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PubMedDate not supplied

Gd-enhanced MR imaging of acute and chronic experimental demyelinating lesions.

Experimental allergic encephalomyelitis, a demyelinating disease with marked similarity to multiple sclerosis, was produced in two of 12 dogs. All dogs were studied with serial MR imaging. T1- and T2-weighted MR images were obtained both before and after IV Gd-DTPA. Multiple, new periventricular white matter demyelinating lesions were observed after each clinical episode of the disease. Like multiple sclerosis, the acute lesions of experimental allergic encephalomyelitis on T2-weighted MR images were indistinguishable from the older, more chronic lesions. However, after Gd-DTPA, there was bright paramagnetic enhancement of the acute lesions and, in one animal, no enhancement of the chronic lesions on T1-weighted MR images. At necropsy, the differences in the MR paramagnetic enhancement correlated well with the relative histologic age of the demyelinating lesions. Our results suggest that MR with Gd-DTPA may be used to differentiate acute, active demyelinating lesions from the more chronic, inactive lesions in this animal model.

Acute Disease↗

PubMedDate not supplied

Solitary asymptomatic plaque of demyelination in the medulla oblongata.

Clinically benign and clinically silent multiple sclerosis is now recognized. The corresponding plaques of demyelination in such cases are usually located in silent areas of the brain. We report a case where a solitary 3 x 3 mm plaque of demyelination was incidentally found in the medulla oblongata at autopsy. Although the plaque should have produced sensory symptoms by virtue of its location, no such history was obtainable even after direct questioning of the spouse of the deceased. The case illustrates that a single episode of demyelination may take place within the CNS without recurrence, and that a demyelinating plaque may be asymptomatic due to a functionally benign local effect, and not only by location in a silent area of the brain.

Humans↗

PubMed1988

[A method of detecting demyelinated nerve tissue in experimental allergic encephalomyelitis].

A method of rapid pathomorphological diagnosis of demyelinization with a simultaneous detection of cell elements in the nervous tissue has been described. The method tested on the model of experimental allergic encephalomyelitis (EAE) is a modified method of Marchi with subsequent staining of histological sections with toluidine blue. Due to a shorter period of nervous tissue exposure to potassium bichromate and osmium acid solutions (from 6-8 weeks to 5 days) the cells preserve their ability to uptake the dye and the endurance of histological sections increases. Their thickness (2-3 microns) makes it possible to examine them in immersion magnification of the light microscope. Using the above method, we succeeded in revealing hematogenic and glial elements in demyelinating foci in the central nervous system of animals with EAE. The method described can be used for studying pathomorphology of multiple sclerosis and other demyelinating diseases in humans and their experimental models, as well as for the express diagnosis of demyelinization in pathoanatomical practice.

Animals↗

PubMed1984

Cytomegalovirus. Induced demyelination associated with acquired immune deficiency syndrome.

We observed three cases of cytomegalovirus (CMV) infection of the nervous system in association with acquired immune deficiency syndrome. The first patient had demyelinating lesions in the spinal cord with relative preservation of axis cylinders. The second patient had a discrete focus of demyelination in the hypothalamic region associated with well-preserved axons and intact neurons. Microglial nodules were absent in both patients. The third patient had subacute encephalomyelitis principally encephalomyelitis principally characterized by microglial nodule formation in the brain and spinal cord, in addition to necrotizing lesions in the thoracic cord and segmental demyelination in the anterior spinal nerve roots. Perivascular lymphocytic infiltration was minimal and was noted mainly within the peripheral nerves. Typical cytomegalic intranuclear inclusion bodies were seen in the nervous tissue of these three patients who all had evidence of disseminated CMV infection. It is possible that these patients had virus-induced demyelination in the face of altered immunoregulation.

Acquired Immunodeficiency Syndrome↗

PubMed1984

Experimental allergic neuritis: demyelination induced by P2 alone and non-specific enhancement by cerebroside.

Experimental allergic neuritis was induced in male inbred Lewis rats immunized with myelin, P2 alone, P2 mixed with galactocerebroside and P2 mixed with glucocerebroside. Neurological deficit started significantly earlier in myelin-immunized rats than in P2-immunized rats. Although myelin-immunized rats appeared most severely affected, differences between the groups in maximum neurological deficit were not significant. The course of the disease of the P2-galactocerebroside-immunized animals did not differ from that of the P2-glucocerebroside-immunized group. Histologically, cellular infiltration and demyelination were more conspicuous 12 days after immunization in the group immunized with myelin than in the other rats. After 21 days, primary demyelination was prominent in all groups: its frequency and severity were similar in the myelin-immunized and P2-immunized animals. The P2-galactocerebroside-immunized group had significantly more frequent demyelination than the P2-immunized group. Wallerian degeneration was prominent in all groups at this stage. We conclude that P2 alone does induce demyelination and that galactocerebroside added to the immunizing emulsion enhances the response but no more than the non-myelin lipid glucocerebroside.

Adjuvants, Immunologic↗

PubMed1995

Myelin oligodendrocyte glycoprotein induces a demyelinating encephalomyelitis resembling multiple sclerosis.

Chronic relapsing experimental autoimmune encephalomyelitis, a demyelinating disease induced by injection of central nervous system (CNS) tissue, is widely used as a model for multiple sclerosis. However, it is unclear which Ag or combination of Ags in the CNS induce the demyelinating immune response. We now show in Lewis rats that a single injection of myelin oligodendrocyte glycoprotein, a specific CNS myelin component, or an appropriately derived myelin oligodendrocyte glycoprotein peptide produces a relapsing remitting neurologic disease with extensive plaque-like demyelination. Igs from affected animals reacted specifically with myelin oligodendrocyte glycoprotein and stimulated a myelin protease activity, leading to myelin basic protein degradation. The demonstrated involvement of myelin oligodendrocyte glycoprotein as a new demyelinating neural Ag may provide a deeper insight into the pathogenesis of multiple sclerosis and its treatment.

Amino Acid Sequence↗

PubMed1997

[Progressive multifocal leukoencephalopathy. Study of the demyelination by magnetization transfer].

PURPOSE: magnetization transfer imaging (MT) has been used to study the degree of demyelination in progressive multifocal leukoencephalopathy (PML). MATERIAL AND METHOD: two groups were studied: a group of 10 HIV + patients with clinical, MR features, biological and/or biopsy proven PML, and a group of 11 normal volunteers with matched age. MT ratio (MTR) were obtained from the center of the PML lesions and 11 areas of normal appearing white matter (NAWM) in the control group. RESULTS: the mean MTR of NAWM in the control group was 46.6% (SD = 2,3). PML lesions demonstrated a strong and significant (p = 0) decreased of the MTR with mean MTR value of 22.4% (SD = 2,3). CONCLUSION: MT characterized the demyelinating process in PML, and can be used to improve diagnosis. Furthermore, MT allowed a quantification of the degree of demyelination which can be helpful in other demyelinating process of CNS such as multiple sclerosis.

Adult↗

PubMed2026

Nimodipine in animal models of demyelination relevant to multiple sclerosis: a systematic review.

BACKGROUND: Multiple sclerosis (MS) is the most common inflammatory neurodegenerative disease in which axonal injury, neuronal death, and demyelination occur. Treatment for MS relapses remains limited, which alleviates acute loss of function but has no impact on long-term disability. This study aimed to perform a systematic review of the effects of nimodipine on experimental demyelination models, including experimental autoimmune encephalomyelitis (EAE) and Cuprizone models in rodents. METHODS: This study was conducted following the PRISMA statement. A systematic search was performed in PubMed, Scopus, the Cochrane Library, and Google Scholar. The primary outcome was EAE clinical disease severity (peak clinical score and/or cumulative disease burden). Secondary outcomes included relapse activity (when reported), histological myelin outcomes, oligodendrocyte lineage markers, neuroaxonal injury markers, and inflammatory readouts. Risk of bias was assessed using the SYRCLE tool. RESULTS: Out of 4660 results, 5 studies were included in the systematic review (four EAE studies and one cuprizone model). Nimodipine was administered using heterogeneous regimens (oral, intravenous, intraperitoneal, subcutaneous, or osmotic pump delivery; 1-30 mg/kg/day). The included studies reported the variable effects of nimodipine on relapse-related outcomes, myelination, inflammatory processes, and neuroprotection in the EAE model of MS. Across EAE studies, nimodipine generally reduced clinical disease severity or cumulative burden, although relapse-related outcomes were inconsistent. CONCLUSIONS: Preclinical evidence suggests that nimodipine may attenuate disease severity and demyelination and may promote repair-related processes in rodent models relevant to MS. However, to evaluate the clinical applicability of nimodipine in MS patients, well-powered, transparently reported preclinical replication and early-phase clinical studies are required before clinical translation.

Animals↗

PubMed2003

Cyclo-oxygenases and prostaglandins in acute inflammatory demyelination of the peripheral nerve.

OBJECTIVE: To investigate the expression of cyclo-oxygenases (COX), key enzymes in propagating inflammatory responses by converting arachidonic acid to prostaglandins, in inflammatory demyelinating disorders of the peripheral nervous system (PNS). METHODS: Expression and distribution of COX messenger RNA (mRNA) and protein were studied in sural nerve biopsies, serum, and CSF samples from patients with Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), or, for comparison, with vasculitic neuropathy (VN), which is a inflammatory nondemyelinating disorder, and noninflammatory neuropathies (NIN) using RT-PCR, immunohistochemistry, and immunoblotting. To confirm functional COX-2 activity, the expression of prostaglandin E(2) (PGE(2)) and prostaglandin F(2alpha) (PGF(2alpha)) was evaluated by ELISA ex vivo and in vitro. RESULTS: Whereas COX-1 expression was unaltered in all investigated groups, a significant upregulation of COX-2 mRNA was detected in sural nerves from patients with GBS, CIDP, or VN but not in control subjects with noninflammatory disorders. Macrophages were identified as its primary cellular source. Increased COX-2 protein levels were detectable in serum and CSF from all patients with GBS and, in smaller numbers only, in samples from patients with CIDP or VN but not from the NIN group studied. Moreover, increased levels of PGE(2) and PGF(2alpha) were measurable in sera from patients with GBS, CIDP, or VN and in cell culture supernatants from in vitro stimulated macrophages, indicative of COX-2 activity. CONCLUSIONS: Cyclo-oxygenase-2, expressed by macrophages, may generate prostaglandins during acute inflammatory demyelination of the peripheral nerve.

Acute Disease↗

PubMed2002

[Immunopathology and treatments of Guillain-Barré syndrome and of chronic inflammatory demyelinating polyneuropathy].

The concepts of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) have changed over the last decade. The spectrum of GBS ranges from acute inflammatory demyelinating polyneuropathy to pure motor, sensory-motor or bulbar variants and the Miller Fisher syndrome. Also CIDP includes different variants in addition to the typical clinical picture with symmetrical proximal and distal weakness, such as a form with predominant distal weakness, a pure sensory form, an asymmetric form and a form with predominant cranial nerve involvement. Detailed immunopathologic features have been described in GBS and CIDP: most current investigations are centered on the hypothesis of molecular mimicry in GBS and together with the pathogenic role of cell-mediated immunity different antibodies have been discovered in GBS which interfere with nerve impulse conduction on neuromuscular transmission. The immunopathogenesis of CIDP remains fragmentary and insufficient for a unified hypothesis. Activated macrophages and T-cells with the participation of T-1 helper cell related cytokines seem to play a fundamental role in demyelination. The nature of antigen presenting cells, T-cell receptors, adhesion molecules and the proinflammatory cytokines need to be explored to design more specific immunotherapies. Established treatments in GBS include intravenous immunoglobulin and plasma exchange. Randomized trials have shown the efficacy of prednisone, intravenous immunoglobulin and plasma exchange in CIDP. New insight in the pathogenetic role of the cytokine-network in CIDP opens new therapeutical possibilities with the modification of the T-1 helper cell reaction with interferon.

Adrenal Cortex Hormones↗

PubMed1978

Subacute demyelinating polyneuropathy responding to corticosteroid treatment.

Ten patients with subacute demyelinating neuropathy responded satisfactorily to corticosteroid treatment. The most prominent features in these cases were (1) subacute progression of diffuse polyneuropathy over weeks and months, (2) high spinal fluid protein level, (3) marked nerve conduction abnormalities, and (4) high rate of relapse. The sural nerve biopsy specimen showed "demyelinating neuropathy." This subacute demyelination neuropathy appears to be a distinct and clinically identifiable entity in which corticosteroid treatment is indicated.

Adult↗

PubMed1983

Pathogenesis of coronavirus SD in mice. I. Prominent demyelination in the absence of infectious virus production.

Following intracerebral inoculation of 3- to 4-week-old C57 B16/J mice with coronavirus SD, 23% exhibited neurologic signs within the first week. However, only 6% died. Within the first week after inoculation (AI), we noted a panencephalitis. Prominent demyelination detected in the spinal cord on day 6 continued through day 29 AI. Demyelinated lesions in the spinal cord were either subpial with few inflammatory cells except for macrophages or perivascular with prominent accumulation of lymphocytes, plasma cells, and macrophages. Beginning on day 6 AI, IgG was detected in the lesions. Although an infectious virus was detectable in the CNS only through day 12 AI, viral antigen expression continued through day 24. We concluded that coronavirus SD persists in a nonrecoverable form throughout the initial phase of demyelination, day 6 to day 24 AI.

Animals↗

PubMed1986

The effect of dexamethasone on L-alpha-lysophosphatidyl choline (lysolecithin)-induced demyelination of the rat spinal cord.

Adult male Sprague-Dawley rats were injected intraspinally with 2 microL of 1% lysolecithin to induce demyelination. This was followed by systemic treatment with dexamethasone acetate for two weeks. Control groups were injected with lysolecithin but not treated. The animals were perfused at 8, 12, 28, and 60 days postoperatively, and the spinal cords were processed and examined histopathologically. The intraspinal injection of lysolecithin produced a focal area of primary demyelination followed by remyelination. In the steroid-treated groups, there was a suppression of the mononuclear phagocytic response, accompanied by slow clearance of the disrupted myelin sheaths and an apparent reduction in lesion size. Remyelination was substantially retarded in comparison with the controls. The findings suggest that steroids interfere with the process of remyelination, as they are known to do with myelination during development. Thus, dexamethasone appears to have a dual effect, decreasing demyelination but delaying remyelination.

Animals↗

PubMed1987

Experimental neuropathology of chronic demyelination induced by a JHM virus variant (DS).

A small plaque variant of JHM virus has a markedly reduced ability to kill mice following intracerebral inoculation. Spinal cords of mice surviving 13 to 16 months following acute infection with this variant were examined ultrastructurally. Multiple subpial areas of demyelination in the anterior and lateral white matter were found in five of 13 mice. The lesions had more gliosis, fewer oligodendrocytes, and less remyelination than has been described following other infections with JHM virus. No conclusive evidence of active demyelination or viral-like particles was found. The pathogenesis of the lesions observed may be due to a persistent, attenuated infection of oligodendrocytes or to immunologic processes. These lesions were similar to chronic multiple sclerosis plaques. Therefore, this variant should prove to be a useful tool for studying the long-term effects of viral-induced demyelinating diseases.

Animals↗

PubMed1989

Osmotic demyelination syndrome. Lack of pathologic and radiologic imaging correlation.

An otherwise healthy diabetic woman developed severe hyponatremia, her serum sodium ion levels were rapidly corrected to normal, and she had a course of improvement then neurologic deterioration, with seizures and coma developing in the subsequent two days. Imaging studies, including computed tomography and magnetic resonance images of the brain as late as 19 days after the osmotic insult, failed to show pathologically demonstrated demyelinating lesions. Osmotic brain injury induces demyelination in areas of gray-white apposition and, clinically, results in a delayed neurologic deterioration one to three days following the osmotic challenge. Even with magnetic resonance imaging, review of the literature and this experience suggest that osmotic demyelination cannot reliably be imaged during the first month after the insult.

Brain↗

PubMed1993

Fatal rabies associated with extensive demyelination.

OBJECTIVE: To compare the clinical course with the neuropathological findings in a patient who died of acute rabies encephalomyelitis with coexisting demyelinating lesions. DESIGN: Patient's history was extensively investigated, during her illness and after death. Details of her previous allergies, postexposure prophylaxis, early use of steroid therapy, 20-day course in an intensive care unit, and autopsy results are clinicopathologically correlated. SETTING: The intensive care unit of an 1100-bed tertiary referral center and teaching hospital. PATIENT: A 55-year-old woman, referred by her family doctor. CONCLUSIONS: Postvaccinal encephalomyelitis and rabies can run similar courses and can be misdiagnosed. On admission to the hospital, this patient was initially diagnosed as having postvaccinal disease. However, autopsy results and postmortem viral cultures disclosed a complex picture, including acute rabies and widespread perivenous demyelination. One other similar report from 1977 in the literature is reviewed. No adequate explanation of the rare coexistence of acute rabies encephalomyelitis and perivascular demyelination is available.

Demyelinating Diseases↗

PubMed1999

Mechanisms of high-dose intravenous immunoglobulins in demyelinating diseases.

Administration of high-dose intravenous immunoglobulins has become one of the most successful new treatment regimens for demyelinating diseases. In a decade of molecular medicine, it came as a surprise that a natural blood product would prove effective in several disorders, including Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and, probably, multiple sclerosis. Many experimental studies, both in vivo and in vitro, have shown that intravenous immunoglobulins can interfere with the immune system at several levels. In addition, intravenous immunoglobulins may promote remyelination in demyelinating disease associated with viral infections. At present, no single mode of action has been identified as the crucial mechanism, which leads us to suggest that multiple effects may act in concert.

Antibodies, Anti-Idiotypic↗

PubMed2002

The "spray can" sign: validation of a clinical observation in chronic inflammatory demyelinating polyneuropathy.

BACKGROUND: The presentation of chronic inflammatory neuropathies is variable. The decision regarding when to intervene with treatment is ideally determined by identifying early markers of loss of function. OBJECTIVE: To test the hypothesis that an observation of functional impairment, defined by a patient with demyelinating neuropathy, can be used as a reproducible and reliable measure of improvement with intravenous immune globulin. DESIGN: A 28-year-old woman presented with a chronic inflammatory demyelinating polyneuropathy. Her first complaint was the inability to use her deodorant spray because of hand weakness. A calibrated pincer gauge fixed on top of her usual spray can was used to objectively test finger flexion. Tip grip and lateral pinch were also measured. A calibrated dynamometer was used to measure grip strength. RESULTS: Power and precision grip force were reproducible in normal control subjects by means of the spray can test. This test proved to be a reliable indicator of reduced muscle strength in the patient and improved after treatment with intravenous immune globulin. CONCLUSIONS: The spray can test objectively quantified the daily function, nominated by the patient, of operating an aerosol can. This measurement, drawn from a functional loss observed by the patient, proved to be a portable and reliable indicator of decline and recovery in chronic inflammatory demyelinating polyneuropathy.

Adult↗