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Sixty-nine cases of Optic Neuritis were studied in order to evaluate the percentage of evolution into multiple sclerosis. We observed an incidence rate of 53.6% which is somewhat high respect to data present in literature. The various findings obtained in the present study were compared with those of the literature and the similarities and discrepancies underlined.
A case of unilateral retrobulbar neuritis was described. The patient, 43-year-old man died because of the extensive postinfarctional changes on the second day of the treatment. Retrobulbar part of the optic nerve and chiasma opticum were investigated. The microscopic pictures represent the correlations between morphological changes and their pressure on the neural fibres connected with visual disturbances.
BACKGROUND: Experimental autoimmune neuritis (EAN) is an animal model of Guillain-Barré syndrome. The mechanisms underlying cellular trafficking and homing of autoreactive immune cells to the peripheral nervous system during EAN and Guillain-Barré syndrome are unknown. We investigated the role of the adhesion molecule lymphocyte function-associated antigen-1 in the pathogenesis of EAN. EXPERIMENTAL DESIGN: EAN was induced in Lewis rats either by immunization with bovine spinal root myelin or by adoptive transfer of P2-specific T cells. Animals were treated intraperitoneally with a monoclonal antibody to lymphocyte function-associated antigen-1 (WT-1) or phosphate-buffered saline and scored for clinical signs. Histology was performed on sciatic nerve and cauda equina and assessed for infiltration and demyelination. Severity of EAN and the corresponding histologic alterations were compared in the different treatment groups. The in vitro effect of WT-1 on T cell proliferation was evaluated. RESULTS: Treatment with WT-1 prevented or efficiently suppressed myelin-induced EAN. In contrast, sham treatment of animals failed to alter the clinical course of EAN. Histologic examination of the peripheral nervous system showed a marked reduction of inflammatory infiltration and perivascular demyelination in animals treated with WT-1. Adoptive transfer EAN was not affected by the administration of WT-1. The differential action in the two models suggests that WT-1 appears to act primarily on the induction phase of the immune response but has no significant impact on the effector phase. In vitro studies with WT-1 revealed that the antibody inhibits the concanavalin A-dependent proliferation of neuritogenic P2-specific T cells. CONCLUSIONS: Our data indicate that lymphocyte function-associated antigen-1 is critically involved in the pathogenesis of EAN. Further analysis of this model may provide insight into the process of immune cell recruitment from the circulation into the peripheral nervous system in immune-mediated neuropathies.
In vitro lymphocyte stimulation reaction to retinal S-antigen was evaluated in 115 patients of anterior uveitis, posterior uveitis/pan-uveitis, and optic neuritis, the positive rate being 34% (18/53), 41.5% (17/41), and 57.1% (12/21) respectively. It is speculated that such immunoresponse may be secondary to the exposition or the release of retinal antigens by various causes, leading to activation or augmentation of meager or low-affinity S-antigen-specific lymphocytes in healthy individuals to start the pathogenic autoimmune process. However, the authors also found that the stimulation index to PHA differed insignificantly between the control and experimental groups, indicating that there was no cellular immuno-hypofunction in the experimental patients.
The author presented results of visual evoked potentials and static perimetry examinations performed in 17 patients with chiasmal tumors and in 27 with retrobulbar neuritis. A comparative analysis of the gathered parameters was done, using computer programs. The results suggest that the applied non-invasive methods of examination could be useful in differential diagnosis of these diseases.
Familial Mediterranean fever (FMF) is an inherited disorder characterized by recurrent attacks of fever and polyserositis of unknown origin. Neuro-ophthalmologic involvement is rare. We describe a previously unreported association of FMF with optic neuritis in two patients.
During the years 1980-1981, 19 patients with a mean age of 39 years, given the diagnosis vestibular neuritis were subjected to a caloric bithermal test, a pure tone audiogram and stapedius reflex measurements within 1 week, 3 weeks, 9 weeks and 1 year after the onset of symptoms, respectively. In a majority of the patients the feeling of dysequilibrium and vertigo diminished within the first 3 weeks and the difference in caloric reaction between the two sides also diminished during this period. In 9 of the patients, a uni- or bilaterally elevated stapedius reflex threshold was found. The return of the caloric response was somewhat slower in this group of patients.
Consecutive subjects 50 to 75 years of age with sudden onset of vertigo but without cochlear or neurological symptoms were investigated with neuro-imaging techniques. Doppler sonography of the vertebral and carotid arteries and recording of voluntary saccades and pursuit eye movements, caloric, spontaneous, gaze and optokinetic nystagmus. Among those studied, 6 out of 24 subjects could be demonstrated to have cerebellar infarctions, another 2 subjects had occlusion of one vertebral artery. Caloric tests could not identify subjects with a cerebellar infarction whereas prominently reduced pursuit eye movements could. Subjects with cerebellar infarction either had a vertebral artery occlusion or prominent cardio-embolic risk factors. It is suggested that subjects with symptoms as vestibular neuritis should be investigated with pursuit eye movements and with at least standard ECG recordings.
A patient with an enhancing, completely intracanalicular mass on MRI was presented. He had noticed progressive hearing loss in the left ear with tinnitus. Neurological examination revealed no abnormality except decreased hearing in the left ear. There were no other cranial nerve or cerebellar signs. An audiogram revealed profound hearing loss on the left ear with no ability of speech discrimination. Brainstem auditory evoked response was absent on the left. MRI enhanced with gadolinium-DTPA demonstrated an intracanalicular enhancing lesion on the left which was presumed to be an intracanalicular acoustic neurinoma. The patient underwent a left suboccipital craniectomy. The eighth cranial nerve appeared normal in the cerebellopontine angle cistern, and was swollen and discolored in the internal auditory canal. It was removed piecemeal. The patient remained deaf in the left ear postoperatively. Histopathologically, the lesion consisted of edematous nerve fiber and inflammatory cells, but no tumor cell was present within the specimen. The patient was diagnosed as having neuritis. The clinical time course of symptoms in our patient was not unusual for an acoustic neurinoma. It seems that the distinction between an intracanalicular acoustic neurinoma and other lesions cannot be made on basis of MR imaging alone. All available imaging modalities should be considered before a definitive surgical procedure is undertaken.
Experimental autoimmune neuritis (EAN) is a monophasic inflammatory disorder of the peripheral nervous system that resolves spontaneously by molecular mechanisms as yet unknown. We have investigated whether the immunosuppressive cytokine transforming growth factor-beta 1 (TGF-beta 1) might be endogenously expressed in the peripheral nervous system of Lewis rats with actively induced and adoptive transfer EAN. TGF-beta 1 mRNA was upregulated to high levels in sensory and motor roots, spinal ganglia, and sciatic nerve as revealed by quantitative Northern blot analysis and in situ hybridization histochemistry, with peak levels just preceding the first signs of clinical recovery. TGF-beta 1 mRNA was localized to scattered round cells and dense cellular infiltrates, but only rarely to Schwann cell profiles. Double labeling studies revealed macrophages and subpopulations of T cells as the major cellular source of TGF-beta 1 mRNA. TGF-beta 1 protein was visualized immunocytochemically and localized to infiltrating mononuclear cells with peak expression around the same time as mRNA, in addition to some constitutive expression in axons and Schwann cells. Our studies suggest that the spontaneous recovery observed in Lewis rat EAN might be mediated by the endogenous elaboration of TGF-beta 1 within the peripheral nerve, and that macrophages might control their own cytotoxicity by expressing TGF-beta 1.
The authors reviewed the records of 20 patients with optic neuritis, all of whom were diagnosed as having clinically definite multiple sclerosis (MS). They were classified into two subgroups: Group A, consisting of 9 patients who had shown acute transverse myelopathy (ATM); and Group B, 11 patients without ATM. Four patients (44%) in Group A had complete visual loss, but none in Group B. Six patients (67%) in Group A had less than 0.1 visual acuity in the affected eye, but only 2 patients (18%) in Group B. Four patients in Group A showed evidence of anticardiolipin antibodies. While both groups were diagnosed as having clinically definite MS, there were differences between them in the clinical features. We assume that the patients with ATM may constitute a different subgroup among MS patients.
In addition to standard pattern-reversal VEPs, the motion-onset VEPs were examined in 50 patients with acute unilateral retrobulbar neuritis (RN) and in 187 patients with possible or definite multiple sclerosis (MS). In MS patients (without sign or history of RN), the results of both types of VEPs correlated only partially. 26.2% of them displayed changes only in the motion-onset VEPs having the pattern-reversal VEPs completely normal. That is why we suppose that the magnocellular system (tested by motion-onset VEPs) can be affected by demyelination separately. In 28 patients with "pure" RN (without any other sign indicating demyelination disease) the always abnormal pattern-reversal VEPs were accompanied by delayed motion-onset VEPs in only 28.6% of patients. In contrast, much higher rate--68.2%--of delayed motion-onset VEPs was found in the 22 RN patients simultaneously suspected of MS These results indicate that RN affects predominantly the parvocellular visual system (tested by reversal VEPs). Distinct latency changes of the motion-onset VEP's in RN patients seem to signal a linkage between RN and demyelination.
Acute monosymptomatic optic neuritis (ON) may be regarded as a specific disease entity, or ON may be viewed as a first manifestation of multiple sclerosis (MS) representing one end of a continuum with fully developed clinically definite MS at the other end. To clarify this, the literature is reviewed, and the relationship between ON and MS is exemplified by examination of a cohort of 50 untreated representative patients with relevant paraclinical tests at onset of monosymptomatic ON. MRI, neurophysiological examinations and CSF analyses are supplementary methods, which together provide evidence that monosymptomatic ON is usually an early manifestation of MS, both being associated with the HLA tissue type DR15. The frequent finding of unenhanced lesions on MRI probably signify that the disease process may start long before the symptoms of ON. CSF may not be representative of the pathological processes in the CNS. Bilateral ON is not particularly liable to herald MS. More attention should be paid to subtle visual disturbances, which may indicate a new attack. It is important that more sensitive evaluations than merely assessing visual acuity be performed in these patients.
Twenty five patients with optic neuritis (ON) of unknown etiology were treated with a high dosage of intravenous vitamin C. We measured blood levels of vitamin A, B1, B2, B6, B12, C, E, folate and zinc. All levels were compared with the normal values of our laboratory. The blood level of vitamin C (p < 0.001) was significantly less than the mean value of the normal. The blood levels of vitamin E, B6 (p < 0.01) and zinc (p < 0.001) also significantly decreased. Intravenous administration of vitamin C was given in those patients with decreased blood level of vitamin C. In order to compare the effect on vision by this treatment, the amplitude of recovery of vision, the time needed to attain the maximum vision, and the speed of visual recovery were analyzed. The results were compared with groups receiving other treatments. That is, Group A received intravenous administration of high dosage of vitamin C, Group B, intravenous pulse administration of corticosterone, Group C, oral administration of corticosterone, and Group D, oral administration of vitamin B12. Vision was significantly improved in all groups. There was no significant difference in improvement of visual acuity. Intravenous administration of vitamin C can be evaluated as the method of choice for the treatment of patients with ON. A possible mode of action by vitamin C on free radicals is discussed.
The authors have described a hypothyroidism clinic event with both non-specific symptoms and retrobulbar neuritis. They conclude that the above-mentioned pathology is somewhat insidious since, affecting the whole body, it can arise with non-specific symptoms thus averting towards a wrong diagnosis.
We reported two early-childhood cases suffering from acute optic neuritis (ON). Case 1 was a 3-year-old girl, who had a preceding upper respiratory infection, headache, nausea and subsequent sudden visual disturbance. Cranial MRI revealed multiple T2-elongated lesions in the white matter. She showed two neurological relapses including ON, leading to the diagnosis of clinically probable multiple sclerosis (MS). Case 2 was a 2-year-old boy, who had an acute onset of visual disturbance without any other neurological deficits. MRI with Gd-DTPA enhancement revealed not only a disorder of optic nerves but involvement of the white matter in the acute phase. It has been suggested that there may be a broad spectrum of demyelinating disorders between ON and MS even in early-childhood. Therefore, we should bear in mind to the subsequent progression to MS in childhood ON cases with silent brain lesions.
Optic neuritis is frequently the first clinical sign of multiple sclerosis (MS). Study results indicate that methylprednisolone pulse therapy reduces the rate of development of MS over a two year period. Patients also experience quicker recovery of vision. This short duration therapy presents immediate and intense nursing care challenges. Coordination of care between three departments at the University of Michigan Medical Center enables many patients to complete IV [intravenous] pulse therapy at home. Although coordination is challenging for providers, ambulatory care and home care benefit patients and their families with potential healthcare cost savings.
Steady-state pattern electroretinograms (PERGs) and visual evoked potentials (VEPs) in response to sinusoidal gratings (2 c/deg), sinusoidally counterphased at closely spaced temporal frequencies (TFs) between 4 and 28 Hz, were recorded from 11 patients with unilateral optic neuritis (ON; 11 affected eyes and 10 healthy fellow eyes) and 7 age-matched normal subjects (7 eyes). Amplitude and phase of responses' second harmonics were measured. Responses' apparent latencies were estimated from the rate at which phase lagged with TF. When compared to control values, mean PERG and VEP amplitudes of ON eyes were reduced (by about 0.4 log units) at both low (5-10 Hz) and high (16-20 Hz) TFs. Mean PERG amplitudes of fellow eyes were selectively reduced at low TFs (by about 0.3 log units). Mean PERG apparent latencies of both ON and fellow eyes were delayed (by 15 and 9 ms, respectively). Mean VEP apparent latency of ON eyes was delayed at both low and high TFs (by 24 and 30 ms, respectively), while that of fellow eyes was selectively delayed at high TFs (by 28 ms). The results in ON eyes indicate non-selective abnormalities of PERG and VEP generators responding at both low and high TFs. VEP TF losses may be in part accounted for by corresponding PERG losses. In the fellow eyes of patients, more selective PERG and VEP TF abnormalities may suggest differential impairment of retinal and postretinal subsystems responding better to low and high TFs (i.e. parvo- and magnocellular streams).