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At least 721 records · Page 40Linked to original sources
PubMed1998

New therapeutic perspectives for demyelinating retrobulbar optic neuritis.

In patients with demyelinating retrobulbar optic neuritis (RON), a spontaneous or corticosteroid-induced improvement is generally observed within the first month, but this is clinically insignificant in 5%-7% of patients. We report the case histories of four patients who were considered to be "non-responders" to corticosteroids because their visus remained unchanged or had improved by only 1/10 after one month from intravenous corticoid therapy begun 2-7 days after disease onset, and who were therefore subsequently administered high intravenous doses of immunoglobulin. Three of these patients completely recovered in a period of 3-9 months; the fourth showed only a partial improvement, but this was consolidated after long-term continuation of the same therapy. These cases suggest the possible efficacy of early administration of intravenous immunoglobulin in RON patients who fail to respond to cortisone therapy. As recently demonstrated in animal models, it can be hypothesised that the result is due to immuno-mediated mechanisms of action that reduce autoimmune responses in the short- and medium-term, and in the long-term favour remyelination.

Acute Disease↗
PubMed1999

Normal-appearing white matter in optic neuritis and multiple sclerosis: a comparative proton spectroscopy study.

We investigated neurochemical abnormalities in the normal-appearing white matter (NAWM) on MRI of patients with optic neuritis (ON) and compared them to those of patients with multiple sclerosis (MS). Patients with ON (42) were classified into three groups according to abnormalities on brain MRI. Patients with MS (55) were divided in two groups: relapsing remitting MS (RRMS) and secondary progressive MS (SPMS). All patients underwent MRI of the brain and localised proton magnetic resonance spectroscopy (MRS) of NAWM. The results were compared to those of 15 controls. Patients with MS had significant abnormalities compared with controls and with patients with ON. Patients with RRMS and those with ON had comparable MRS parameters, while patients with SPMS had significant spectroscopic abnormalities in comparison with controls, but also with patients with RRMS. These changes consisted of a decrease in N -acetylaspartate, a neuronal marker, which may reflect axonal dysfunction and/or loss. MRS abnormalities were detected in 14 patients with ON (27 %). The main abnormalities consisted of a decrease in N -acetylaspartate, an increase in choline-containing compounds at long echo times, and the presence of free lipid peaks at short echo times. MRS of the NAWM on MRI may prove useful for detecting neurochemical brain abnormalities in ON not visible on MRI.

Adult↗
PubMed1999

Bilateral optic neuritis in a child diagnosed with Gd-enhanced MR imaging using fat-suppression technique.

A 4-year-old boy developed bilateral optic neuritis. Although precise neuro-ophthalmological evaluation was difficult, the diagnosis was made with gadolinium-enhanced MR imaging using fat-suppression technique in the initial stage of the disease. Enhancement and enlargement of the intraorbital and intracanalicular optic nerve were demonstrated bilaterally as well as protrusion of the optic nerve head. The disease responded dramatically to intravenous steroid therapy. The etiologies in children usually differ from those in adolescent and adult patients.

Adipose Tissue↗
PubMed1998

[Bilateral simultaneous acute amaurosis in neuritis nervi optici. Initial manifestation of encephalomyelitis disseminata].

BACKGROUND: Bilateral simultaneous acute amaurosis as a primary manifestation of demyelinating disease is extremely rare. PATIENT: The clinical course of a 24-year-old patient who initially presented with a bilateral complete loss of vision is demonstrated. Morphologically both optic discs appeared slightly blurred and prominent. Otherwise there were no anterior and posterior segment abnormalities. Examination of the cerebrospinal fluid revealed an increased number of cells and protein without oligoclonal bands. On MRI multiple white matter lesions were visible. Laboratory tests showed no specific abnormalities, especially with respect to infectious or vasculitic diseases. Under intensive steroid therapy (initially 1000 mg prednisolone/day), visual acuity recovered almost completely. Nine months after onset of the disease visual acuity was 1.0 in both eyes. CONCLUSIONS: Even in patients with a fulminant onset of the disease almost complete visual recovery is possible. Differential diagnosis should rule out vasculitic autoimmune optic neuritis, infections, tumors, processes of the paranasal sinuses, toxic, and hereditary causes.

Adult↗
PubMed2002

Adoptive transfer-experimental allergic neuritis in newborn Lewis rats results in inflammatory infiltrates, mast cell activation, and increased Ia expression with only minor nerve fiber degeneration.

Experimental allergic neuritis (EAN) induced in the Lewis rat by the adoptive transfer of a P2-specific T cell line (AT-EAN) is considered an animal model of Guillain-Barré syndrome. It is not yet known whether AT-EAN is inducible at early stages in the development of the peripheral nervous system (PNS) or whether disease activity is modified because of immaturity of either the nervous system or the immune system. We therefore compared the susceptibility of neo-natal and adult Lewis rats to AT-EAN induced by the adoptive transfer (intraperitoneally) of 10(6) activated P2-specific T cells. P2 antigen was already present in 7 day old Lewis rats and P2-specific T cell transfer into 3-day-old rats induced clinical disease associated with an inflammatory response (sciatic nerves and spinal ganglia). In injected newborn rats we observed local activation of mast cells, infiltration of the PNS by inflammatory cells, and induction of Ia antigen expression in Schwann cells. Unlike in adults, segmental or paranodal demyelination despite occasional nerve fiber degeneration did not occur. However, the difference between newborn and adult rats could not be ascertained statistically because of the relative rarity of the lesions, their focal character, the admixture of fiber demyelination and degeneration, and most importantly, size differences of the myelinated fibers, which result in a large developmental decrease in fiber density in adults compared to newborns.

Adoptive Transfer↗
PubMed2001

Glucocorticosteroids modulate antigen-induced T cell apoptosis in experimental autoimmune neuritis and cause T cell proliferation in situ.

Treatment of experimental autoimmune disorders of the nervous system with high doses of glucocorticosteroids (GC) or with administration of the specific antigen is effective and associated with marked T cell apoptosis in situ. Here we investigated in adoptive transfer-experimental autoimmune neuritis (AT-EAN) of the Lewis rat whether induction of T cell apoptosis resulting from T cell activation by antigen therapy can be further augmented by glucocorticosteroids (GC). AT-EAN was induced by intravenous injection of P2-specific T cell blasts. At the maximum of disease two pulses of the antigen recombinant human P2 (rhP2) were given within 12 h. Methylprednisolone was administered simultaneously or 2 h after the antigen and animals were killed 6 h after the second antigen injection. Using an in situ tailing technique followed by immunocytochemical analysis, the presence of DNA fragmentation in T lymphocytes was confirmed. The bromodeoxyuridine (BrdU) technique was employed to detect in situ proliferating cells. T cell apoptosis in sciatic nerve was enhanced after monotherapy with either antigen or GC compared to the control group receiving an irrelevant myelin protein, recombinant human P0. In combination therapy, a synergistic effect on T cell apoptosis in sciatic nerve was obtained when methylprednisolone was injected sequentially, 2 h after rhP2 protein. BrdU incorporation in the sciatic nerve as well as in the spleen, a major lymphoid organ, was significantly enhanced in animals treated with antigen followed by GC 2 h later as compared to rats receiving rhP2 only, speaking for T cell proliferation in situ associated with T cells undergoing apoptosis. Our findings underscore that different proapoptotic stimuli may act synergistically, depending on the timing of the second treatment. In this scenario even local T cell proliferation in the inflamed nervous system occurs. These results support the paradigm of antigen presentation in the nervous system.

Adrenal Cortex Hormones↗
PubMed1996

In situ demonstration of T cell activation and elimination in the peripheral nervous system during experimental autoimmune neuritis in the Lewis rat.

The mechanisms of activation and termination of autoimmune responses are poorly understood. We have studied the sites and mode of activation and elimination of T cells in actively induced experimental autoimmune neuritis (EAN) and in adoptively transferred by P2-specific T cells (AT-EAN). The bromodeoxyuridine (BrdU) technique was employed to detect in situ proliferating cells in spleen and sciatic nerve. We assessed the nuclear morphology of infiltrating T cells using morphological criteria of apoptotic cell death. Apoptosis of lymphoid cells was also investigated using molecular labeling techniques. In AT-EAN, the number of BrdU positive cells in splenic germinal centers peaked at day 2 after cell transfer [554 +/- 267] (mean +/- SEM per mm2, controls 98 +/- 35), 1 day before disease onset, and declined thereafter. BrdU incorporation in spleens from animals with active EAN peaked at day 11, around disease onset, but reached lower total values (165 +/- 29 per mm2). In neither model did we observe a significant proportion of BrdU-positive T cells in the peripheral nervous system. However, T cells exhibiting morphological signs of apoptosis were detected in the sciatic nerve immediately after disease onset. The number of these cells was highest on day 7 in AT-EAN (6.6 +/- 3.2 per mm2) and on day 17 in active EAN (11.2 +/- 2.2 per mm2) corresponding to the maximum of T cell infiltration in both animal models. T cell activation occurs systematically and not just in the autoimmune lesion. Infiltrating T cells are eliminated by apoptosis in situ, terminating the inflammatory process. Further insight into these mechanisms may help to develop new therapeutic strategies for autoimmune disorders of the peripheral nervous system.

Animals↗
PubMed1998

Systemic complement depletion reduces inflammation and demyelination in adoptive transfer experimental allergic neuritis.

The effect of systemic complement depletion by cobra venom factor (CVF) was evaluated in adoptive transfer experimental allergic neuritis (AT-EAN). Spleen cells of rats immunized with a neuritogenic peptide SP26 were injected into naive rats. On days 3 and 6 after cell transfer AT-EAN rats were treated with CVF or saline intraperitoneally. AT-EAN rats treated with CVF had significantly lower scores for histological inflammation (0.25 +/- 0.25 vs 1.9 +/- 0.4, mean +/- SEM, P < 0.03) and demyelination (0.13 +/- 0.13 vs 1.6 +/- 1.4, P < 0.02) than saline-treated AT-EAN rats. Immunocytochemistry of lumbosacral nerve roots showed significantly less ED1-positive macrophages (0.5 +/- 0.3 vs 1.6 +/- 0.6, P < 0.04) and CD11bc-positive (expressing complement receptor 3 or CR3) inflammatory cells (0.6 +/- 0.4 vs 1.7 +/- 0.5, P < 0.03). Our data suggest that complement plays a crucial role in inflammatory demyelination since systemic complement depletion significantly reduces recruitment of macrophages into the nerve and subsequent macrophage-mediated demyelination.

Animals↗
PubMed1999

Effects of autoantigen and dexamethasone treatment on expression of endothelial-monocyte activating polypeptide II and allograft-inflammatory factor-1 by activated macrophages and microglial cells in lesions of experimental autoimmune encephalomyelitis, neuritis and uveitis.

Endothelial-monocyte activating polypeptide II (EMAP II) and allograft-inflammatory factor-1 (AIF-1) are two proteins produced by activated monocytes and microglial cells. We now report expression of these factors during experimental therapy of rat neuroautoimmune diseases. Comparative analysis of two therapeutic strategies, treatment with high doses of recombinant autoantigens or with dexamethasone, revealed unexpected differences. High doses of autoantigen were most effective in experimental autoimmune encephalomyelitis and neuritis (EAE and EAN), but less effective in experimental autoimmune uveitis (EAU). Low and high doses of dexamethasone treatment greatly reduced the severity of EAE, EAN and EAU at day 11, but a relapse was observed between days 21 and 26. Only rather limited expression of EMAP II and AIF-1 is seen in the normal central nervous system (CNS). This constitutive expression is not abolished by dexamethasone treatment. In inflammatory autoimmune lesions of the rat CNS, prominent AIF-1 and EMAP II staining was seen with macrophages and monocytes. In particular, parenchymal microglial cells were now activated to express AIF-1 and EMAP II. In accordance with prevention of neurological signs, histological observations revealed that accumulation of activated monocytes expressing EMAP II and AIF-1 in the CNS or peripheral nervous system and the massive expression of these factors by parenchymal microglial cells is inhibited by high doses of autoantigen. Dexamethasone prevented or abolished local expression of EMAP II and AIF-1 at days 10-16. However, an acute and severe relapse occurred in encephalomyelitis between days 20-26. In these cases, a smoldering expression of EMAP II and AIF-1 persisting long after cessation of neurological signs was observed. Thus, expression of EMAP II and AIF-1 by infiltrating activated macrophages is a marker of disease activity and expression of these factors could be used to demonstrate 'silent' lesions in the CNS and prolonged microglial cell activation. Apparently, AIF-1 and EMAP II immunoreactivity are tools to stage activation of monocytes and microglial cells in inflammatory lesions.

Animals↗
PubMed1999

Increased lipocortin-1 (annexin-1) expression in the sciatic nerve of Lewis rats with experimental autoimmune neuritis.

Lipocortin-1 exerts a potent immunosuppressive effect on pathogenic T cells. In multiple sclerosis and experimental autoimmune encephalomyelitis levels of lipocortins are raised, suggesting their involvement in the recovery from an immunological insult or in neural regeneration. To further understand the role of lipocortins in the peripheral nervous system we have characterized lipocortin-1 levels and cellular distribution of lipocortin-1 immunoreactivity in sciatic nerves of rats with experimental autoimmune neuritis (EAN), a model of human Guillain-Barré syndrome. EAN was induced actively by immunization with bovine peripheral myelin (active EAN) or by adoptive-transfer (AT-EAN) of P2-specific T cells. Cellular infiltrates in serial and semithin cryosections were characterized by immunohistochemistry. In parallel, lipocortin-1 levels in tissue extracts were quantified by a sandwich-ELISA. Only weak lipocortin-1 immunoreactivity was found in nerves of control animals injected with non-pathogenic T cells. The majority of macrophages and lymphocytes in EAN lesions exhibited lipocortin-1 immunoreactivity. Some very heavily stained cells showed a distribution and morphology similar to ED-2-positive macrophages which were abundant during early stages of EAN. Lipocortin-1 expression in T cells and macrophages was proven by immunocytochemical studies in semithin serial sections. In tissue extracts, lipocortin-1 levels increased from 0.24 +/- 0.14 micrograms/mg protein in controls receiving non-pathogenic T cells to a maximum of 0.55 +/- 0.1 micrograms/mg protein in AT-EAN at the peak of disease, and then slowly decreased during clinical recovery but still remained elevated. In dose-response studies in AT-EAN, highest values of lipocortin-1 (0. 71 +/- 0.23 micrograms/mg protein) were recorded after transfer of 2 x 10(7) T cells. Increased levels of lipocortin-1 were also measured in active EAN but occurred during the recovery phase (0.65 +/- 0.27 micrograms/mg protein). By analogy with other immune-mediated disorders, increased lipocortin-1 expression in the inflamed sciatic nerve in EAN may exert immunoregulatory functions in-situ and contribute to the termination of the autoimmune response.

Adrenal Cortex Hormones↗
PubMed2001

Blockade of signaling via the very late antigen (VLA-4) and its counterligand vascular cell adhesion molecule-1 (VCAM-1) causes increased T cell apoptosis in experimental autoimmune neuritis.

We characterized the early effects of anti-very late antigen (VLA-4) and its counterligand vascular cell adhesion molecule-1 (VCAM-1) antibody therapy on T cell infiltration and apoptosis in adoptive transfer experimental autoimmune neuritis of female Lewis rats. At the peak of disease, animals were treated with anti-VCAM-1 monoclonal antibody (mAb), anti-VLA-4 mAb, or the respective isotype mAb controls 18, 12, or 6 h before perfusion. Anti-VCAM-1 led to a rapid, significant increase of apoptotic T cells in the sciatic nerve with a maximum after 6 h, preceding the significant decrease of T cell infiltration seen after 18 h. This was accompanied by a significant reduction in mRNA levels for IFN-gamma and inducible nitric oxide synthase. The results for anti-VLA-4 treatment showed a similar trend. The early increase of T cell apoptosis following disruption of VLA-4/VCAM-1 interaction may reflect a novel signaling component of proapoptotic pathways.

Animals↗
PubMed2002

Multiple sclerosis and optic neuritis: CCR5 and CXCR3 expressing T cells are augmented in blood and cerebrospinal fluid.

A role for chemokines as mediators of Th1 cell recruitment to the central nervous system (CNS) is probable in MS. Therefore we studied expression of Th1-related CCR5 and CXCR3 chemokine receptors in patients with MS and controls. Patients with untreated MS had elevated percentages of CCR5 and CXCR3 expressing T cells vs. healthy controls (HC) in blood, and vs. other non-inflammatory neurological diseases (OND) patients in CSF. Such elevation was not found in MS patients examined during ongoing treatment with IFN-beta. Patients with optic neuritis (ON), a common first manifestation of MS, had elevated percentages of CXCR3 expressing T cells in blood compared with HC, and of CCR5 expressing T cells in CSF compared with OND patients. High chemokine receptor expression may be one prerequisite for Th1 cells to migrate to the CNS. Inhibition of chemokine receptor expression may constitute a potentially important therapeutic effect of IFN-beta.

Adult↗
PubMed2005

Predicting the outcome of optic neuritis: evaluation of risk factors after 30 years of follow-up.

BACKGROUND: Multiple sclerosis (MS) is a common disease with considerable risk for disability. Optic neuritis (ON) is a common first symptom of MS but it can also remain an isolated episode. Therefore, predicting the outcome of ON has gained in importance, particularly in light of current discussions of early disease modifying treatments in individuals at risk of developing MS. We reported previously on our cohort of 86 patients with acute monosymptomatic unilateral ON of whom 33 had progressed to MS after up to 18 years. Three patients had died. The present study extends the observation period to 31 years. METHODS: Patients were followed for up to 31 years or until a diagnosis of MS was made. Cerebrospinal fluid (CSF) was examined at onset. HLA class I and II antigens were determined. Magnetic Resonance Imaging (MRI) was performed during follow up. FINDINGS: Only one of 50 patients at risk developed clinical manifestations of MS during the extended follow up period. The estimated 15-year-risk of MS was 40 % (confidence interval [CI] 31%-52%). Most cases, 20 of 34 or 60%, occurred within three years. Among factors present at onset, CSF with mononuclear pleocytosis and/or oligoclonal Ig increased the risk for subsequent MS significantly, 49% (CI 38%-65%) compared with 23 % (CI 12%-44%) for those with normal CSF, p=0.02. Younger patients and those with winter onset also had greater risk. Recurrence of ON similarly elevated the risk significantly, p<0.001. After 19-31 years MRI lesions suggestive of demyelinating disease were detected in 20 of 30 individuals although no clinical manifestations of MS had occurred. CONCLUSION: The risk of MS in this large population-based prospective ON patient series was 40% and significantly higher in those with inflammatory CSF abnormalities at onset. Clinically silent MRI lesions suggestive of MS were detected in a majority of those with "ON-only". This finding should be taken into account when discussing prognosis and early intervention in patients with clinically isolated ON.

Age Factors↗
PubMed1999

Long-term follow-up of isolated optic neuritis: the risk of developing multiple sclerosis, its outcome, and the prognostic role of paraclinical tests.

We evaluated the risk of developing clinically definite multiple sclerosis (CDMS) after an acute attack of isolated optic neuritis (ON) in 112 patients, in relation to demographic and paraclinical findings. Patients were examined by brain MRI, CSF analysis, and multiple evoked potentials (EPs); 10 were lost to follow-up, and the other 102 were enrolled in a prospective study (follow-up duration 6. 3 +/- 2.2 years). Of these, 37 (36.3%) developed CDMS after a mean interval of 2.3 +/- 1.6 years. The risk of developing CDMS was 13% after 2 years, 30% after 4, 37% after 6, and 42% after 8 and 10 years. Gender, age, and season of ON onset did not affect the risk. MS occurred in 37 of 71 patients (52.1%) with one MRI lesion or more; no patient with a normal MRI developed the disease. MS developed more frequently in patients with intrathecal IgG synthesis than in those without (43% vs. 28%), but the difference was not statistically significant. Multiple EPs showed a slight predictive value only including somatosensory EPs of the lower limb. Multiple sclerosis was mild in most cases (EDSS 2.2 +/- 1.9). The EDSS was less than 4 in 32 cases (86%), between 4 and 6 in 2 (5%), higher than 6.5 in 3 (8%).

Adult↗
PubMed1998

Visual field defects in optic neuritis and anterior ischemic optic neuropathy: distinctive features.

BACKGROUND: We analyzed the value of visual-field defects in the differential diagnosis of optic neuritis (ON) and non-arteritic anterior ischemic optic neuropathy (AION). METHODS: Ninety-nine consecutive patients with acute-onset optic neuropathy formed the basis for this study. Compressive and vasculitic neuropathies were excluded. Eighty-six patients fulfilled the criteria for either ON (50 patients): < or = 35 years, normal disk, recovery of visual function, or AION (36 patients): > or = 60 years, swelling of the disk, no recovery of visual function. Without knowledge of other clinical data, visual fields obtained by Gold-mann perimetry were classified into five types of defects (forced choice). With the correct diagnosis at hand, fields were reviewed for characteristic features. RESULTS: Forced-choice classification into defect types [%]: Central scotoma ON 68, AION 18; superior altitudinal defect ON 13 AION 7; inferior altitudinal defect ON 8, AION 52; peripheral defect ON 1, AION 5; diffuse defect ON 10, AION 18. Search for pathognomonic defects: a scotoma centered on the fixation point with a sloping border occurred exclusively in ON (25 of 50 patients). An inferior altitudinal defect with a sharp border along the horizontal meridian, particularly in the nasal periphery, occurred only in AION (10 of 36 patients). A steep centrocecal scotoma occurred in 3 of the 36 AION cases and not at all in the ON cases. Scotomas in the center breaking through to the periphery, superior altitudinal defects (with a sloping border along the horizontal meridian) and diffuse depressions verging on blindness occurred in both ON and AION. CONCLUSION: A sctoma centered on the fixation point with a sloping border is highly characteristic of ON, while an inferior altitudinal defect with a sharp border along the horizontal meridian, particularly in the nasal periphery, is highly characteristic of AION. To identify these diagnostic criteria, it can be necessary to examine full fields. With restriction of perimetry to 30 degrees a large central scotoma can be mistaken for a diffuse defect and the border in the nasal periphery can be missed.

Acute Disease↗
PubMed2004

Optic neuritis: diagnostic criteria application in clinical practice.

Optic neuritis (ON) refers to any inflammatory optic neuropathy. In clinical practice ON is mainly diagnosed by ophthalmologists and less frequently by neurologists. ON diagnostic criteria are included in the Classification of International Headache Society (IHS) and in other classification systems, both in neurological and ophthalmologic fields. The aims of this study were to verify the application of IHS ON diagnostic criteria in clinical practice and the role of the ocular pain qualitative aspects. We performed a partially retrospective (140 cases) and prospective (43 cases) study analysing the clinical characteristics of patients with ON. We observed retro orbital pain in a huge percentage of patients; it was provoked or spontaneous and worsened by eye movements. We found that the new IHS classification criteria (IHS 2004) do not fully satisfy the requirements for ON diagnosis. Further study is necessary to validate the diagnostic criteria of ON in clinical practice.

Eye Movements↗
PubMed2005

Controversies in optic neuritis pain diagnosis.

Optic neuritis (ON) refers to any inflammatory disorder of the optic nerve. In clinical practice ON is mainly diagnosed by ophthalmologists and less frequently by neurologists. ON diagnostic criteria are included in different classification systems both in neurologic and ophthalmologic fields. Diagnosis of ON is still very unsatisfactory. Indeed diagnostic criteria are not uniform and therefore the diagnosis is still mainly formulated according to the clinical experience only. A consensus on practice guidelines for ON diagnosis might be useful. Ocular pain is a milestone in ON diagnosis, but it is too often mistreated by both the patient and the clinician. The International Headache Society (IHS) Classification of Headache Disorders provides in its 1988 and 2004 versions the diagnostic criteria for ON. These criteria are not spread and followed by the large majority of neurologists, but they are mainly applied by the experts in headache disorders. On the other hand, ON is a disorder widely encountered by neurologists and ophthalmologists. The latest IHS version defines the criteria of the pain features more precisely, but it is still unsatisfactory. In a future revision, the pain should be further detailed. Further studies aimed at validation of the diagnostic criteria of ON are strongly needed.

Diagnosis, Differential↗