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PubMed1997

Diameter of the optic nerve in idiopathic optic neuritis and in anterior ischemic optic neuropathy.

PURPOSE: There is considerable overlap in the clinical profile of patients with idiopathic optic neuritis (ON) and anterior ischemic optic neuropathy (AION). We tested the hypothesis that the retrobulbar diameter of the optic nerve may be a criterion for the differential diagnosis between ON and AION. METHODS: The diameter of the optic nerve was measured by B-scan ultrasonography with the eye in an abducted position. Only patients with a unilateral optic neuropathy were included, 16 ON patients (mean age 24 years, 5 with and 11 without disc swelling) and 9 patients with AION (mean age 72 years). As controls for the ON patients 10 young normal subjects (mean age 25 years) and as controls for the AION patients 10 elderly subjects with eye problems not related to the optic nerve (mean age 76 years) were examined. RESULTS: In the ON patients with disc swelling the diameter of the optic nerve was 5.4 +/- 0.5 mm in the affected and 3.0 +/- 0.3 mm in the unaffected side. This difference was significant (Wilcoxon-test, p = 0.043). In the ON patients without disc swelling the diameter of the optic nerve was 4.4 +/- 0.4 mm in the affected and 3.0 +/- 0.3 mm in the unaffected side. This difference was significant (Wilcoxon-test, p = 0.003). In the AION patients the diameter of the optic nerve was 3.0 +/- 0.3 mm on the affected and 2.8 +/- 0.4 mm on the unaffected side. This difference was not significant (Wilcoxon-test, p = 0.093). Comparing the optic nerves with ON and AION to those of the controls, the diameter was significantly enlarged in the nerves with ON and normal in the nerves with AION (one factor repeated ANOVA). CONCLUSION: The diameter of the optic nerve is increased in ON without disc swelling and even more so in ON with disc swelling. The enlargement is probably due to edema of the nerve itself, not the surrounding subarachnoidal space. In AION, the diameter of the optic nerve is normal. Measuring the diameter of the optic nerve by B-scan ultrasonography is particularly useful in the differential diagnosis between ON with disc swelling and AION.

Adolescent↗
PubMed2003

Optic neuritis in children--clinical and electrophysiological follow-up.

Optic neuritis (ON) in children usually presents with visual loss, relative afferent pupillary defect (RAPD), abnormal optic disc appearance, defects of visual field and colour vision, as well as with abnormalities of visual evoked potentials (VEP). Both, clinical and VEP parameters, improve after the attack; the time until recovery, however, is as yet unknown. The aim of this study was to follow-up children with ON for 1 year and to determine clinical and VEP recovery. Twelve children (six with bilateral, six with unilateral ON) were studied in the acute phase and systematically followed-up for 1 year. The results show that initially, visual acuity was diminished in all eyes, while after 1 year, in only 14% of them. Optic disc appearance was abnormal in 83.3% of the eyes in the acute phase, and in 85% after 1 year. At the disease onset RAPD could be detected in 67%, visual field defects in 58.5%, and colour vision defects in 50% of eyes, but none of these abnormalities persisted in any eye until the end of study. VEP were abnormal in 83% of eyes in the acute phase and in 56% at the final follow-up (at 6 or 12 months). VEP normalization, when occurred, was mostly observed during the first 6 months. Complete clinical and VEP recovery was observed in three children. Both, clinical and electrophysiological recovery in children with ON were relatively substantial and fast within the first year. VEP improvement may indicate better prognosis.

Acute Disease↗
PubMed2003

Evidence favoring the involvement of CC chemokine receptor (CCR) 5 in T-lymphocyte accumulation in optic neuritis.

OBJECTIVE: To define the relationships between levels of chemokine receptor (CCR)5+ T-cells in blood and cerebrospinal fluid (CSF) of optic neuritis (ON) and control patients (CON). MATERIALS AND METHODS: Expression of CCR5 and related receptors CCR1 and CCR3 on CD4- and CD8-positive T-cells in peripheral blood mononuclear cells (PBMC) and CSF was determined by flow cytometry in 20 patients with ON, 16 control patients with lumbar spondylosis, 20 healthy controls (HC) and 16 patients with rheumatoid arthritis (RA). RESULTS: CCR5+CD4+ and CD8+ T-cells were enriched in CSF, compared with PBMC, in both ON and CON patients (all P < 0.001), and the percentages of CD4+/CCR5+ (r = 0.917) and CD8+/CCR5+ (r = 0.828) cells in PBMC and CSF were strongly and directly correlated. CCR5+ T-cells produce high amounts of tumor necrosis factor-alpha (TNF-alpha) and very low amounts of interleukin-5 (IL-5). Closely related receptors (CCR1, CCR3) were not altered. CONCLUSIONS: Our data suggest an involvement of CCR5 in T-cell accumulation in the inflamed central nervous system.

Adult↗
PubMed2001

Optic neuritis and multiple sclerosis.

PURPOSE: Review of the association between optic neuritis (ON) and multiple sclerosis (MS). RESULTS: MS often presents as acute unilateral ON. While it is clear that many patients with ON suffer from a generalized disease of the central nervous system that will go on to clinically definite MS (CDMS), it is also clear that others do not. With more and more well-informed patients and the emerging pharmacotheraphy for MS, the distinction between those patients with ON who have MS and those who do not, has become more important than ever before. Recently, a large randomized clinical trial on patients with ON or other clinically isolated syndromes suggestive of MS and evidence of prior subclinical demyelination on magnetic resonance imaging of the brain, found that treatment with recombinant interferon-beta-1a is beneficial by reducing the development of CDMS. CONCLUSION: Ophthalmologists should refer their patients with acute ON to a neurologist for MS-directed investigations and decisions regarding early institution of disease modifying therapy.

Acute Disease↗
PubMed1999

Linomide suppresses experimental autoimmune neuritis in Lewis rats by inhibiting myelin antigen-reactive T and B cell responses.

Linomide (quinoline-3-carboxamide) is a synthetic immunomodulator that suppresses several experimental autoimmune diseases. Here we report the effects of Linomide on experimental autoimmune neuritis (EAN), a CD4+ T cell-mediated animal model of acute Guillain-Barré syndrome (GBS) in humans. EAN induced in Lewis rats by inoculation with bovine peripheral nervous system (PNS) myelin and Freund's complete adjuvant was strongly suppressed by Linomide administered daily subcutaneously from the day of inoculation. Linomide dose-dependently delayed the interval between immunization and onset of clinical EAN, as well as the severity of EAN symptoms. These clinical effects were associated with dose-dependent down-modulation of PNS antigen-induced T and B cell responses and with suppression of the proinflammatory cytokines IL-12, interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) mRNA. In PNS sections, Linomide suppressed IL-12 and TNF-alpha, and up-regulated IL-10 mRNA expression. These findings suggest that Linomide could be useful in certain T cell-dependent autoimmune diseases.

Adjuvants, Immunologic↗
PubMed2001

Transfer of myelin-specific cells deviated in vitro towards IL-4 production ameliorates ongoing experimental allergic neuritis.

A causal role of IL-4 (Th2) production for recovery in experimental allergic neuritis (EAN) was indicated by experiments where Th1-like autoreactive cell populations, taken from the induction phase of the disease, were deviated to extensive secretion of IL-4 in a selective fashion, by ex vivo stimulation with autoantigen in the presence of IL-4. The deviated cells were adoptively transferred to EAN rats at a time just prior to the onset of clinical signs. This treatment ameliorated EAN compared with sham treatment. This therapeutic approach, with generation of autoreactive IL-4-secreting cells ex vivo followed by subsequent adoptive transfer, may become a new selective treatment of organ-specific autoimmune diseases since, in contrast to previous attempts, it is done in a physiological and technically easy way.

Adoptive Transfer↗
PubMed2002

Elevated expression of CCR5 by myeloid (CD11c+) blood dendritic cells in multiple sclerosis and acute optic neuritis.

Myeloid and plasmacytoid dendritic cells (DC) are present in cerebrospinal fluid (CSF) in non-inflammatory neurological diseases (NIND) and elevated in clinically definite multiple sclerosis (MS) and in early MS - acute monosymptomatic optic neuritis (ON). Here, we show that expression of CCR5, a chemokine receptor for regulated on activation, normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein (MIP)-1alpha/beta, is elevated on blood myeloid (CD11c+) DC in MS and ON compared to non-inflammatory controls. In contrast, expression of CXCR4, a receptor for stromal cell-derived factor (SDF)-1alpha, is similar in all groups. Blood myeloid DC from MS patients respond chemotactically to RANTES and MIP-1beta, which are expessed in MS lesions. In active MS and ON, expression of CCR5 by myeloid DC in blood correlates with numbers of these cells in CSF. Thus, elevation of CCR5 may contribute to recruitment of myeloid DC to CSF in MS and ON. Recruitment of plasmacytoid DC to CSF appears to be CCR5-independent.

Acute Disease↗
PubMed1999

Suppression of chronic experimental autoimmune neuritis by nasally administered recombinant rat interleukin-6.

Experimental autoimmune neuritis (EAN) is a CD4+ T-cell-mediated demyelinating disease of the peripheral nervous system (PNS) and serves as experimental model for human immune-demyelinating neurophathies, especially the Guillain-Barré syndrome. In this study, we examined the effect of recombinant rat interleukin-6 (rrIL-6) on chronic EAN in Lewis rats induced by immunization with P2 peptide 57-81 and Freund's complete adjuvant (FCA). Nasal administration of rat rIL-6 (1 microg/rat/day) beginning in the initial phase of EAN as a therapeutic agent, decreased the severity and the duration of clinical EAN. Low-grade inflammation and suppression of regional demyelination within the sciatic nerves were seen in rrIL-6-treated rats. Hyporesponsiveness of lymph node T cells, down-regulation of serum tumour necrosis factor-alpha (TNF-alpha) and increased levels of P2-specific immunoglobulin G1 (IgG1) antibodies document that nasal administration of rrIL-6 was effective systemically. However, because of the non-specific nature of the treatment and multiple effects of IL-6, more experience and great caution are needed, before nasal administration of IL-6 can be considered as a treatment of human autoimmune demyelinating neurophathies.

Administration, Intranasal↗
PubMed2002

Accumulation of immunoglobulin across the 'blood-nerve barrier' in spinal roots in adoptive transfer experimental autoimmune neuritis.

At the onset of Guillain-Barré syndrome, disruption of diffusion barriers, such as the blood-nerve barrier, probably increases the exposure of spinal roots and peripheral nerves to macromolecules, some of which might be pathogenic. As a measure of such disruption, we measured the accumulation in the endoneurium of spinal roots and sciatic nerve of systemically administered 125I-labelled immunoglobulin in adoptive transfer experimental autoimmune neuritis (AT-EAN) in the rat. AT-EAN is a model of Guillain-Barré syndrome, induced by injection of activated T lymphocytes sensitized to myelin P2 protein. Immunoglobulin accumulation was expressed as counts/min/mg in fixative-perfused roots as a percentage of that in serum, measured 24 h after intraperitoneal injection of 0.1 micro Ci 125I-labelled immunoglobulin. Immunoglobulin accumulation in the roots of normal rats was 3 +/- 1% (mean +/- SE), but this first increased 3(1/2) days after cell injection, peaked at 22 +/- 2% on day 4(1/2), and declined to normal by day 8. T lymphocytes and polymorphonuclear leucocytes first appeared within the endoneurium at day 3(1/2), and macrophages and a few erythrocytes at day 4. Neurological deficit appeared on day 4 and was maximal on day 6. Demyelination and axonal degeneration began at day 5. The first abnormality detected in AT-EAN was a rapid increase in the passage of immunoglobulin into spinal roots, together with endoneurial infiltration of T lymphocytes and polymorphonuclear leucocytes. Accumulation of immunoglobulin was maximal during the worsening of neurological deficit, and declined rapidly before the onset of neurological recovery.

Adoptive Transfer↗
PubMed1998

Thalidomide prolongs experimental autoimmune neuritis in Lewis rats.

Thalidomide is reported to have immunomodulatory and anti-inflammatory effects, which have led to its use in the treatment of a number of immune-mediated disorders, including leprosy, discoid lupus and Behcet's disease, and to prevent immunological rejection phenomena following skin and bone marrow grafts. Experimental autoimmune neuritis (EAN) is a CD4+ T-cell-mediated demyelinating autoimmune disease, which represents an animal model for the study of the immunopathogenesis and immunotherapy of Guillain-Barré syndrome (GBS) in humans. We examined the effect of thalidomide in Lewis rats with EAN, which was induced by immunization with bovine peripheral nerve myelin (BPM) and complete Freund's adjuvant (CFA). Thalidomide prolonged clinical EAN when given at a dose of 200 mg/kg/day by gavage. This clinical effect was associated with increased numbers of inflammatory cells in sciatic nerve sections and elevated numbers of interferon-gamma (IFN-gamma) mRNA-expressing cells among lymph node mononuclear cells from thalidomide-treated EAN rats on day 17 postimmunization, i.e. at the peak of clinical EAN. The finding that thalidomide prolongs clinical EAN is in agreement with the clinical polyneuropathy reported in patients receiving treatment with thalidomide and limits its clinical usefulness.

Animals↗
PubMed2000

Intranasal administration of recombinant mouse interleukin-12 increases inflammation and demyelination in chronic experimental autoimmune neuritis in Lewis rats.

To examine whether interleukin (IL)-12 modulates ongoing chronic experimental autoimmune neuritis (EAN), we evaluated the effects of recombinant mouse IL-12 (rmIL-12) in Lewis rats with chronic EAN, induced by immunization with P0 peptide (180-199) plus complete Freund's adjuvant. Rats were treated intranasally with either 0.1 or 1 microg/rat/day rmIL-12 for 6 days from the onset of clinical chronic EAN, on days 5-10 postimmunization (p.i.). Only high-dose rmIL-12 exacerbated chronic EAN. This clinical effect was associated with higher numbers of inflammatory cells and more severe demyelination in sciatic nerve sections on days 15 and 80 p.i. compared with low-dose rmIL-12-treated rats and phosphate-buffered saline (PBS)-treated control rats. High-dose rmIL-12 increased significantly the lymph node mononuclear cell proliferation in response to P0 peptide 180-199 and IFN-gamma production in the sciatic nerves. These data indicate that intranasally administered IL-12 acts as a proinflammatory cytokine in chronic EAN. Effective inhibition of IL-12 in vivo could be considered for therapeutic use in chronic inflammatory demyelinating polyradiculoneuropathy.

Administration, Intranasal↗
PubMed2000

Augmented expression of daintain/allograft inflammatory factor-1 is associated with clinical disease: dynamics of daintain/allograft inflammatory factor-1 expression in spleen, peripheral nerves and sera during experimental autoimmune neuritis.

Experimental autoimmune neuritis (EAN) is an animal model of Guillain-Barré syndrome, characterized by inflammation and demyelination of the peripheral nervous system (PNS). Daintain/allograft inflammatory factor-1 (daintain/AIF-1) is a novel interferon-gamma-inducible protein expressed by macrophages during organ specific autoimmune diseases. To study the involvement of daintain/AIF-1 in EAN we induced EAN in Lewis rats by immunizing with bovine PNS myelin (BPM) and complete Freund's adjuvant (CFA). The expression of daintain/AIF-1 was examined in the spleen, peripheral nerves and sera during the course of EAN by immunohistochemistry and radioimunoassay (RIA). The expression of daintain/AIF-1 in the spleen and in the sciatic nerves peaked at the preclinical stage (day 7 post immunization (p.i.)) and at the height (day 15 p.i.) of clinical EAN, consistent with a disease promoting role for daintain/AIF-1. Daintain/AIF-1 expressing cells represented a subset of ED1+ or CD11b/c+ mononuclear cells. A significant increase of daintain/AIF-1-like immunoreactivity in sera occurred at the preclinical stage of EAN. Taken together, these data indicate that daintain/AIF-1 may play a proinflammatory role in the pathogenesis of EAN.

Animals↗
PubMed2000

Magnetic resonance imaging features of subacute idiopathic brachial neuritis.

A 60-year-old man presented with sudden onset of left shoulder pain followed 2 weeks later by the development of left shoulder girdle weakness. A clinical and electrophysiological diagnosis of subacute idiopathic brachial neuritis was made. The MRI features of subacute muscular denervation in this patient are discussed and the relevant literature reviewed.

Brachial Plexus Neuritis↗
PubMed2001

The presentation, aetiology, management and outcome of optic neuritis in an Asian population.

PURPOSE: To analyse the presentation, aetiology, management and outcome of patients with optic neuritis (ON) in Singapore. METHODS: This was a retrospective study involving consecutive patients with ON presentng at the Singapore National Eye Centre between January 1997 and May 1999. The presenting features, investigatons, treatment and visual outcome after 6 months were studied. RESULTS: A total of 31 patents (39 eyes) presented with ON during this period, 17 of whom had anterior ON. No aetiology was found in 26 patients (83.9%), two patients (6.5%) had multiple sclerosis, one had active syphilis, one had rheumatoid arthritis and another had pan-sinusitis. Seventeen patients (54.8%) were treated with intravenous methyl-prednisolone followed by oral prednisolone. Within the follow-up period 26 of 31 eyes (83.9%) wth idiopathic ON attained visual acuity of 6/12 or better with 12 (38.7%) recovering to 6/6 or better and only one eye ending with less than 6/60 visual acuity. The one patient with syphilis recovered 6/6 visual acuity bilaterally. Both patients with multiple sclerosis also had good visual recovery at 6 months. The visual outcome in those cases of ON associated with rheumatoid arthritis and pan-sinusitis was poor with visual acuity of less than 6/60 at 6 months follow up in each instance. CONCLUSION: The majority of the cases of ON in this study were idiopathic. There was a low association with multiple sclerosis. Most patients had good visual recovery within 6 months.

Adolescent↗
PubMed2002

Functional MRI of the visual cortex and visual testing in patients with previous optic neuritis.

The volume of cortical activation as detected by functional magnetic resonance imaging (fMRI) in the visual cortex has previously been shown to be reduced following optic neuritis (ON). In order to understand the cause of this change, we studied the cortical activation, both the size of the activated area and the signal change following ON, and compared the results with results of neuroophthalmological testing. We studied nine patients with previous acute ON and 10 healthy persons served as controls using fMRI with visual stimulation. In addition to a reduced activated volume, patients showed a reduced blood oxygenation level dependent (BOLD) signal increase and a greater asymmetry in the visual cortex, compared with controls. The volume of visual cortical activation was significantly correlated to the result of the contrast sensitivity test. The BOLD signal increase correlated significantly to both the results of the contrast sensitivity test and to the Snellen visual acuity. Our results indicate that fMRI is a useful method for the study of ON, even in cases where the visual acuity is severely impaired. The reduction in activated volume could be explained as a reduced neuronal input; however, the greater asymmetry might point to a cortical reorganization as a consequence of neuronal damage. Future fMRI studies in ON will add to the understanding of the neural adaptive behaviour following ON.

Adult↗
PubMed1988

Cluster headache-like headache, Hageman trait deficiency, retrobulbar neuritis, and giant aneurysm. Autonomic function studies.

A 56-year-old, previously reported woman with cluster headache-like headache with bouts of unilateral (the side of predominance changing through the years) severe headache had a familial history (three generations) of partial Hageman factor deficiency and bleeding episodes. A giant aneurysm was found to be lodged in the anterior communicating artery on the left side. Clinically, the features were atypical for cluster headache: onset at a young age (14 years), episodes of retrobulbar neuritis appearing at the side of pain, etc. Studies of forehead sweating indicated that the right side was the pathologic one, from an autonomic point of view, as did pupillometric studies. However, during attacks, which were left-sided at the time, forehead sweating was marked laterally on the left side and on the upper eyelid, but not on the right. The "signal" usually reaching the autonomically stigmatized side during attacks of cluster headache, therefore, did not seem to reach the sweat glands on that (the right) side during the attack in the present case. This headache may, therefore, be distinct from cluster headache, both from a clinical and from an autonomic function point of view.

Autonomic Nervous System↗
PubMed2000

Molecular mimicry in infectious encephalitis and neuritis: binding of antibodies against infectious agents on Western blots of human nervous tissue.

OBJECTIVES: To study the occurrence of cross-reactivities of antibodies against infectious agents with human nervous tissue. METHODS: Binding of 25 antibodies against 17 neurotropic pathogens comprising Borrelia burgdorferi, Toxoplasma gondii, and various DNA and RNA viruses to Western blots of human cortex and myelin from central and peripheral nervous system was investigated. RESULTS: Fourteen of the 25 antibodies tested showed binding to Western blots of human nervous tissue, suggesting the presence of shared epitopes. Binding of 11 antibodies against 10 pathogens to cortex and/or myelin correlated with the tissue targeted by neuropathological lesions. Three antibodies did not show such correlation; 11 antibodies did not bind at all. CONCLUSIONS: Our results suggest that shared epitopes between infectious agents and human nervous tissues are more common than previously expected. Thus, molecular mimicry should be considered more frequently as a possible pathogenetic mechanism, among others, inducing tissue damage in encephalitis and neuritis caused by various pathogens.

Aged↗