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[Neuritis nervi optici--results of an etiological inquiry and therapeutical results (author's transl)].

The authors report on the results of an etiological inquiry in 71 patients from 1970 to 1977 suffering from neuritis nervi optici. The study includes also the therapeutical results. The findings demonstrate that modern examination techniques did not bring a definite progress of the clarification of the etiological relation: Approximately 50% stay without causality. The identificated causes are on all fours with those found by Rönne (1930) except the diseases following the application of modern drugs, e. g. contraceptives. Therapeutically a combination of systemic and parabulbar application of corticosteroids, drugs for stimulating the blood flow (e. g. Trental, Cosaldon retard), Vitamin-B-complex, and antibiotics are recommended.

Adolescent↗

Factors likely to affect the development of multiple sclerosis in patients presenting with optic neuritis in a tropical and subtropical area.

The relationship between optic neuritis (ON) and multiple sclerosis (MS) in a subtropical climate is examined. 105 cases of ON were followed for varying periods over 26 years. The factors studied included place of birth, sex, age at onset, presence of recurrent ON, the interval to the onset of MS, and HLA antigen typing. 55% of cases developed evidence of definite MS. The majority of cases who went on to develop MS had their onset of ON between 21 and 40 years of age. The subtropical climate did not cause any significant variation in incidence. However those case who had HLA Bw4 appear to be protected from developing MS.

Adolescent↗

Allergic neuritis: a neuritogenic peptide from the P2 protein that induces disease in rats.

Peptide CN1, a large 93 residue peptide, derived from residues 21-113 of the bovine and rabbit P2 protein of sciatic nerve myelin, induces severe allergic neuritis in Lewis rats. When complexed with phosphatidylserine and tested at 50 microgram dosage in Freund's complete adjuvant, it induces severe clinical and histologic signs (cellular infiltration and demyelination of the sciatic nerve) in most animals. It is as potent in disease induction as the P2 protein on a weight basis. In contrast, when not complexed with phosphatidylserine, Peptide CN1 induced only mild clinical signs and histologic lesions in 3 of 10 rats. CNBr peptides CN2 and CN3, derived from the carboxyl and amino terminal ends, respectively, were not active. Spleen and lymph node cells from rats sensitized to Peptide CN1 responded to both P2 and Peptide CN1 in culture in the mitogenic assay. These data show that the major neuritogenic domain for the rat resides in the CN1 region.

Animals↗

Electrophysiological and immunological studies in optic neuritis.

Serial clinical and electrophysiological examinations and immunological investigations have been performed on 34 patients with primary optic neuritis. In 8 patients, the latency of visual evoked responses was normal after the resolution of clinical symptoms, and in a further 5 patients improvement in VER latency occurred although the response remained abnormal. In 17 patients, VER's abnormal and did not alter over the period of clinical recovery; in 4 patients there was a progressive increase in the latency of the VER's through both eyes although a satisfactory clinical recovery occurred. The frequency of histocompatibility antigens was similar in the group of ON patients to that in the normal population. Immunological function was normal in patients with ON as assessed by levels of immunoglobulins. T and B lymphocyte numbers and by lymphocyte blastogenesis in response to PHA and myelin basic protein. Three patients have developed multiple sclerosis, all of whom had either HLA-A3 or -B7 antigens; the clinical and electrophysiological pattern of recovery was different in each case.

Cerebrospinal Fluid Proteins↗

Effects of chronic demyelination on axonal transport in experimental allergic optic neuritis.

Axonal transport studies were undertaken to determine the effect of chronic demyelination on axonal function in experimental allergic optic neuritis in the guinea pig, an animal model for multiple sclerosis. Fast and slow components of axonal transport over the prelaminar, laminar, and retrolaminar portions of the optic nerve head and at the foci of demyelination in the retrobulbar optic nerve were evaluated by the autoradiographic grain-counting technique. At 6 hr there was a significant increase in grain counts over the demyelinated foci and in the regions proximal to the demyelination, including the swollen disc. At day 1 there was no significant difference in the grain counts at the site of demyelination when compared to the myelinated portion of the nerve. However, at days 3 and 7 there was a decrease in the number of grains over the demyelinated areas. These results indicate impairment of axonal function in chronic demyelination. Moreover, in this pathologic process, most of the synthesized materials appear to move in the fast transport phase, unlike in the normal optic nerve where the bulk of materials move by slow transport.

Animals↗

Experimental allergic neuritis: demyelination induced by P2 alone and non-specific enhancement by cerebroside.

Experimental allergic neuritis was induced in male inbred Lewis rats immunized with myelin, P2 alone, P2 mixed with galactocerebroside and P2 mixed with glucocerebroside. Neurological deficit started significantly earlier in myelin-immunized rats than in P2-immunized rats. Although myelin-immunized rats appeared most severely affected, differences between the groups in maximum neurological deficit were not significant. The course of the disease of the P2-galactocerebroside-immunized animals did not differ from that of the P2-glucocerebroside-immunized group. Histologically, cellular infiltration and demyelination were more conspicuous 12 days after immunization in the group immunized with myelin than in the other rats. After 21 days, primary demyelination was prominent in all groups: its frequency and severity were similar in the myelin-immunized and P2-immunized animals. The P2-galactocerebroside-immunized group had significantly more frequent demyelination than the P2-immunized group. Wallerian degeneration was prominent in all groups at this stage. We conclude that P2 alone does induce demyelination and that galactocerebroside added to the immunizing emulsion enhances the response but no more than the non-myelin lipid glucocerebroside.

Adjuvants, Immunologic↗

A permanent rat T cell line that mediates experimental allergic neuritis in the Lewis rat in vivo.

A rat T cell line of the "helper" phenotype (W3/25-positive, OX 8-negative) has been derived from Lewis rats inoculated with P2 protein isolated from bovine PNS myelin. The line LiP2/A is exquisitely specific for P2 protein, exhibiting no reactivity to bovine basic protein or to PPD. In addition to responding strongly to the intact P2 protein, the line cells show some response to a synthetic peptide containing the neuritogenic amino acid sequence of P2 protein (SP-B, residues 66-78). Intravenous inoculation of naive rats with as few as 10(4) activated LiP2/A cells leads to the onset of mild clinical signs of experimental allergic neuritis. Higher doses of cells lead to more severe clinical disease. Histologic examination of clinically ill animals confirmed the disease as EAN. The pathologic lesions were confined to the PNS and spared the central nervous system. The lesions consisted of marked perivascular cuffs and infiltrates of inflammatory cells associated with marked degenerative changes--demyelination and some axonal degeneration.

Animals↗

Treatment of toxocaral optic neuritis.

An 8-year-old male with poor vision from presumed toxocaral optic neuritis is presented. The diagnosis is supported by positive serum ELISA testing. Subtenon's depot injections of Kenalog resulted in excellent improvement and final visual acuity of 20/20. Early diagnosis with serum ELISA tests and vigorous treatment with subtenon's steroids are recommended.

Ascariasis↗

Optic neuritis or ophthalmic artery aneurysm? Case presentation with histopathologic documentation utilizing a new staining method.

An elderly woman was admitted to the hospital with a presumptive diagnosis of optic neuritis following abrupt loss of vision in her left eye. Noninvasive studies were unrevealing, and she was put on a course of prednisone. Further visual loss 2 weeks later prompted a second course of prednisone therapy. Six years later the patient died from cardiac arrest. The autopsy revealed an aneurysm arising from the origin of the left ophthalmic artery. Selected brain specimens were histologically examined by application of a newly developed staining technique capable of identifying degenerated axons in human brain tissue even after long survival periods. We traced degeneration from the site of compression at the left optic nerve to five primary visual nuclei. Furthermore, transsynaptic cellular changes were observed in the lateral geniculate nucleus.

Aged↗

Equine adenovirus 1 isolated from cauda equina neuritis.

Equine adenovirus 1 was recovered after four to six passages from two out of three cases of cauda equina neuritis (CEN) using kidney monolayers. Similar treatment of lumbo-sacral spinal cord from six normal horses did not yield adenovirus. All three cases of CEN had antibodies to the neuritogenic myelin protein P2 while immunofluorescence demonstrated that autologous IgG bound to the myelin of affected nerves. Adenovirus was not detected in neural tissue by immunofluorescence.

Adenoviridae↗

Superficial radial neuritis and De Quervain's disease. Report of three cases.

Three patients with De Quervain's disease developed superficial radial neuritis, a complication which seems not to have been considered in the literature. All 3 patients were women. One responded to conservative therapy and the other 2 required tenolysis of the abductor pollicis longus and extensor pollicis brevis tendon sheaths to relieve symptoms.

Adult↗

Dichotomy of psychophysical responses in retrobulbar neuritis.

Thirty cases of retrobulbar neuritis (RBN) with varying degrees of myelin loss have been analyzed in terms of loss of chromatic function, loss of spectral flicker detection and reduction in visual acuity. We suggest, from the preliminary results of this study, that there may be two distinct types or stages in RBN. Both stages include moderate to severe impairment or damage to the colour-opponent (and most likely the fine-acuity) system. The second type or stage also involves a conduction block or failure, severely reducing sensitivity to fast flicker, although other luminance functions not involving fast-flicker detection may be spared.

Adolescent↗

Systemic lupus erythematosus presenting as optic neuritis.

A 57-year-old white man presented with unilateral optic neuritis. General physical examination and neurologic consultation revealed no further findings. Laboratory investigation, however, yielded an elevated sedimentation rate, positive LE preparation, elevated ANA titer, false-positive VDRL, and red blood cell casts in the urine. A diagnosis of systemic lupus erythematosus (SLE) was made. The patient was treated with sub-Tenon and systemic corticosteroids. There was a moderate improvement in central visual acuity. The suspected pathophysiology of SLE is reviewed. The papillitis presumably reflects the generalized vasculitis of SLE and may be responsive to corticosteroids as are other signs and symptoms of this disease.

Fluorescein Angiography↗

Second Louis H. Clerf Lecture. Vestibular neuritis.

Vestibular neuritis is a discrete degenerative neuropathy of the vestibular nerve trunks. The clinical manifestations consist of one or more severe prolonged episodes of vertigo, sometimes in association with milder periodic or constant unsteadiness. The atrophic changes in the vestibular nerves are usually sufficiently severe to create vestibular test abnormalities. The clinical and pathological features are consistent with a viral etiology.

Adult↗

[Microcirculation and permeability of the pulmonary capillaries in the dynamics of experimental neuritis of the vagus nerve].

Intravital biomicroscopy was used to study permeability and microcirculation of pulmonary vessels during experimental neuritis of the vagus nerve. The study lasted 14 days. Vascular permeability was evaluated from the changes in adhesion capacity of capillary endothelium with respect to India ink. The microhemodynamics was explored by visual observation and appraisal of the photo and film documents. The most pronounced changes were noticed on the 3d day. In the following days the changes were phasic in nature, repeating on days 6, 9 and 12. All the changes were synchronous.

Animals↗

[Idiopathic and zoster vestibular neuritis. Course and prognosis].

112 cases of vestibular neuritis were studied. 77% were relatively pure lesions, whilst in 23% of cases there were more extensive lesions with abnormalities of the saccadic oculomotor system and BERA abnormalities. Spontaneous nystagmus disappeared in 2 to 3 months in general. In 54% of cases there was complete recovery of absolute reflex activity within normal limits on the affected side. There was restoration of normal difference of reflectivity in 22%. In 13% there was normal absolute reflex activity, normal hypovalence and normal directional preponderance. Age appeared to influence the course of directional preponderance and the extent of lesions on the course of hypovalence. Early mobilisation of the patient is of primordial importance.

Acoustic Impedance Tests↗

Electrophysiological tests and CSF examination in patients with optic neuritis.

Electrophysiological tests (visual and somatosensory evoked potentials, flicker fusion test) and electrophoretic examination of cerebrospinal fluid were performed in 17 patients who previously suffered from one or more attacks of optic neuritis. The association of the tests revealed the demyelinating inflammatory pathogenesis in eight cases. In the remaining nine cases the CSF oligoclonal pattern was absent. The evidence that a bilateral delayed VEP, suggesting a subclinical contralateral involvement of optic pathways, could be related to multiple sclerosis, is discussed. A case was finally ascertained as being affected by Leber's optic atrophy.

Adolescent↗