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PubMed1980

Antigen-induced suppression of experimental allergic neuritis in the guinea pig.

Treatment of guinea pigs suffering from a fatal form of experimental allergic neuritis (EAN) using P2 basic protein of PNS myelin reduced the clinical severity, the overall mortality and the incidence of respiratory problems. The large basic protein (MBP) common to the CNS and PNS had no suppressive effect on EAN. Cyanogen bromide cleavage of P2 destroyed its suppressive activity. P0 protein of PNS myelin had marginal suppressive activity but Cop 1, a synthetic copolymer effective in suppressing EAE, was without significant effect on EAN. The suppression with P2 protein of a milder form of EAN (induced with a reduced amount of PNS myelin) was less marked. Increasing the treatment period from 10 to 15 days did not increase the suppressive effect of P2 in the milder form of EAN.

Animals↗
PubMed1988

Membrane plasma exchange in experimental allergic neuritis: effect on antibody levels and clinical course.

The effect of membrane plasma exchange on the course of chronic experimental allergic neuritis in rabbits is described. Using miniature membrane plasma separators conscious animals were treated with 4 exchanges over 5 days removing one plasma volume per procedure and using a non-immunogenic gelatin plasma solution as replacement. Comparisons of clinical scores between control and treated groups indicated that treated animals received significant benefit from plasma exchange (day 1 post-treatment P less than 0.002; day 3 post-treatment P less than 0.01). However, relapse was observed in all plasma exchanged animals such that by day 8 post-treatment there was no significant difference in clinical scores between the two groups. Quantitation of anti-myelin IgG and IgM by ELISA assay showed that 55-60% of circulating antibody was removed per exchange. Rapid post-exchange antibody rebound was observed for both IgG and IgM so that pre-exchange levels were re-established within 24-48 h. However, no significant overshoot in circulating levels of anti-myelin IgG nor IgM could be observed. It is probable that long-term remission as a result of therapeutic plasma exchange is a function of effective circulating plasma removal and if present, the suppression of ongoing antigenic stimuli.

Animals↗
PubMed1988

Disease patterns in experimental allergic neuritis (EAN) in the Lewis rat. Is EAN a good model for the Guillain-Barré syndrome?

Lewis rats develop experimental allergic neuritis (EAN) when injected with bovine dorsal root (BDR) emulsified in complete Freund's adjuvant (CFA). In this study the susceptibility to EAN and subsequent relapse was studied in animals ranging from 4 to 25 weeks of age. Older animals exhibited a severe acute illness which was monophasic over the period of observation, whereas younger animals developed a less severe and frequently relapsing illness. Very young animals often relapsed more than once and sometimes to a more severe degree than shown in their first attack. Older animals which were in the late recovery stage of EAN (44 days after injection with BDR/CFA) were completely resistant to a second challenge with antigen. Young adult animals also developed resistance but not as strongly as the older animals. Animals first injected at weaning developed resistance as in the adults, but the analysis is complicated by the occurrence of spontaneous relapses. Because of differences in disease pattern between EAN and acute inflammatory polyneuropathy (Guillain-Barré syndrome) in man, caution should be exercised in drawing too close a parallel between the animal model and the human disease. The affinities may be closer to chronic relapsing inflammatory polyradiculopathy in man.

Aging↗
PubMed2004

Vestibular neuritis in a child with otitis media with effusion; clinical application of vestibular evoked myogenic potential by bone-conducted sound.

Vestibular evoked myogenic potential (VEMP) has been applied for patients with vestibulo-cochlear disorders. The impairment of the sound transmission due to middle ear pathology affects VEMP results. In children, otitis media with effusion (OME) is well documented and it is difficult to apply conventional VEMP in such cases. To overcome the attenuation of stimulation due to middle ear pathology, VEMP by bone-conducted sound has been developed. We report a 3-year-old girl with vestibular neuritis and OME as a representative case of clinical application of VEMP by bone-conducted sound. VEMP by bone-conducted sound can be an alternative method to elicit vestibular-dependent potential.

Bone Conduction↗
PubMed2004

In vivo monitoring of macrophage infiltration in experimental autoimmune neuritis by magnetic resonance imaging.

We report on the in vivo assessment of macrophage infiltration in adoptive transfer experimental autoimmune neuritis (AT-EAN), a prototypic Th-1-mediated autoimmune disorder of the peripheral nervous system (PNS). Lewis rats received systemic injections of superparamagnetic iron oxide (SPIO) particles at days 2, 3, 4, 5, or 9 after adoptive transfer of P2-specific T-cells and were scanned by standard 1.5 T magnetic resonance imaging (MRI) always 24 h later. MRI revealed focal signal loss of the cauda equina indicating iron accumulation in spinal nerves already at the preclinical stage (day 3). Signal loss peaked at day 4, when first clinical signs developed. At the maximum of clinical disease, signal loss already declined and disappeared on days 6 and 10. In spinal nerve sections, Perl's iron stain showed focal cellular accumulation of SPIO at days 3, 4, and 5 in ED1-positive macrophages. Spinal nerves at days 6 and 10 exhibited massive macrophage infiltrates, but no more iron deposition. In conclusion, SPIO-enhanced MRI provides a novel in vivo tool to assess the timing of macrophage entry into target tissues during an immunopathologic attack and holds promise to monitor immunotherapeutic interventions.

Animals↗
PubMed2005

Enhanced expression of netrin-1 protein in the sciatic nerves of Lewis rats with experimental autoimmune neuritis: possible role of the netrin-1/DCC binding pathway in an autoimmune PNS disorder.

Netrin-1 is a chemotropic factor that plays an important role as a survival factor in the adult nervous system. To investigate whether netrin-1 is involved in autoimmune injury of the peripheral nervous system (PNS), the temporal expression of netrin-1 protein was analyzed in the sciatic nerves of Lewis rats with experimental autoimmune neuritis (EAN). Western blot analysis revealed a significant increase in the level of netrin-1 protein in the sciatic nerves of rats on days 11 to 24 post-immunization (p.i.) compared to controls; netrin-1 expression declined by day 30 p.i. Immunohistochemistry revealed that netrin-1 protein was expressed weakly in Schwann cells and vessels in the sciatic nerves of normal and CFA-immunized control rats. In the sciatic nerves of EAN-affected rats, netrin-1 immunoreactivity was increased mainly in the cell membrane and extracellular matrix of OX42-positive macrophages and S100-positive Schwann cells at the peak and recovery phases of EAN. Moreover, the putative netrin-1 receptor, deleted in colorectal cancer (DCC), was expressed mainly in axons, some macrophages, and Schwann cells in EAN-affected sciatic nerves, although the level of protein expression did not change significantly over the course of EAN. We suggest that a significant increase in netrin-1 expression contributes to host cell survival and axon regeneration to counter autoimmune injury and inflammation, which may play a role in recovery from EAN-induced paralysis.

Animals↗
PubMed2004

A case of isolated nodulus infarction presenting as a vestibular neuritis.

We reported a patient with cerebellar infarction who presented with purely isolated vertigo, ipsilesional spontaneous nystagmus, and contralesional axial lateropulsion without usual symptoms or signs of cerebellar dysfunction. An MRI of the brain showed a small left cerebellar infarct selectively involving the nodulus. A pure vestibular syndrome in our patient may be explained by ipsilateral involvement of nodulo-vestibular inhibitory projection to vestibular nucleus. Clinicians should be aware of the possibility of a nodulus infarction in patient with acute vestibular syndrome, even if the pattern of nystagmus and lateropulsion is typical of a vestibular neuritis.

Adult↗
PubMed2005

What accounts for vertigo one year after neuritis vestibularis - anxiety or a dysfunctional vestibular organ?

One year after neuritis vestibularis, 29% from a sample of 75 patients still complained of vertigo. The objective of this investigation was to study why patients suffer from persisting vertigo. The alternative hypotheses were that the vertigo experienced could be explained either by a persisting vestibular dysfunction or by psychopathological changes. To elucidate this question, patients were examined with dynamic posturography, the symptom check list (SCL 90 R), the state-trait anxiety inventory (STAI), the agoraphobic cognitions questionnaire (ALQ) and the body sensations questionnaire (BSQ). After one year, only two patients had overall pathological results in the posturography. Following the assumption that sub-clinical dysfunction of the organs of balance can also lead to an altered body perception in combination with anxiety, the pathological results of posturographic sub-tests were related to experiences of vertigo. Here also there were no significant associations. However, vertigo correlated highly significantly with body-related anxiety and anxiety-related apprehension. In conclusion, chronic vertigo after an acute vestibular disorder could be regarded as a somatopsychic process. Persisting experience of vertigo is not explained by sub-clinical organic changes. Anxiety seems to be the crucial factor in persisting vertigo.

Anxiety↗
PubMed2001

P0 glycoprotein peptides 56-71 and 180-199 dose-dependently induce acute and chronic experimental autoimmune neuritis in Lewis rats associated with epitope spreading.

Two synthetic peripheral nerve myelin P0 protein peptides, an immunodominant (amino acids 180-199) and a cryptic (amino acids 56-71) one, induced an acute or chronic course of experimental autoimmune neuritis (EAN) in Lewis rats, when given at low dose (50-100 microg/rat) or high dose (250 microg/rat), respectively. Corresponding to the different clinical course, pathological changes and immune responses were found: (1) Onset of clinical signs of P0 peptide 56-71 (P0 56-71) induced EAN was 1-3 days later than in P0 peptide 180-199 (P0 180-199) induced EAN at all immunizing doses, whereas the peak of the disease occurred at a similar time point post immunization (p.i.), i.e. at days 14-16 p.i. in P0 56-71 induced EAN and at day 16 p.i. in P0 180-199 induced EAN. (2) Intramolecular epitope spreading as assessed by delayed type hypersensitivity response occurred in P0 56-71 induced EAN at both low and high antigen doses and in P0 180-199 induced EAN at high antigen dose (250 microg/rat) only. (3) P0 180-199 stimulated higher levels of interferon-gamma production in P0 180-199 induced EAN than in P0 56-71 induced EAN and vice versa. (4) Histopathologic evaluation revealed a similar grade of mononuclear cell infiltration in the sciatic nerves of both types of EAN, but more severe demyelination was found in P0 180-199 induced EAN compared to P0 56-71 induced EAN. The results support the hypothesis that high dose autoantigen immunization induces extensive determinant spreading and chronic course of autoimmune diseases.

Acute Disease↗
PubMed2001

A new model of sciatic inflammatory neuritis (SIN): induction of unilateral and bilateral mechanical allodynia following acute unilateral peri-sciatic immune activation in rats.

Immune activation near healthy peripheral nerves may have a greater role in creating pathological pain than previously recognized. We have developed a new model of sciatic inflammatory neuritis to assess how such immune activation may influence somatosensory processing. The present series of experiments reveal that zymosan (yeast cell walls) acutely injected around the sciatic nerve of awake unrestrained rats rapidly (within 3h) produces low threshold mechanical allodynia in the absence of thermal hyperalgesia. Low (4 microg) doses of zymosan produce both territorial and extra-territorial allodynia restricted to the ipsilateral hindpaw. Higher (40-400 microg) doses of zymosan again produce both territorial and extra-territorial allodynia. However, allodynia is now expressed both in the ipsilateral as well as contralateral hindpaws. Several lines of evidence are provided that the appearance of this contralateral ('mirror') allodynia reflects local actions of zymosan on the sciatic nerve rather than spread of this immune activator to the general circulation. Since many clinical neuropathies result from inflammation/infection of peripheral nerves rather than frank physical trauma, understanding how immune activation alters pain processing may suggest novel approaches to pain control.

Acute Disease↗
PubMed2006

The impact of cognitions on the development of panic and somatoform disorders: a prospective study in patients with vestibular neuritis.

BACKGROUND: There is a high incidence of panic and somatoform disorders after vestibular neuritis. However, the occurrence of psychiatric disorders has been shown to be unrelated to persistent functional vestibular impairment. The aim of the present study was to examine the role played by cognitions in the development of panic and somatoform disorders. METHOD: In a 2-year prospective study, cognitions were recorded at various stages using the Agoraphobic Cognitions Questionnaire and Body Sensations Questionnaire. Our analysis focused on whether body-related anxiety or panic-related thoughts can predict the development of a panic or somatoform disorder. RESULTS: Fear arising on the first day of an acute vestibular episode did not predict the development of panic or somatoform disorders. One week after the dysfunction, however, the fear of vertigo was a significant predictor, explaining 20% of the variance in the development of either disorder. After 6 weeks, persistent fear of vertigo or vomiting predicted approximately 30% of the variance, and after 6 months panic-related thoughts predicted 40% of the variance and, with the inclusion of body-related fears, as much as 60% of the variance in the development of panic or somatoform disorders. CONCLUSION: Our data confirm prospectively a number of fundamental assumptions of cognitive theory concerning the development of anxiety disorders. Subjects who experience vertigo as particularly alarming focus more intensely than other patients on the negative symptoms they perceive as being related to the disorder. Patients with panic-related cognitions were prone to develop panic or somatoform disorders.

Acute Disease↗
PubMed2001

Sciatic inflammatory neuritis (SIN): behavioral allodynia is paralleled by peri-sciatic proinflammatory cytokine and superoxide production.

We have recently developed a model of sciatic inflammatory neuritis (SIN) to assess how immune activation near peripheral nerves influences somatosensory processing. Administration of zymosan (yeast cell walls) around a single sciatic nerve produces dose-dependent low-threshold mechanical allodynia without thermal hyperalgesia. Low (4 microg) doses produce both territorial and extraterritorial allodynia restricted to the injected hindleg. In contrast, higher (40 microg) doses produce territorial and extraterritorial allodynias of both hindlegs, an effect not accounted for by systemic spread of the zymosan. The aim of these experiments was to determine whether these behavioral allodynias were correlated with immunological and/or anatomical changes in or around the sciatic nerve. These experiments reveal that zymosan-induced bilateral allodynia was associated with the following: (a) increased release of both interleukin-1beta and tumor necrosis factor-alpha from peri-sciatic immune cells; (b) increased release of reactive oxygen species from perisciatic immune cells; (c) no change in circulating levels of proinflammatory cytokine; (d) no apparent zymosan-induced influx of immune cells into the sciatic nerve from the endoneurial blood vessels; (e) mild edema of the sciatic, which was predominantly restricted to superficial regions closest to the peri-sciatic immune cells; and (f) no anatomic evidence of changes in either the ipsilateral saphenous nerve or contralateral sciatic nerve that could account for the appearance of extraterritorial or contralateral ("mirror") allodynia, respectively. No reliable differences were found when the low-dose zymosan was compared with vehicle controls. Taken together, these data suggest that substances released by peri-sciatic immune cells may induce changes in the sciatic nerve, leading to the appearance of bilateral allodynia.

Animals↗
PubMed2006

Recovery of vestibular evoked myogenic potentials after a vertigo attack due to vestibular neuritis.

CONCLUSIONS: Inferior vestibular nerve functions could recover in patients with vestibular neuritis (VN). OBJECTIVES: Although the recovery of superior vestibular nerve functions has been reported, there is little information about the recovery of inferior vestibular nerve functions in patients with VN. This study was done to clarify if inferior vestibular nerve functions recover after an attack of VN. METHODS: Neuro-otological tests including vestibular evoked myogenic potential (VEMP) testing and caloric testing were sequentially performed in 13 patients with VN, who showed absence of VEMP on the affected side at the initial examination (7 men and 6 women, 28-82 years of age). VEMPs to click stimulation (95 dBnHL) were recorded with surface electrodes over each sternocleidomastoid muscle. RESULTS: Among the 13 patients, 5 patients (4 men and 1 woman) showed recovery of VEMP responses. Four of the five patients (three men and one woman) showed recovery of VEMP to the normal range. It takes 6 months to 2 years to recover within the normal range. On the other hand, caloric responses recovered to the normal range only in one patient.

Adult↗
PubMed1999

Vestibular neuritis: a follow-up study.

Seven to eight years after a disease period of vestibular neuritis 19 patients previously examined at our department were given a questionnaire about whether they had experienced any audiovestibular symptoms since they first fell ill. All 19 patients responded and 18 consented to participate in the long-term follow-up study. The patients were subjected to a clinical evaluation, a bithermal caloric test and audiological examinations with stapedius reflex measurements with use of the same technique as at the first examinations. Ten of the 18 patients had experienced recurrent vestibular symptoms with sensation of dysequilibrium and vertigo. Six of these 10 patients also had periods of positional vertigo. The remaining nine patients were free of symptoms. None of the patients had noticed any change in their hearing ability. The mean caloric side difference at the 7- or 8-year follow-up was not significantly higher in the group of patients with symptoms than in the group without symptoms. Neither did the group of patients with pathologically elevated stapedius reflex thresholds at onset display a larger mean caloric side difference than the group of patients with normal thresholds. However, a small caloric side difference at onset of the disease served as a predictor for residual vestibular symptoms. It is speculated whether the group of patients with residual symptoms had a different pathophysiological localization of their disease within the vestibular system than the group of patients with no symptoms at follow-up.

Adult↗
PubMed1998

Effect of lipids on the conformation of an antigenic determinant for experimental autoimmune neuritis.

The conformation of SP-26, the synthetic peptide (residues 53-78) of myelin P2 protein that causes experimental autoimmune neuritis (EAN) in the peripheral nervous system, has been studied in lipid environments and in water/trifluoroethanol (TFE) mixture using circular dichroism (CD) spectroscopy and Fourier transform infra-red (FTIR) spectroscopy. SP-26 becomes more structured on binding with micelles formed from anionic lipids and in the presence of TFE. On the other hand, zwitterionic lipids have a denaturing effect or no effect on the conformation of SP-26. The present results suggest that the disease-modulating effects of various lipids are closely related to their ability to induce conformational change in the antigenic region of P2 protein.

Circular Dichroism↗
PubMed1996

T cell directed immunotherapy of inflammatory demyelination in the peripheral nervous system. Potent suppression of the effector phase of experimental autoimmune neuritis by anti-CD2 antibodies.

Experimental autoimmune neuritis (EAN) of Lewis rats, an inflammatory demyelinating neuropathy and model of the human Guillain-Barré syndrome (GBS), was used to evaluate the novel T cell directed immunotherapy with the anti-CD2 monoclonal antibody (mAb) OX34. Clinical signs of EAN actively induced by immunization with bovine peripheral nerve myelin in complete Freund's adjuvant (CFA) were totally prevented or markedly suppressed by preventative injections of OX34 starting 8 days post-immunization (p.i.). Moreover, therapeutic application of the mAb beginning on the day of first clinical signs of EAN markedly inhibited progression of disease. Electrophysiological and histological investigation of sciatic nerves 17 and 18 days p.i. respectively, also revealed an inhibitory effect of OX34 on EAN-associated functional and morphological nerve damage. Similarly, therapeutic injections of OX34 after onset of EAN actively induced by immunization with a neuritogenic peptide of the P2 protein completely halted further deterioration of clinical disease. Finally, clinical, electrophysiological and histological signs of adoptive transfer EAN mediated by injection of neuritogenic T helper line cells were prevented or strongly suppressed by OX34-application on the day of cell transfer and 4 days later, underlying the impact of the mAb on the effector phase of the disease. Since the anti-CD2 mAb did not exert its effect by inhibition of T cell activation, induction of anergy, modulation of CD2 antigens, or by T cell depletion, we assume that it may affect migration of T lymphocytes across the blood-nerve barrier. The immediate and marked suppression of ongoing EAN by the mAb lead to the recommendation of anti-CD2 mAbs as candidates for T cell directed immunotherapy of the GBS.

Animals↗
PubMed1979

Experimental allergic neuritis in the Lewis rat.

Purified myelin from the peripheral nervous system of guinea pig, frog (Rana catesbeiana), rat, rabbit, beef, and human in Freund's adjuvant were injected into the Lewis rat. Groups of rats receiving injections of myelin from different species were examined for signs of dysfunction and lesions in the PNS and CNS. Injection of frog PNS myelin into the Lewis rat did not produce any clinical signs or lesions typical of experimental allergic neuritis (EAN) or experimental allergic encephalomyelitis (EAE). Injection of myelin from the PNS of rat, rabbit, beef, and human elicited clinical signs and lesions characteristic of EAN, while guinea pig myelin injection caused superimposed conditions of EAE and EAN. The myelin proteins from the various species were separated by polyacrylamide gel electrophoresis, the gels were scanned and the individual proteins measured. There did not appear to be a correlation between the amount of P2 protein contained in the different myelin species and the severity of the EAN symptoms and lesions produced. Although the Lewis rat is far more susceptible to EAE caused by guinea pig CNS myelin than by any other species, EAN can be easily induced in this animal by injection of PNS myelin from a number of species.

Animals↗
PubMed1993

The Farnsworth-Munsell 100 hue test in the first episode of demyelinating optic neuritis.

The Farnsworth-Munsell 100 hue test (F-M 100) was used to examine 30 patients with their first episode of unilateral demyelinating optic neuritis (DON) at presentation, after 6 weeks and after 6 months. Twelve patients satisfactorily completed the test with the affected eye at presentation. This number had increased to 23 by 6 weeks and to 27 by 6 months. No patient with a visual acuity of LogMAR 0.86 (Snellen equivalent approx 6/43) or worse, could complete the test. The mean total error score of affected eyes showed significant improvement at each subsequent examination but was always worse than the non-affected eyes. There was a significant correlation between total error scores and visual acuities of affected eyes at presentation and after 6 months. Fourteen patients recovered a visual acuity of LogMAR 0.0 (Snellen equivalent 6/6) or better but the total error scores of the affected eyes were significantly worse than the non-affected eyes (p = 0.017), indicating that defective colour vision is an indicator of a previous episode of DON despite the recovery of normal visual acuity. DON is reported to produce a red-green (Type II) axis of colour defect but individual F-M 100 polar diagrams were usually generally abnormal and did not show any predominance of recognisable axis of colour defect at any examination. Group averaging of the F-M 100 data from such a well-defined group of patients with acute DON revealed a significant bipolar abnormality in the tritan (blue-yellow) axis at presentation which was not demonstrated at the subsequent examinations or at any examination of the non-affected eyes.

Adult↗