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PubMed1985

Changes in lymphocyte subsets during the course of experimental allergic neuritis.

The percentages of various leucocyte subsets in the blood, spleen and popliteal lymph nodes of animals with experimental allergic neuritis (EAN) were determined at various times between the initiation of the disease and recovery. The total cell yield from these tissues and the weights of the spleens and lymph nodes were recorded. Clinical and histological signs of disease were assessed at the same time points. Normal and adjuvant control animals were also studied. The most marked change observed was that the percentage of MRC OX 8+ ('suppressor/cytotoxic') cells in the blood of animals with EAN was significantly below the normal value during the most severe clinical disease, and then returned to normal during recovery. Adjuvant controls did not show this change. No significant differences were observed in the other lymphocyte subsets studied (surface Ig+, Ia+, W3.13+ and W3.25+ cells) or in the total white cell count in the blood. There were no changes from normal values in any of the parameters examined in the spleen. The popliteal lymph nodes were enlarged in both adjuvant controls and animals with EAN and both showed a decrease in the percentage of W3.25+ lymphocytes from normal unenlarged nodes.

Animals↗
PubMed1985

Temporal frequency discrimination in optic neuritis and multiple sclerosis.

The temporal contrast sensitivity function and temporal frequency discrimination have been studied in normals and in 7 cases of multiple sclerosis or optic neuritis. Sinusoidal gratings of two spatial frequencies (0.2 and 2.0 cycles/deg) were used. The abnormalities demonstrated in the patients varied between individuals but overall a picture has emerged of four principal anomalies. The temporal transfer function of the 2 cycles/deg medium spatial frequency grating has a band-pass appearance, whereas it is low-pass in normal subjects (5 out of 8 eyes). The peak of temporal frequency discrimination function (i.e. the temporal frequency at which discrimination is most acute) occurs at a lower temporal frequency in the patients than in normal subjects particularly at the higher spatial frequency (5 out of 8 eyes for a spatial frequency of 2.0 cycles/deg; 2 out of 8 eyes for a spatial frequency of 0.2 cycles/deg). It was found that normal subjects were able to discriminate between the maximum temporal frequency used as a standard in the discrimination experiments (16 Hz) and a higher temporal frequency. In the patients, however, a cut-off in the discrimination function occurred at a temporal frequency well below this (8 out of 8 eyes for a spatial frequency of 2.0 cycles/deg; 2 out of 8 eyes for a spatial frequency of 0.2 cycles/deg). Further to the above result, in a number of patients an attempt was made to ascertain how the gratings were perceived in this abnormally extensive region of ambiguity in the high temporal frequency range. It was found that high temporal frequencies, at a constant contrast level above threshold and constant apparent contrast, were perceived either as flickering at a slower rate than did an intermediate temporal frequency or even appeared stationary. This effect was rare at the lower spatial frequency (1 out of 8 eyes) but was demonstrated in 4 out of 8 eyes at the spatial frequency of 2.0 cycles/deg. It was not specifically sought in all individuals. These results are discussed in the context of an information channelling model of temporal frequency processing in the visual system.

Discrimination, Psychological↗
PubMed1986

Colour and luminance vision in human optic neuritis.

A comparison of sensitivities to chromatic and luminance stimuli has been carried out in patients with a past history of optic neuritis. Patients were selected with differing degrees of stable residual visual deficits, and with marked interocular differences in sensitivity. Threshold contrast sensitivity was measured to sinusoidal luminance gratings and to chromatic red/green and blue/yellow gratings, all with the same spatial frequency of 1 cycle per degree. A psychophysical criterion was used to ensure that detection of the chromatic grating was determined only by its colour differences. When the difference between the sensitivity to luminance and chromatic gratings was compared between the more and less severely affected eyes of each subject, it was found that, overall, chromatic sensitivity was more severely impaired than luminance sensitivity in the disorder. Sensitivities to the red/green and the blue/yellow stimuli were found to be affected equally.

Color Perception↗
PubMed1987

Retinal venous sheathing in optic neuritis. Its significance for the pathogenesis of multiple sclerosis.

A systematic study of the frequency of retinal vascular abnormalities and cells in the media has been made in 50 patients presenting with acute optic neuritis. Abnormalities were found in 14 (fluorescein leakage in 10, perivenous sheathing in 6, cells in the vitreous in 6 and in the anterior chamber in 4; in 2 the cells in the media were seen without vascular changes). After a mean follow up of 3.5 years multiple sclerosis (MS) had developed in 8/14 patients with vascular abnormalities and/or evidence of inflammation and in 5/32 without; the difference is significant (P less than 0.02). The occurrence of perivenular abnormalities in a region free of myelin and oligodendrocytes provides evidence that the vascular changes in MS can occur independently of contiguous demyelination, and may be the primary event in the formation of a new lesion.

Adolescent↗
PubMed1988

The role of macrophages and eicosanoids in the pathogenesis of experimental allergic neuritis. Serial clinical, electrophysiological, biochemical and morphological observations.

Experimental allergic neuritis (EAN) can be prevented or ameliorated by global blockade of macrophages. How these cells damage peripheral nervous tissue in this autoimmune demyelinating polyneuropathy is not fully understood. Since macrophages exert a number of their inflammatory actions by the release of arachidonic acid-derived eicosanoids, we investigated the possible role of these mediators in the pathogenesis of EAN. Lewis rats with myelin-induced EAN were treated before and after onset of clinical signs. Administration of corticosteroids or of the cyclo-oxygenase inhibitors indomethacin and BW755c before the onset of neurological signs suppressed the disease, as judged by clinical assessment, serial electrophysiological testing and histological examination, while initiation of drug treatment on day 13 postimmunization still markedly attenuated the course of EAN. The selective lipoxygenase blocker nafazatrom had only a slight effect. Determination of the production by macrophages ex vivo of eicosanoids corroborated the predicted site of action of the pharmacological compounds applied. We infer that macrophage-derived proinflammatory arachidonic acid metabolites significantly contribute to functional and tissue damage in EAN. Our results may be relevant to future pharmacological treatment of the acute Guillain-Barré syndrome.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1989

Effect of ion channel blockers on immune response and course of experimental allergic neuritis.

The influence of the K+ channel blocker quinidine and the Ca++ channel blocker verapamil on in vivo and in vitro immune responses was tested in experimental allergic neuritis (EAN) of Lewis rats. Daily intraperitoneal injections of 4 mg quinidine produced a significant reduction of neurological deficits in EAN rats, whereas verapamil had no effect. In contrast, both drugs inhibited the in vitro proliferative response of regional lymph node cells to specific antigens of bovine peripheral myelin and purified protein derivative of tuberculin in a similar dose-dependent manner. Quinidine-treated EAN rats revealed considerably less inflammatory infiltration in target tissue than untreated EAN rats, shown immunohistochemically. Single injections of ion channel blockers into EAN rats did not improve nerve cell functions as measured by electrophysiological recordings of sciatic nerve. It is concluded that the dominant effect of quinidine in vivo is attributed to a reduction of the demyelinating autoimmune process. Hence ion channel blocking drugs can exert immunomodulatory effects, which may have implications for their clinical application.

Animals↗
PubMed1990

Optic neuritis: variations in temporal modulation sensitivity with retinal eccentricity.

Temporal modulation sensitivity functions were measured centrally and at eccentricities of 2.5 degrees, 5 degrees and 10 degrees in the temporal visual field of 12 patients with recovered optic neuritis and in a group of matched normal controls. A circular, spatially uniform stimulus of 1 degree angular subtense was presented with sinusoidal modulation at 5, 8, 14 and 23 Hz. The general pattern of results in patients was a loss of sensitivity relative to normal controls at all temporal frequencies at 0 degree and 2.5 degrees eccentricity, with rather greater losses occurring at the medium-to-lower temporal frequencies. At 5 degrees eccentricity, the losses were confined to medium temporal frequencies only, and at 10 degrees eccentricity there was no significant loss at any temporal frequency. These findings may be explained by a greater vulnerability of optic nerve fibers of small diameters to the effects of demyelinating disease.

Adult↗
PubMed1990

Visual loss in multiple sclerosis and its relation to previous optic neuritis, disease duration and clinical classification.

Visual function was investigated in a group of 58 clinically classified cases of multiple sclerosis (MS). Psychophysical measures of luminance and chromatic threshold sensitivity and temporal contrast sensitivity were undertaken, together with visual evoked potentials and Bjerrum screen perimetry. The patient group was divided on the basis of optic neuritis (ON), clinical disease duration and clinical classification. A comparison of the results of all visual measures suggested a nonuniform loss of function in the patient group without ON and a more consistent loss of function in the group with ON. The various measures were equally efficient in detecting abnormal function, albeit from different areas of the central visual field. Clinical disease duration was not a significant independent factor in predicting visual dysfunction. In contrast, a comparison of clinical classification categories revealed significantly fewer abnormalities of visual function in the suspected MS category (31%) than in the ON, early probably and clinically definite categories (75-100%), a result which indicated the importance of clinical classification as a predictor of visual dysfunction.

Adult↗
PubMed1991

Chronic relapsing experimental allergic neuritis induced by repeated transfer of P2-protein reactive T cell lines.

Chronic relapsing experimental allergic neuritis (crEAN) was induced by repeated transfers of P2-protein reactive T lymphocyte lines. Clinically, each intravenous transfer of P2-reactive T cells induced a relapse of the disease with weight loss and flaccid paresis of the hindlimbs followed by recovery. After multiple transfers, recovery from disease was incomplete, leading to increasing neurological deficit during the remissions. The pathology of the lesions during exacerbations was characterized by massive inflammation in the peripheral nervous system, associated with extensive endoneurial oedema, nerve fibre destruction and wallerian degeneration. Selective primary demyelination and remyelination was found in the minority of affected nerve fibres. No onion bulbs were present in chronic lesions. In the central nervous system partial degeneration of the posterior columns reflected the extent of wallerian degeneration in the peripheral nerves and spinal roots. In addition, during stages of active disease some T lymphocytes and upregulation of Ia antigen expression were found in the spinal cord.

Animals↗
PubMed1991

Recognition of motion-defined shapes in patients with multiple sclerosis and optic neuritis.

We have developed a simple procedure for assessing the ability of the visual pathway to extract a two-dimensional shape from motion. The test requires a patient to read motion-defined (MD) letters. These letters differ physically from the familiar contrast-defined (CD) letters that are dimmer or brighter than their surroundings in that the boundaries of MD letters are rendered visible exclusively by a step in velocity while the boundaries of CD letters are rendered visible by a step in luminance. Subjects viewed a random pattern of bright dots containing a perfectly camouflaged letter. Then the letter was revealed by moving dots within and outside the letter at equal speeds in opposite directions. Letter reading scores for 50 eyes of 25 patients with multiple sclerosis (MS) or optic neuritis were compared with norms based on 50 control subjects. When tested with large (50 arc min, i.e., 6/60) MD letters, 34/50 eyes of patients required abnormally high dot speeds to read letters, visual loss being sufficiently selective in 10 eyes that contrast sensitivity, Snellen acuity, 11%-contrast and 4%-contrast acuity were all spared. Four eyes were effectively motion blind in the sense that they could not read large letters even at our highest relative speed of 0.9 deg/s and the failure could not be attributed to reduced Snellen acuity. Our normal limit was 2.5 SD from the control mean and there were 1/50 false positives. Of the 34/50 eyes with elevated speed thresholds, 23 had normal Snellen acuities. The number of eyes abnormal for intermediate (11%) contrast CD letters, was 19/50 of which 8 had normal Snellen acuity, confirming our previous finding that MS can degrade the ability to see low-contrast objects while sparing Snellen acuity. We conclude that MD test letters can detect lesions that are not picked up by testing with CD test letters of high or low contrast. We suggest that the MD letter test can detect dysfunction in the human equivalent of a pathway in monkey brain that originates in large retinal ganglion cells, passes through the magnocellular layers of the lateral geniculate body, includes cortical area MT, and is involved in processing motion.

Adult↗
PubMed1991

The visual defect in multiple sclerosis and optic neuritis. A combined psychophysical and electrophysiological investigation.

Chromatic and achromatic visual function were investigated using psychophysical and evoked potential techniques in 32 patients with multiple sclerosis (MS) or optic neuritis. There was no evidence for either chromatic or achromatic vision being selectively damaged. There was, however, some evidence that demyelination of the optic nerve causes a visual defect in which the transmission of high temporal frequencies is imparied. In some patients either a red or blue deficit was evident, but overall there was no evidence of a wavelength specific colour vision defect in our patient group. Reduction of chromatic sensitivity as determined psychophysically had a statistically significant correlation with the amplitude and latency of the chromatic visual evoked potential.

Adult↗
PubMed1991

The pathophysiology of acute optic neuritis. An association of gadolinium leakage with clinical and electrophysiological deficits.

Eighteen patients with acute optic neuritis underwent optic nerve magnetic resonance imaging (MRI) before and after injection of gadolinium-diethylene triamine pentacetic acid (Gd-DTPA). Ten were re-examined 4 weeks later. Leakage of Gd-DTPA across the blood-optic nerve barrier was a consistent finding in the acute lesion, and its presence was associated with abnormal visual acuity and colour vision, retro-ocular pain on eye movement, and afferent pupillary defect, and a reduced amplitude of the P100 component of the visual evoked potential. Gd-DTPA leakage had ceased in 9/11 nerves when restudied 4 wks later, and this evolution was associated with improved visual acuity and an increased P100 amplitude. Leakage is likely to reflect inflammation, and we conclude that the latter plays an important part in the production of conduction block and clinical deficit, and that its resolution is an important step in clinical remission from acute episodes of demyelination.

Adolescent↗
PubMed1992

Acute optic neuritis. A cognitive and magnetic resonance imaging study.

Forty-two patients with acute optic neuritis (ON) (mean duration of symptoms 14.5 d) were compared with a matched, normal control group on a battery of tests of attention and information processing speed. Approximately half the sample (55%) had brain abnormalities shown by magnetic resonance imaging (MRI) and were more impaired across a variety of tests compared with those patients without brain lesions or normal controls. There was no difference in psychometric performance other than the pegboard task between the normal control group and those ON patients without brain involvement. Significant correlations were found between total lesion area in the brain and some tests of attention. Results from the Symbol Digit-Substitution Test were particularly sensitive in this regard and could correctly identify 70% of the sample with brain lesions.

Adult↗
PubMed1992

Transient cellular expression of gamma-interferon in myelin-induced and T-cell line-mediated experimental autoimmune neuritis.

This study reports the cellular localization of gamma-interferon (gamma-IFN) in nerve roots during the course of experimental autoimmune neuritis induced either by active immunization (EAN) or adoptive transfer of P2-specific T-cells (AT-EAN). One micrometre thick cryosections of ventral roots of EAN and AT-EAN animals were labelled with the monoclonal antibodies DB-1 and DB-12 recognizing different epitopes of rat gamma-IFN. In EAN numerous gamma-IFN-positive cells were present before overt clinical signs and demyelination (days 11-13 after immunization). Concomitantly, raised gamma-IFN levels were measured in the serum of these animals. However, systemically increased gamma-IFN serum levels were not specific for a neuritogenic T-cell response. At subsequent stages when many axons were demyelinated (day 16 and later) gamma-IFN-positive cells had disappeared and gamma-IFN serum levels returned to normal value. gamma-Interferon positive cells could be identified as W3/13 positive T-cells and polymorphonuclear leukocytes. Additionally, a considerable number of ED1-positive macrophages showed gamma-IFN immunoreactivity. The majority of macrophages and all Schwann cells were gamma-IFN negative. Similar results were obtained in AT-EAN 4 d and 6 d following cell transfer. After nerve transection no gamma-IFN-positive cells were found in the distal stumps. The localization of gamma-IFN in nerve roots indicates an important role of this lymphokine in acute immune-mediated demyelination. gamma-Interferon most likely locally affects macrophage functions such as migration, major histocompatibility complex (MHC) class II antigen (Ia) expression, and production of cytotoxic molecules in nerves, and thereby contributes to myelin damage.

Animals↗
PubMed1993

Suppression of experimental allergic neuritis by an antibody to the intracellular adhesion molecule ICAM-1.

Experimental allergic (autoimmune) neuritis (EAN) was induced in Lewis rats either by inoculation with bovine spinal root myelin or injection of neuritogenic P2-specific T cells. Injection of a purified monoclonal antibody (1A-29) to the intercellular adhesion molecule-1 (ICAM-1) prevented or transiently suppressed myelin-induced EAN depending on the timing of antibody application. Administration of 1A-29 suppressed moderate adoptive transfer EAN (AT-EAN) but not severe AT-EAN. In contrast, treatment with phosphate buffered saline or an unrelated IgG1 had no effect on the course of the disease. Histological sections of the peripheral nervous system (PNS) showed a marked reduction of inflammatory infiltrates and perivascular demyelination in rats injected with 1A-29. The effect of 1A-29 on the concanavalin A (Con A)- and P2-dependent proliferation of neuritogenic P2-specific T cells was studied in vitro. Our data suggest that antibodies to ICAM-1 act on the induction and effector phase of the immune response by inhibiting both early interactions between immunocompetent cells after exposure to foreign antigen and transendothelial migration of primed T cells into the peripheral nerve. Treatment with antibodies to leucocyte adhesion molecules could be a useful therapeutic approach to autoimmune disease of the PNS.

Animals↗
PubMed1993

The neurotrophic analogue of ACTH(4-9), Org 2766, protects against experimental allergic neuritis.

Demyelinating diseases such as multiple sclerosis or the Guillain-Barré syndrome originate from an autoimmune response resulting in the degradation of myelin and impaired neuronal function. Prophylactic administration of the neurotrophic peptide, H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH [an ACTH(4-9) analogue], to rats with experimental allergic neuritis, a model for the Guillain-Barré syndrome, markedly suppresses the clinical symptoms, protects against loss of motor coordination and prevents the degeneration of myelinated axons in the affected peripheral nerve. Therefore, this peptide may provide a new approach to the therapy of peripheral demyelinating polyneuropathies.

Adrenocorticotropic Hormone↗
PubMed1994

Effective use of a neurotrophic ACTH4-9 analogue in the treatment of a peripheral demyelinating syndrome (experimental allergic neuritis). An intervention study.

Demyelinating syndromes are an important group of nerve disorders for which no effective therapy exists and which are life threatening in a substantial proportion of the patients. In the present experiments we assessed the ameliorative effect of Org 2766, a degradation resistant ACTH4-9 analogue devoid of corticotrophic and melanotrophic action in experimental allergic neuritis (EAN), an animal model for a human demyelinating disease, the Guillain-Barré syndrome (GBS). In order to mimic the clinical situation, peptide treatment was initiated at the first appearance of neurological symptoms in each animal. The ACTH4-9 analogue treatment substantially suppressed the neurological symptoms in animals with EAN, as assessed by clinical scoring and resulted in a significant improvement of motor performance. Furthermore, histological examination of the sural nerve provided a morphological basis for the beneficial functional effect of peptide treatment: more myelinated fibres were present in EAN animals treated with the ACTH4-9 analogue in comparison with EAN animals treated with saline. Further analysis of the sural nerve indicated a complete preservation of the diameter distribution of myelinated fibres in sural nerves of peptide-treated animals. In contrast, saline-treated EAN animals exhibited a significant loss of small and intermediate size myelinated fibres in the sural nerves. This study provides first evidence for the amelioration of the functional and anatomical deficits in an animal model of the GBS syndrome by an interventive synthetic neurotrophic peptide treatment.

Adrenocorticotropic Hormone↗
PubMed1994

Optic neuritis. Differential losses of luminance and chromatic function near a scotoma.

Visual sensitivity to achromatic and chromatic stimulus flashes was determined at sites just inside, on the boundary and just outside scotomata in 11 patients with recovered optic neuritis. The colour of the flashes and the size of the steady background on which they appeared were such that detection was more likely to be mediated by either the large-diameter, magnocellular fibres or the small-diameter, parvocellular fibres of the anterior visual pathway. The spacing of the test sites ranged from 0.5 degrees to 4 degrees visual angle, depending on the shape and location of the scotomata. The greatest differences in sensitivity were between sites just inside and just outside the scotoma and in response to achromatic stimuli more likely to involve the magnocellular fibres. This effect may be due to the size of magnocellular fibres or to their relatively smaller numbers.

Adult↗