found that micturitional disturbance in ADEM seemed to be as common and as severe as in MS. Supranuclear as well as nuclear types of pelvic and pudendal nerve dysfunction seemed to be responsible for micturitional disturbance in our patients with ADEM. Micturitional disturbance seemed to be related to the pyramidal tract involvement, and probably reflecting the severity of spinal cord lesions.
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PMID:Micturitional disturbance in acute disseminated encephalomyelitis (ADEM). 891 71

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

A 7-year-old female presented with fever, urinary incontinence, mental regression, gait disturbance, and lethargy after diarrhea. Magnetic resonance imaging revealed multifocal T(2)-weighted hypersignal lesions supportive of acute disseminated encephalomyelitis. Her mother had been diagnosed with hereditary neuropathy with susceptibility to pressure palsy. The girl was also determined to have hereditary neuropathy with liability to pressure palsy, with a 1.5-Mb deletion in chromosome 17p11.2 encompassing the gene for peripheral myelin protein 22 detected by fluorescent in situ hybridization. Hereditary peripheral neuropathies may be a factor in triggering the autoimmune demyelinating disorder of the central nervous system.
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PMID:Acute disseminated encephalomyelitis in a female with hereditary neuropathy with susceptibility to pressure palsy. 1078 48

A 6-year-old female patient with acute disseminated encephalomyelitis associated with poliomyelitis vaccine virus is reported. She had a history of high fever, headache, and gait disturbance. Neurologic examination confirmed spastic triparesis, urinary incontinence, diminution of tactile sensation, and vision deterioration. Hemography, serum laboratory findings, and urinalysis were normal. The cerebrospinal fluid was clear, with normal pressure, 9 leukocytes/mm(3), and 27 mg/dL protein, but the myelin basic protein was elevated to 10.7 ng/mL. T(2)-weighted magnetic resonance imaging disclosed multifocal high-intensity lesions of the spinal cord. The serum polio virus type 2 antibody titer was raised in the acute phase, and polio vaccine virus type 2 was detected in viral cultures of the cerebrospinal fluid and pharynx swab and had undergone an A-G neurovirulence mutation at nucleotide 481. Finally, she had human leukocyte antigen (HLA)-Cw3 and HLA-DR2, to which multiple sclerosis is related in Japan. Thus the cause of ADEM may have been related to her HLA type.
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PMID:Acute disseminated encephalomyelitis associated with poliomyelitis vaccine. 1141 5

Multiple sclerosis (MS) is characterized by inflammatory lesions throughout the central nervous system. Spinal cord inflammation correlates with many neurological defecits. Most MS patients suffer from micturition dysfunction with urinary incontinence and difficulty in emptying the bladder. In experimental autoimmune encephalomyelitis (EAE) induced in female Lewis rats, a model of MS, we investigated at distinct clinical severity scores the micturition reflex by cystometrograms. All rats presenting symptomatic EAE suffered from micturition reflex alterations with either detrusor areflexia or hyperactivity. During pre-symptomatic EAE, a majority of rats presented with detrusor areflexia, whereas at onset of clinical EAE, detrusor hyperactivity was predominant. During progression of EAE, detrusor areflexia and hyperactivity were equally expressed. Bladder hyperactivity was suppressed by activation of glycine and GABA receptors in the lumbosacral spinal cord with an order of potency: glycine > GABA(B) > GABA(A). Detrusor areflexia was transformed into detrusor hyperactivity by blocking glycine and GABA receptors. Spinalization abolished bladder activity in rats presenting detrusor hyperactivity and failed to induce activity in detrusor areflexia. Altogether, the results reveal an exaggerated descending excitatory control in both detrusor reflex alterations. In detrusor areflexia, a strong segmental inhibition dominates this excitatory control. As in treatment of MS, electrical stimulation of sacral roots reduced detrusor hyperactivity in EAE. Blockade of glycine receptors in the lumbosacral spinal cord suppressed the stimulation-induced inhibitory effect. Our data help to better understand bladder dysfunction and treatment mechanisms to suppress detrusor hyperactivity in MS.
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PMID:Characterization and restoration of altered inhibitory and excitatory control of micturition reflex in experimental autoimmune encephalomyelitis in rats. 1706 3

The vast majority of patients with multiple sclerosis (MS) develop bladder control problems including urgency to urinate, urinary incontinence, frequency of urination, and retention of urine. Over 60% of MS patients show detrusor-sphincter dyssynergia, an abnormality characterized by obstruction of urinary outflow as a result of discoordinated contraction of the urethral sphincter muscle and the bladder detrusor muscle. In the current study we examined bladder function in female SWXJ mice with different defined levels of neurological impairment following induction of experimental autoimmune encephalomyelitis (EAE), an animal model of central nervous system inflammation widely used in MS research. We found that EAE mice develop profound bladder dysfunction characterized by significantly increased micturition frequencies and significantly decreased urine output per micturition. Moreover, we found that the severity of bladder abnormalities in EAE mice was directly related to the severity of clinical EAE and neurologic disability. Our study is the first to show and characterize micturition abnormalities in EAE mice thereby providing a most useful model system for understanding and treating neurogenic bladder.
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PMID:Bladder dysfunction in mice with experimental autoimmune encephalomyelitis. 1870 33


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