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At least 1,243 records · Page 69Linked to original sources
PubMed1990

The dyschromatopsia of optic neuritis is determined in part by the foveal/perifoveal distribution of visual field damage.

Most hypotheses of acquired dyschromatopsia invoke the mechanism of selective damage to specific components of the afferent visual system to explain the predominance of red-green and blue-yellow hue-discrimination defects found in neural and retinal disorders, respectively. However, this pattern of hue-discrimination disturbance in ocular disease may vary. There are frequent exceptions which are inadequately explained by existing hypotheses. In an effort to explain the pattern and pathogenesis of acquired dyschromatopsias better, the authors examined patients with nonproliferative diabetic retinopathy (DR) and late-stage retrobulbar neuritis (RBN) using age-corrected Farnsworth-Munsell 100-hue testing and threshold static perimetry. As expected, most DR eyes showed some degree of relative blue-yellow dyschromatopsia (89%) with few showing a greater weighting towards red-green dyschromatopsia (11%). However, an approximately equal number of RBN eyes had a relative blue-yellow (48%) versus red-green dyschromatopsia (52%). For RBN, the authors found a strong association between the spatial distribution of field defect and the type of relative hue-discrimination disturbance. Eyes with greater field depression at the fovea relative to the perifovea showed a relative preponderance of red-green dyschromatopsia (68%) as opposed to blue-yellow dyschromatopsia (32%), whereas eyes with greater relative perifoveal impairment showed a relative preponderance of blue-yellow dyschromatopsia (100%). This relationship between the relative spatial distribution of visual field damage and the relative hue-discrimination deficit in RBN was statistically significant (P = 0.002). Such an association was not found for DR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

[Comparison of the Aulhorn flicker test with visual evoked potentials in the diagnosis of optic neuritis].

The Aulhorn flicker test and visual evoked cortical potentials (VEP) are of great value for the diagnosis of optic neuritis (ON). In the present study, the two methods were compared for the first time within the same group of patients. The study comprised 405 eyes (175 suffering from active or subsided ON). The results were evaluated with a double-blind procedure. With the flicker test, the subjective brightness of flickering light is determined as a function of the flicker frequency. This test gives pathological results only in active ON and normalizes when the active phase is over. The test can discriminate between active and subsided ON as well as between the recurrent and chronic courses of the disease. Differentiation is not possible with the VEP, since the VEP latencies are prolonged even after the end of the active period of the disease. The sensitivity of the flicker test was 84.4%. The sensitivity of the VEP was 72.7% for our group of patients suffering from ON if the criterion of increased latency was used alone. In the diagnosis of multiple sclerosis (MS), the proportion of correctly identified pathological VEP results is increased because of the detection of demyelination of the optic nerve that causes no clinical symptoms. The specificity of the flicker test was 97.8% and that of the VEP 86.5%. If both methods were combined, the sensitivity was 98.4% and specificity 99.6%. The two methods obviously have different characteristics and seem to rely upon different demyelination effects. Each method has its advantages and disadvantages as well as optimal indications.(ABSTRACT TRUNCATED AT 250 WORDS)

Evoked Potentials, Visual↗
PubMed1990

[Pathologic studies of Guillain-Barre syndrome (GBS) and 13 rabbits with experimental allergic neuritis].

Pathological studies were carried out of Guillain-Barré syndrome (GBS) and 13 rabbits with experimental allergic neuritis. It was shown that the postmortem pathological findings in the patients, who died at different stages of GBS, varied in the degree of axon degeneration, the amount of plasmocyte infiltration, the appearance of phagocytes and the proliferation of Schwann cells and fibroblast. But in all the cases in this series segmental demyelination of the peripheral nerve with lymphocyte infiltration occurred without exception. In the rabbits with EAN, it was found that there were small foci of demyelination in the cerebral white matter and diffuse hemorrhage in the grey matter of the spinal cord. Lymphocyte infiltration in the EAN rabbit group was seen in a much more extensive manner than that found in cases of the patients with GBS, but the proliferation of Schwann cells and fibroblast seemed to take place more slowly in comparison with the similar process as was revealed in the patients who died from GBS.

Adolescent↗
PubMed1985

Morphologic study on experimental allergic neuritis mediated by T cell line specific for bovine P2 protein in Lewis rats.

Light and electron microscope studies were performed on experimental allergic neuritis (EAN) passively induced in Lewis rats by the intravenous injection of T line cells specific for bovine P2 protein. Histologic changes were almost entirely restricted to the peripheral nervous system, being most severe in the sciatic nerve and lumbosacral nerve roots, whereas the brachial nerve and cervical nerve roots were involved to a lesser extent. The lesions were composed of edema, cellular infiltrates, demyelination, and, subsequently, axonal degeneration. Infiltrated macrophages were observed actively stripping the myelin, and the Schwann cell cytoplasm of affected nerve fibers was pushed to the periphery without distinct evidence of degeneration. The first evidence of pathologic change was severe edema in the sciatic nerve 4 days postinoculation. This edema was demonstrated immunohistochemically by the presence of albumin and fibrinogen in the endoneurial space. Mast cell degranulation was observed in these edematous nerve lesions. The cellular infiltrates which formed perivascular cuffs were composed of not only mononuclear cells but also many granulocytes. In the central nervous system, meningeal cell infiltration was also observed in the spinal cord, and after 7 days postinoculation degeneration of the posterior column was also found. This latter observation is thought to represent degeneration due to axonal damage of lumbosacral posterior roots. These pathologic findings in a T cell-mediated model of EAN were essentially the same as those previously reported in conventionally induced EAN or human Guillain-Barré Syndrome. Thus, T cells specific for bovine P2 protein can induce typical EAN lesions in the Lewis rat. The further investigation of this transfer model of EAN will enable us to clarify the pathogenesis of EAN and Guillain-Barré syndrome.

Animals↗
PubMed1986

Anti-galactocerebroside antibody in rabbits with experimental allergic neuritis.

Serum antibodies to P2 protein, myelin basic protein (MBP) and galactocerebroside (GC) were examined to study the role of humoral factors in experimental allergic neuritis (EAN). Out of 19 outbred rabbits sensitized with peripheral nerve homogenate, 14 developed EAN and the remaining 5 rabbits did not develop the disease. Anti-P2 protein and anti-MBP antibodies were detected not only in the EAN rabbits but also in the nonresponders. On the other hand, anti-GC antibody was detected in 7 of 14 EAN rabbits but not in the nonresponders. This antibody appeared near the onset of the clinical signs. As 7 rabbits developed EAN in the absence of the antibody and the titer did not correlate with the clinical severity, it is unlikely that anti-GC antibody is the major factor in inducing EAN. However, this antibody, along with other factors, may play a role in EAN.

Animals↗
PubMed1986

Induction of experimental allergic neuritis in the BN rat: P2 protein-specific T cells overcome resistance to actively induced disease.

T lymphocyte lines specific for the peripheral nerve myelin protein P2 were selected from the lymph nodes of Brown Norway (BN) rats immunized with bovine P2 protein in complete Freund's adjuvant. These T cells expressed the W3/25+, OX8-phenotype and responded specifically to bovine P2 protein, but not to PPD or bovine basic protein, in T cell proliferation assays. When injected i.v. into syngeneic recipients, BN P2-specific T cell lines induced both clinical and histologic signs of experimental allergic neuritis (EAN), overcoming the resistance of this rat strain to actively induced EAN. Although the histopathology of the disease was indistinguishable from that seen in T cell-mediated EAN in the Lewis rat, disease onset was considerably later, 7 to 8 days after cell transfer, as opposed to 4 days in Lewis. This lag phase between inoculation and disease onset could not be further reduced even by raising the cell dose to 50 X 10(6) cells/host. The fine specificity of the T cell response to P2 differs between Lewis- and BN-derived T cell lines. At least one neuritogenic epitope for each strain was present in the cyanogen bromide-derived peptide CB2 (residues 21-113), as shown by the ability of CB2-specific T cell lines derived from each strain to transfer EAN to the appropriate host strain. However, neuritogenic BN T lines fail to mount a response to the sequence 53-78 (SP4), which encompasses an epitope that is neuritogenic for Lewis rats. These results demonstrate that the resistance of BN rats to actively induced EAN is not due to the lack of appropriate P2-specific autoreactive T cell clones in the normal T repertoire. Furthermore, the results suggest that two distinct epitopes of P2 are responsible for EAN in Lewis and BN rats.

Animals↗
PubMedDate not supplied

Myelin basic protein in the CSF of patients with multiple sclerosis, optic neuritis and various neurological diseases.

We tested 104 patients for myelin basic protein (MBP) content in the CSF. Of these subjects 14 were selected as control group, 36 were affected by multiple sclerosis (MS), 14 by optic neuritis (ON) and 42 presented other not primarily demyelinating neurological diseases (ND ND). CSF MBP level was significantly higher in the MS group than in the other groups of patients, while no statistical difference was found between the MS patients with acute exacerbation and those in remission.

Humans↗
PubMed1977

Virus antibody levels in serum and cerebrospinal fluid specimens from patients with optic neuritis.

Virus antibody levels in serum specimens from 77 patients with optic neuritis (ON) were compared with those in healthy controls which had been matched with regard to sex, age and place of residence. A group of 58 patients with various neurological diseases other than multiple sclerosis (MS) or infectious diseases of the central nervous system (CNS) served as a second control group. The ON patients had significantly higher measles antibody titers in serum than the two control groups in both measles HI and HLI tests. Tests of cerebrospinal fluid (CSF) specimens revealed similar differences between ON patients and controls. Tests for antibodies to other viruses showed no statistically significant differences between ON patients and controls. There were several ON patients with normal serum/CSF albumin ratios but low serum/CSF IgG and measles antibody ratios. An increase in measles antibody CSF titers was observed during the study time in two ON patients. The results support the hypothesis that local production of measles antibodies takes place in the CNS of some patients with ON as has been earlier suggested to occur in patients with MS.

Antibodies, Viral↗
PubMed1989

Bilateral chorioretinitis, centripetal optic neuritis, and encephalitis in a llama.

Blindness characterized by dilated, unresponsive pupils and ophthalmoscopic evidence of optic nerve atrophy and retinal degeneration developed in a 5-year-old llama. Lesions were not progressive during 2 months of observation. The llama was euthanatized and necropsied. Histopathologic findings included chorioretinitis, optic neuritis, and encephalitis characterized by mononuclear perivascular infiltration. Attempts to prove an infectious cause were unsuccessful.

Animals↗
PubMed1989

Experimental allergic neuritis: effect of plasma infusions.

The effect of intravenous fresh frozen plasma (FFP) and artificial plasma infusions upon the clinical course of chronic experimental allergic neuritis (EAN) in the rabbit was investigated. A total of 12 animals allocated to treatment groups received rabbit FFP or a gelatin plasma expander Haemaccel (Hoechst) and were compared to 13 control non-treated animals. Animals receiving Haemaccel at a rate of 15 ml/kg/day for 7 days showed no significant clinical benefit at any stage. However, animals receiving 15 ml/kg/day FFP for 8 days showed significant clinical benefit during treatment initiated at the onset of definite neurological symptoms of EAN (Mann-Whitney U test, day 4 post-allocation P less than 0.05; day 6 post-allocation P less than 0.01; day 8 post-allocation P less than 0.05). Relapse was observed after cessation of treatment such that comparisons of clinical scores at day 14 and 22 post-allocation revealed no significant differences. Analysis of plasma anti-myelin IgG levels by ELISA showed that non-immunogenic plasma volume expansion decreased anti-myelin IgG concentrations immediately by an average of 34% but had no long-term effect. In contrast, anti-myelin IgG concentrations in FFP infused animals were significantly decreased, compared to controls, when measured 24 h after the last infusion (Student's t-test P less than 0.05). Identical percentage weight losses for both control and treatment groups post-allocation indicated that this decrease was immunologically mediated and not due to plasma dilution. Similar plasma cortisol concentrations measured in both groups showed no significant artifactual induction of endogenous steroid production. Infusions of FFP during early disease progression are able to mediate clinical remission in animals with chronic EAN.

Animals↗
PubMed1989

[Magnetic resonance imaging (MRI) in the diagnosis of optic neuritis and neuropathy].

Magnetic resonance imaging (MRI) was performed in thirty patients who had been suffering from optic neuritis (ON). Twenty-one cases were caused by multiple sclerosis (MS) and in 9 cases the causes been defined. In MRI, abnormalities were found in 17 out of 21 MS cases in several places such as near the ventricles, mid-brain, spinal cord etc. Increased signals from the optic chiasm to optic radiation were found in 5 cases. However, abnormal MRI findings did not always correspond to Goldmann visual field defects. In 3 out of 9 cases of ON with unknown causes, high signals in the white matter of the brain were found, and it was suggested that those may develop to MS. MRI was, thus, proved to be very useful for the diagnosis of MS.

Adolescent↗
PubMed1989

Optic neuritis in the two northernmost counties of Norway. A study of incidence and the prospect of later development of multiple sclerosis.

A study of the incidence of uncomplicated optic neuritis (ON) in the period 1972-1984 and the subsequent risk of later developing of multiple sclerosis (MS) was performed in the two northernmost counties of Norway. The incidence of ON was stable during the period. Of the 36 ON patients available to follow-up, 42% later developed MS. Mean time from debut of ON to the next symptom of MS was 2.2 years, median 1 year. There was one ethnic Lapp among the ON patients. The number of Lapps in the area is estimated to be about 26,000.

Adult↗
PubMed1986

Treatment of optic neuritis with megadose corticosteroids.

Difficulty in distinguishing between monosymptomatic optic neuritis due to autoimmune disease or to intrinsic demyelination in young adults prompted a trial administration of megadose corticosteroids in a series of patients. Treatment with 1 g daily of intravenous methylprednisolone (Solu-Medrol) for 2 to 5 days led to the rapid resolution and restoration of visual function in five patients. Two untreated patients suffered irreversible loss of vision. One patient with known autoimmune disease required a higher dose. The author suggests a trial of megadose, intravenous corticosteroids in patients between the ages of 21 and 45 years with optic neuropathies of uncertain or suspected autoimmune etiology after appropriate neuro-ophthalmologic evaluation.

Adrenal Cortex Hormones↗
PubMed1977

[Electrostimulation and stimulation electromyography in the complex treatment of facial neuritis with rheographic control].

The author treated 60 patients with facial nerve neuritis with the aid of a "Bion" apparatus. For control over the changes seen due to the use of electrostimulation, stimulational EMG was used with the registration of a rheogram of the mimical muscles. During the study the following data were obtained: a shortening of the latent period of the facial nerve in an electrostimulation was an objective criterion, permitting to control the restitution of the damaged neuro-muscular face structures. Under the effect of treatment there was also an improvement in the biolectrical activity of the superciliary muscle and an increase in the amplitude of the rheographical wave. In most cases (53 patients) there was a recovery, in 6--a significant improvement. In 1 case the state was not altered.

Electric Stimulation Therapy↗