Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuritis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,063 records · Page 59Linked to original sources
PubMed1994

Optic neuritis and multiple sclerosis: the T cell repertoires to myelin proteins and MBP peptides change with time.

Autoreactive T cells recognizing myelin basic protein (MBP), proteolipid protein (PLP) and MBP peptides have been described in multiple sclerosis (MS) and optic neuritis (ON), but their role in disease pathogenesis, if any, is unknown. A consistency of the T cell repertoire over the course of MS and ON should facilitate the development of specific immunotherapies. We have examined the T cell responses to autoantigens in two consecutive blood specimens taken from patients with ON and MS, and in two consecutive CSF specimens obtained from ON patients. As read-out numbers of T cells responding to antigen stimulation by the secretion of interferon-gamma were estimated. Pronounced differences in occurrence and numbers of T cells recognizing MBP, MBP peptides with the amino acid sequences 63-88, 110-128 and 148-165, and PLP were noticed in individual ON and MS patients over the course of disease. The MBP peptide among those three included, that was predominantly recognized by T cells in the individual patient, also varied over the course. The quantitative and qualitative changes of the myelin antigen-specific T cell response in MS and in ON, the latter to a certain extent reflecting the situation in early MS, do not favor the future useful development of specific immunotherapies in these diseases.

Adult↗
PubMed1994

Th1-like cell responses to peripheral nerve myelin components over the course of experimental allergic neuritis in Lewis rats.

Experimental allergic neuritis (EAN) is a T cell-mediated animal model of Guillain-Barré syndrome characterized by inflammation and demyelination of peripheral nerves. EAN can be induced by immunization of rats with bovine peripheral nerve myelin (BPM) or the myelin proteins P2 or P0, but the extent of T cell responses over the course of EAN is incompletely defined. We studied the T cell responses to these proteins and the glycolipid GM1 by enumerating T helper type 1 (Th1)-like cells secreting interferon-gamma (IFN-gamma) after short-term culture of mononuclear cells (MNC) in presence of antigen. Already 7 days post immunization (p.i.) with BPM and before onset of clinical EAN, lymph nodes contained elevated levels of P2 responsive T cells. At the height of EAN on day 14 p.i. and during recovery, T cell levels responding to BPM, P0 and GM1 were also elevated. The same temporal profiles and specificities were registered for antigen reactive spleen MNC. The results implicate that Th1-like cells with multiple specificities including the glycolipid GM1 occur at increased levels in lymphoid organs in EAN rats, and that IFN-gamma may be an important effector molecule in the induction of nerve damage.

Animals↗
PubMed1996

Serial MRI, VEP, SEP and biotesiometry in acute optic neuritis: value of baseline results to predict the development of new lesions at one year follow up.

INTRODUCTION: In an attempt to establish the value of MRI, VEP, SEP, and biotesiometry in monitoring disease evolution we undertook a one year follow up study of 70 untreated patients with acute optic neuritis (ON). MATERIAL & METHODS: ON was monosymptomatic in 48 patients (bilateral in 10) and part of clinically definite multiple sclerosis (CDMS) in 22 patients, examined as mentioned below. RESULTS: Results are given at onset and at follow up (in brackets). In monosymptomatic ON, brain MRI was abnormal in 53% (53%), VEP in the eye with acute ON in 79% (71%), VEP in the clinically unaffected eye in 34% (47%), SEP in 25% (23%), and biotesiometry in 29% (17%). In CDMS, brain MRI was abnormal in 95% (95%), VEP in the eye with acute ON in 86% (77%), VEP in the clinically unaffected eye in 50% (64%), SEP in 55% (50%), and biotesiometry in 63% (53%). Only minor changes in test scores were observed after one year except for significant improvement of VEP in eyes with acute ON. Eight of 32 patients, characterized by at least one abnormal paraclinical test at onset of monosymptomatic ON, had developed CDMS versus none of 16 patients with normal paraclinical results (p = 0.03; Fisher). CONCLUSION: Patients with monosymptomatic ON with paraclinical signs of multifocal involvement at onset had an increased risk of developing CDMS. No single test predicted the evolution of CDMS, perhaps due to the relatively short follow up time.

Acute Disease↗
PubMed1996

Distribution of HLA-Dw2 in optic neuritis and multiple sclerosis indicates heterogeneity.

UNLABELLED: The human leukocyte antigen (HLA) phenotype Dw2 is known to be increased in multiple sclerosis (MS), but only slightly in optic neuritis (ON). MATERIAL AND METHODS: 127 consecutive patients with unilateral monosymptomatic ON were typed genomically for HLA-DR and -DQ genes. RESULTS: The frequency of HLA-Dw2 among ON patients (47%) was found to be significantly higher than among 250 controls (30%) but significantly lower than in a group of 245 MS patients (60%), all of the same ethnic origin. At the group level, these figures can be calculated to indicate that 53% of the ON patients belong to the group of "MS-type ON" (95% confidence limits 25-78%). A compilation of published data on the frequency of the HLA-DR17(3), DQ2 haplotype, prompted by a slight increase in this material, revealed a significant association with this haplotype in ON, after compensation for the increase of Dw2. CONCLUSION: ON differs from both MS and controls regarding HLA-Dw2. Thus, a substantial number of patients with ON may suffer from conditions not immuno-genetically related to MS, which might be designated as non-MS type ON. This condition may be more common in men and in young patients of both sexes.

Adult↗
PubMed1997

Optic neuritis progressing to multiple sclerosis.

We report a partially retrospective and longitudinal study of patients with optic neuritis (ON) that developed multiple sclerosis (MS). We assessed clinical features or factors that might differentiate these patients from those with ON that did not develop MS. Of the cases followed, 110 (67%) were found to have an idiopathic origin of the disease; whereas 55 (33%) were found to develop it secondary to another disease. Of the 110 idiopathic cases, 13 (12%), developed MS over an average of 2 years. The results of these patients in the laboratory analyses of blood and CSF as well as the results of the MRI and evoked potential studies, were significantly different from the ON patients without MS. We conclude that the percentage of patients with ON in our sample that developed MS is similar to that found in Japan and is relatively low in comparison to other reports.

Adult↗
PubMed1997

Absence of seven human herpesviruses, including HHV-6, by polymerase chain reaction in CSF and blood from patients with multiple sclerosis and optic neuritis.

Several members of the herpesvirus family have been implicated in the pathogenesis of multiple sclerosis (MS). Recently, HHV-6 viral antigen has been demonstrated in association to MS plaques, as well as DNA from human herpesvirus 6 (HHV-6) in cerebrospinal fluid from a few MS patients by polymerase chain reaction (PCR). In the present study, CSF from patients with MS, optic neuritis and other neurological diseases, as well as consecutive CSF and serum samples from MS patients included in a clinical trial with acyclovir, were analysed by nested PCR for the presence of DNA from herpes simplex virus 1 and 2, Epstein-Barr virus, varicella zoster virus, cytomegalovirus, human herpesvirus 6 and 7. No virus DNA was found in any CSF (n = 115) or serum (n = 116) sample. These findings argue against a continuous disseminated herpesvirus infection in MS, but do not rule out a lesion-associated, low-grade herpesvirus infection within the MS brain.

Adolescent↗
PubMed1997

Serial Gadolinium-enhanced MRI in untreated patients with acute optic neuritis: implications for natural history.

INTRODUCTION: Serial brain MRIs with and without Gadolinium (Gd)-DTPA were performed in acute optic neuritis (ON). MATERIAL AND METHODS: Fifty-nine untreated patients (44 female) aged 20-57 years with ON underwent MRI median 16 d from onset of symptoms of ON and at 1 and 12 months follow-up. RESULTS: At onset of monosymptomatic ON (AMON), 13 of 40 (33%) patients had lesions on MRI without Gd-DTPA compared with 15 of 19 (79%) patients with ON as part of clinically definite multiple sclerosis (CDMS). An initially abnormal MRI never normalized, whereas 3 patients with AMON with initially normal MRI had lesions at follow-up. In AMON enhancing lesions were seen in 5% of patients at onset, in 12% after 1 month, and in 11% after 12 months. The corresponding figures in CDMS were 21%, 38%, and 33%. All enhancing lesions were also seen on MRI without Gd-DTPA. The number of lesions on MRI without Gd-DTPA increased significantly with time in the 8 patients with AMON with enhancing lesions at one or more MRIs. New enhancing lesions appeared in 11 patients (6 AMON), of whom 3 (2 AMON) had an exacerbation. In contrast, 12 (5 AMON) patients had an exacerbation, being accompanied by new enhancing lesions in only 3 (2 AMON) patients. CONCLUSION: Gd-DTPA did not increase the sensitivity of MRI, which was significantly higher in CDMS than in AMON, but improved the understanding of the natural history of AMON and CDMS. The dynamics of enhancing lesions did not correlate well with exacerbations. Serial MRI and clinical assessment are supplementary in monitoring disease activity.

Acute Disease↗
PubMed1999

Changes in the retinal veins in acute optic neuritis.

OBJECTIVE: To investigate patients with acute optic neuritis (ON) for changes of the retinal veins. MATERIAL AND METHODS: Seventy-six patients with acute ON were extensively neuro-ophthalmologically examined. RESULTS: Multiple sclerosis (MS) was found in 41 patients of whom 1 had periphlebitis retinae (PR) and 2 had venous sheathing (VS). Probable MS was found in 15 patients without prior symptoms of MS. One had PR and VS, and 2 had VS. Twenty patients had mono-symptomatic ON, none had retinal changes. CONCLUSION: Changes of the retinal veins should alert the clinician to a probable diagnosis of MS. ON appears frequently as the initial symptom of MS. Our observation of VS in these patients suggest that clinically silent retinal disease activity had occurred prior to the ON.

Acute Disease↗
PubMed2006

Optical coherence tomography versus automated perimetry for follow-up of optic neuritis.

PURPOSE: To evaluate the usefulness of optical coherence tomography (OCT) for follow-up of optic neuritis (ON) compared with subjective visual function tests. METHODS: Twelve patients with ON underwent a complete ophthalmological evaluation at initial diagnosis, including best corrected visual acuity (VA), visual fields testing and OCT examination. These examinations were repeated periodically over 6 months. Retinal nerve fibre layer (RNFL) thickness evolution was analysed and correlated with VA and visual field mean deviation. RESULTS: Six months after ON, mean RNFL in the affected eye decreased significantly compared with that in the fellow eye (24.54%). A significant correlation was found between RNFL thinning and final VA (r = 0.807, p = 0.005), with a 1-line drop in VA for every 5.4-micro m decrease. All patients with an altered visual field had an abnormal RNFL value; of the seven patients with normal visual fields, 57% had an abnormal RNFL value (p < 5%). CONCLUSIONS: Optical coherence tomography can detect axonal damage as early as the third month after an isolated initial episode of ON, even in the presence of normal visual fields. Mean RNFL thinning is correlated with final VA.

Adult↗
PubMed2006

Isolated bilateral optic neuritis in acute disseminated encephalomyelitis.

PURPOSE: We present a 4-year-old girl with isolated visual loss related to a bilateral oedematous optic neuropathy of unknown origin, occurring after an episode of viral illness. METHODS: A cerebral MRI was performed, showing bilateral enhancement of the optic nerves and bilateral, diffuse, cerebral white matter lesions. RESULTS: The MRI scan suggested acute disseminated encephalomyelitis. Treatment with intravenous steroids and immunoglobulins resulted in favourable visual recovery. CONCLUSIONS: Bilateral isolated optic neuritis in childhood may be the only presenting symptom in acute disseminated encephalomyelitis, which requires appropriate evaluation and therapeutic management.

Blindness↗
PubMed1988

A case of angioimmunoblastic lymphadenopathy associated with a long spontaneous remission, retrobulbar neuritis, a clonal rearrangement of the T-cell receptor gamma chain gene and an unusual marrow infiltration.

A man with angioimmunoblastic lymphadenopathy entered a spontaneous remission that lasted 18 yr, ending in retrobulbar neuritis followed by a generalized relapse. After another remission was induced by prednisolone he developed marrow infiltration with a lymphoid cell of novel surface-marker phenotype. His lymph node cells demonstrated a clonal rearrangement of the T-cell receptor gamma chain (TcR gamma) genes whereas the TcR beta genes were heterogeneously rearranged. The marrow cells did not contain the rearranged TcR gamma gene. He died of pulmonary emboli 21 yr after his original presentation. We propose a model whereby the original event was the development of a lymphoid stem cell clone with no TcR gene rearrangement. Subsequently, a sub-clone bearing the TcR gamma gene rearrangement proliferated in the lymph nodes and further heterogeneous rearrangement of the TcR beta genes occurred within this subclone. Proliferation in the marrow of the original clone finally supervened.

Adult↗
PubMed1995

Astrocytes upregulate glial fibrillary acidic protein (GFAP), but not insulin-like growth factor-I (IGF-I) during experimental autoimmune neuritis (EAN).

T cell-mediated autoimmune neuritis produces rapid activation of spinal cord microglia. To determine whether this microglial response upregulates astrocytic expression of IGF-related proteins, we induced EAN and used in situ hybridization and immunocytochemistry to examine the mRNAs and peptides for glial fibrillary acidic protein (GFAP), insulin-like growth factor-I (IGF-I), IGF-I receptor (IGFR-I) and IGF binding protein-2 (IGFBP-2). Relative levels of GFAP mRNA and peptide were highest in the lumbar spinal cord 4-10 d following T cell transfer and significant GFAP elevations were still present after three weeks. The astrocytes expressing GFAP mRNA and peptide were localized around motoneurons which were related topographically to axons in peripheral nerve inflammatory lesions. In the nucleus gracilis, where terminals of dorsal root ganglion neurons are located, astrocytic levels of GFAP mRNA and peptide rose later and did not reach their highest levels until 21 d after T cell transfer. Even though microglia were activated in both locations 2-4 d after transfer, astrocytic levels of IGF-I, IGFR-I and IGFBP-2 mRNA and peptide did not differ significantly from those observed in controls. The dissociation of GFAP and IGF-I expression in EAN suggests that these astrocytic responses may be independently regulated. We also suggest that the type and severity of remote neuronal injury are probably more important inducers and regulators of these astrocytic responses than microglial cell activation.

Animals↗
PubMed2002

The critical role of IL-12p40 in initiating, enhancing, and perpetuating pathogenic events in murine experimental autoimmune neuritis.

Interleukin 12 (IL-12) is a proinflammatory cytokine with important immunoregulatory activities and is critical in determining the differentiation and generation of Th1 cells. For the present study, we investigated the role of endogenous IL-12 in the pathogenesis of experimental autoimmune neuritis (EAN), which is a CD4+ T-cell mediated autoimmune inflammatory disease of the peripheral nervous system. EAN is used as an animal model for Guillain-Barré syndrome of humans. Here, EAN was established in IL-12 p40 deficient mutant (IL-12-/-) C57BL/6 mice by immunization with P0 peptide 180-199, a purified component of peripheral nerve myelin, and Freund's complete adjuvant. In these IL-12-/- mice the onset of clinical disease was delayed, and the incidence and severity of EAN were significantly reduced compared to that in wild-type mice.The former group's clinical manifestations were associated with less P0-peptide 180-199 induced secretion of interferon-gamma (IFN-gamma) by splenocytes in vitro and low production of anti-P0-peptide 180-199 IgG2b antibodies in serum. Fewer IFN-gamma and TNF-alpha producing cells, but more cells secreting IL-4, were found in sciatic nerve sections from IL-12-/- mice, consistent with impaired Th1 functions and response. However, the IL-12 deficiency appeared not to affect P0 peptide 180-199-specific T-cell proliferation. These results indicate that IL-12 has a major role in the initiation, enhancement and perpetuation of pathogenic events in EAN by promoting a Th1 cell-mediated immune response and suppressing the Th2 response. This information augments consideration of IL-12 as a therapeutic target in Guillain-Barré syndrome and other T-cell-mediated autoimmune diseases.

Animals↗
PubMed1980

Lymphocyte subpopulations in peripheral blood and cerebrospinal fluid from patients with acute optic neuritis.

Ten patients with acute optic neuritis (AON) were examined for T and B lymphocytes in blood and cerebrospinal fluid by means of rosette techniques. The percentage of T lymphocytes in blood was significantly decreased (54+/-3%) compared to controls (66+/-2%). Absolute numbers of T lymphocytes, and relative and absolute B lymphocyte concentrations were not significantly different from controls. The cerebrospinal fluid (CSF) T lymphocyte percentage was significantly increased (88.8% compared to 78.0% in controls). The relative CSF immunoglobulin G concentration was elevated in four patients (40%). On agarose gel electrophoresis, bands in the gamma globulin region were found in two patients (20%).

Acute Disease↗
PubMed1980

Correlation of visual evoked potentials, ophthalmological and neurological findings after unilateral optic neuritis.

Forty-two patients were tested with pattern reversal visual evoked potentials (VEPs) 1--8 years after an episode of acute unilateral optic neuritis. The stimulation was produced by dot as well as checker-board pattern. An unexpectedly large proportion (12 cases) showed normal VEP latencies from the affected eye. In these patients the initial visual acuity was on the average significantly better than in cases with prolonged VEP latencies. They also had significantly fewer remaining ocular signs than the patients with abnormal VEPs. On the other hand, no correlation was found between the VEP findings and the incidence of CSF abnormalities, multiple sclerosis and HLA types. In 14 patients of which 13 belonged to the group above, repeated VEP tests were performed from the acute onset of the disease and up to 2 years afterwards confirming that a considerable normalization of VEP latencies occurs.

Adult↗
PubMed1982

Pattern VEP in two immunochemical subtypes of optic neuritis.

Visual functions and visual evoked potentials (VEP) were compared in 2 groups of patients with optic neuritis (ON). The subdivision was based on the occurrence of oligoclonal IgG in the cerebrospinal fluid in some patients [the ON (+) group] but not in others [the ON (-) group]. At the onset of ON there were no other signs of neurological disease in these patients. Later the majority of those in the ON (+) group had developed multiple sclerosis but only one patient in the ON (-) group. Recovery after the acute optic inflammation was the same in both groups with respect to visual acuity and fields, but better in the ON (-) than in the ON (+) group with respect to colour vision and pattern VEP. A closer correlation between colour vision defects and VEP latency changes was found for the ON (+) than the ON (-) group, suggesting demyelinating disease as a more probable cause of the optic nerve inflammation in the former than in the latter group.

Adolescent↗
PubMed1991

Chiasmal optic neuritis.

We describe two cases of chiasmal optic neuritis. The presenting symptoms were reduced visual acuity and bitemporal visual field defects. The enlargement of the optic chiasm in the acute stage and normalization after recovery is demonstrated by magnetic resonance imaging (MRI).

Adrenal Cortex Hormones↗
PubMed1991

Acute optic neuritis with normal visual acuity. Comparison of symptoms and signs with psychophysiological, electrophysiological and magnetic resonance imaging data.

In a prospective study of hitherto 70 patients with acute optic neuritis (ON), 18 patients aged 15-49 years (12 women, 6 men) were diagnosed as having very subtle form of ON (bilateral in 4 patients), characterized by normal visual acuity. However, their symptoms were sudden functional visual disturbances, most frequently blurred vision accompanied by pain in or around the affected eye(s). In 5 patients, the ON was a manifestation of clinically definite multiple sclerosis (MS); the remaining 13 patients had monosymptomatic ON. The duration of visual symptoms ranged from 2 to 28 days (median 7 days) at the time of examination. Although 18 patients had a normal visual acuity, i.e. 6/6 c.c. (Snellen's notation) or better, extensive studies of the visual functions (using sensitive supplementary tests) revealed various abnormalities, primarily various visual field defects, abnormal contrast sensitivity, abnormal VEP and colour vision deficiencies (often of blue-yellow type). Magnetic resonance imaging (MRI) of the brain revealed demyelinating lesions in 10 of the 13 patients with monosymptomatic ON, and in all 5 patients with definite MS. The extended disease spectrum gives reason to hypothesixe that ON may occur more frequently than previously reported, and that the described subtle form of ON could be an unnotified precocious manifestation of the demyelinating disease.

Acute Disease↗