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PubMed2005

Anatomic differences in the lateral vestibular nerve channels and their implications in vestibular neuritis.

HYPOTHESIS: Anatomic differences may render the superior division of the vestibular nerve more susceptible to injury during vestibular neuritis. BACKGROUND: Neural degeneration has been identified in temporal bone studies of vestibular neuritis. Previous anatomic and physiologic studies of vestibular neuritis have demonstrated that the superior division of the vestibular nerve is preferentially affected, with sparing of the inferior division. A preliminary temporal bone study has implicated neural entrapment as a possible cause for this preferential injury. METHODS: Two independent unbiased observers performed histologic analysis of 184 temporal bones from our temporal bone library. Measurements of the medial, midpoint, and lateral portions of the superior vestibular, inferior vestibular, and the singular nerves and their bony channels lateral to the internal auditory canal were made. These measurements included the length and width of each bony channel and an estimated percent of each channel occupied by bony spicules at each location. RESULTS: The lengths of the bony channels of the singular nerve (0.598 mm) and the inferior vestibular nerve (0.277 mm) were significantly shorter than the average length of the superior vestibular channel (1.944 mm; p < 0.0001). The total percent of the channel occupied by bone at the midpoint was significantly greater for the superior vestibular (28%) compared with either the singular (0%) or the inferior vestibular channel (18%) (p < 0.0001). CONCLUSION: The lateral bony channel of the superior vestibular nerve is seven times longer than the inferior vestibular and more than three times longer than the singular channel. There are a larger percentage of bony spicules occupying the superior vestibular compared with the inferior vestibular or singular channels. In addition, the superior nerve passes through a longer area of severe narrowing compared with the inferior or singular nerves. This anatomic arrangement of a longer bony channel with more interspersed bony spicules could make the superior vestibular nerve more susceptible to entrapment and ischemia.

Humans↗
PubMed2003

Vestibular-evoked myogenic potential in patients with unilateral vestibular neuritis: abnormal VEMP and its recovery.

The incidence of inferior vestibular nerve disorders in patients suffering from unilateral vestibular neuritis and the recovery of these disorders were evaluated by monitoring the vestibular-evoked myogenic potential (VEMP). Eight patients ranged from 21 to 73 years that suffered from unilateral vestibular neuritis underwent VEMP and caloric testing. Abnormal VEMP was observed in two of the eight patients with unilateral vestibular neuritis. Two patients were diagnosed as having an inferior vestibular nerve disorder. One of these patients showed recovery of the inferior vestibular nerve function as assessed by the VEMP. Disorders of the inferior vestibular nerve function and their recovery was confirmed by our current results. The time course of recoveries of the superior and inferior vestibular nerve systems were similar in the two patients.

Adult↗
PubMed2004

[Factors influencing long-term progress in patients with vestibular neuritis].

We previously reported that platform stabilometry was effective in evaluating the condition of patients with vestibular neuritis. In the present study, we increased the patient population (n = 31) and followed them up for long-term (253.5 +/- 36.5 days after admission) to determine factors influencing prognosis. We examined the stability of patients with vestibular neuritis using platform stabilometry at 5 time points: P1, (5.3 +/- 0.7 days after admission); P2, (22.2 +/- 1.2 days); P3, (73.2 +/- 2.5 days); P4, (159.2 +/- 9.2 days); and P5, (258.3 +/- 23.5 days). For some elements--the total length of locus and the area of surroundings with open or closed eyes--the total length of locus with open eyes decreased significantly (P<0.05) following disease amelioration. Important factors for improving elements of platform stabilometry in patients with vestibular neuritis were age, presence of upper respiratory infection, and the duration of nystagmus.

Adult↗
PubMed2005

[Observation on therapeutic effect of plum-blossom needle therapy on peripheral facial neuritis at acute stage].

OBJECTIVE: To compare difference between plum-blossom needle therapy and hormonotherapy in the The treatment group of 32 cases with periphtherapeutic effect on peripheral facial neuritis at acute stage. METHODS: eral facial neuritis at acute stage were treated with plum-blossom needle therapy and the control group of 32 cases with oral administration or intravenous drip of dexamethasone. Their therapeutic effects were compared. RESULTS: The total effective rate was 100.0% in the treatment group and 93.4% in the control group, with a significant difference between the two groups (P < 0.05). CONCLUSION: The therapeutic effect of plum-blossom needle therapy on peripheral facial neuritis at acute stage is better than that of the hormonotherapy.

Acupuncture Therapy↗
PubMed2005

Vestibular neuritis: etiopathogenesis.

Vestibular neuritis presents as sudden unilateral vertigo in the absence of hearing loss or neurologic involvement and is thought to be due to neurotropic viruses. Its morbidity is unknown and it affects both sexes equally, with the highest incidence at 40-50 years of age. The etiology of this condition has been ascribed to viral, bacterial and protozoan infections, as well as allergic and auto-immune causes. Inflammation of the vestibular nerve is followed by demyelination and loss of function, which is not always reversible. Higher plasma fibrinogen and CRP levels in the acute phase, longer BERA latency and I-III interval and increased gadolinium uptake in the vestibular nerve and Scarpa's ganglion on enhanced MRI confirm the inflammatory nature of the process. An animal model of vestibular neuritis using retroauricular inoculation of herpes simplex virus in mice, histologic findings in the temporal bone of individuals who had vestibular neuritis, and influenza A virus infection in cultured Schwann's cells suggest viral infection as the main aetiologic cause.

Animals↗
PubMed1978

Antiserum-mediated demyelination in vivo: a sequential study using intraneural injection of experimental allergic neuritis serum.

Primary segmental demyelination accompanied by mononuclear phagocytes was induced by injection of antiserum into rat peripheral nerve, and the morphologic sequence of events was studied. Antisera were obtained from rabbits with experimental allergic neuritis (EAN) produced by the inoculation of emulsified bovine peripheral nerves in complete Freund's adjuvant. Sera were injected directly into rat sciatic nerve to circumvent the blood-nerve barrier. Recipient rats developed sensorimotor paralysis on the side injected with experimental allergic neuritis sera. Intense focal demyelinative lesions resulted from injection of experimental allergic neuritis sera. Control sera obtained from rabbits inoculated with bovine serum albumin in complete Freund's adjuvant did not produce paralysis or demyelination. The earliest change was damage to Schwann cells, seen 20 minutes after antiserum injection. Within a few hours lamellar splitting and vacuolation of myelin began to paranodal regions and Schmidt-Lanterman clefts and there were infiltrating polymorphonuclear cells. By 8 hours without the detectable presence of monocytes or macrophages, myelin vesiculation became advanced and widespread. By 15 hours, endoneurial edema had reached its maximum. Macrophages were found in association with myelinated nerve fibers. From that time through the next 5 days, demyelination progressed to complete denudation of axons by macrophage phagocytosis of myelin. Activated cytoplasm of Schwann cells reinvested demyelinated axons, often in concert with persisting phagocytic macrophages. Peripheral nerve demyelination thus transferred evolved rapidly, and myelin destruction occurred prior to the appearance of monocytes or macrophages. Demyelinating activity was lost after absorption by purified peripheral nerve myelin but not by liver or kidney and was heat-labile and complement dependent (T. Saida, K. Saida, D. H. Silberberg, and M. J. Brown: Nature 272: 639, 1978).

Animals↗
PubMed1992

Neurotoxic treatment in a patient with brachial neuritis associated with Hodgkin's disease.

Brachial neuritis is a rare form of neuropathy associated with Hodgkin's disease. In the patient we describe, a brachial neuritis occurred during chemotherapy for Hodgkin's disease. He later developed a marked sensory peripheral neuropathy with vincristine. Lhermitte's sign also developed following modest doses of radiotherapy (35 Gy in 20 fractions to the whole cervical cord). We suggest that neurotoxic treatment must be given with extra care to patients with non-metastatic tumour induced neuropathies.

Adult↗
PubMed1983

Parainfectious optic neuritis. Report and review following varicella.

Severe loss of vision and bilateral optic disc edema occurred in a 10-year-old girl 38 days after the rash of varicella first appeared and subsequent encephalitis developed. Recovery of visual function was nearly complete, but optic atrophy persisted. Parainfectious optic neuritis following other viral infections, with the exception of herpes zoster, has a similar clinical profile: delayed onset, severe visual loss, optic disc edema, bilaterality, good recovery, and residual optic atrophy. Conduction delays in our patient's patterned visual evoked potentials implicated demyelination within the optic nerves. The often favorable recovery, frequency of delayed onset, and bilateral involvement of the optic nerves support an autoimmune process in the pathogenesis of parainfectious optic neuritis.

Chickenpox↗
PubMed1986

Silent brain lesions in patients with isolated idiopathic optic neuritis. A clinical and nuclear magnetic resonance imaging study.

Eight of 16 patients with isolated idiopathic optic neuritis were found to have one to several brain lesions by nuclear magnetic resonance scanning. The brain lesions were predominantly located in the periventricular white matter; their appearances, locations, and extents were similar to those seen in recent nuclear magnetic resonance studies of patients with definite multiple sclerosis. All of these brain lesions were clinically silent and were missed by computerized tomography. Idiopathic optic neuritis may be the only manifestation of a multicentric disease process that is disseminated in the central nervous system in the majority of cases.

Adolescent↗
PubMed1988

Paraneoplastic optic neuritis and encephalomyelitis. Report of a case.

A 63-year-old man developed bilateral paresis of horizontal and upward eye movements. He was found to have a small oat cell carcinoma of the lung. Four months later he experienced acute visual blurring on the right side. Examination of the right eye at that time revealed a visual acuity of 3/200 and a central scotoma. There was swelling of the right optic disc. Three weeks after the onset of the visual loss, the acuity of the right eye spontaneously improved to 20/60, the field deficit lessened, and there was a decrease in the swelling of the optic disc. Subsequently, his neuro-ophthalmologic condition remained unchanged but his general health deteriorated, and he died nine months after the onset of the disease. Neuropathologic examination showed mild perivascular lymphocytic infiltration and fibrosis of the meninges throughout the central nervous system, loss of neurons and gliosis in the third and fourth cranial nerve nuclei, perivascular inflammation and gliosis of the optic nerves, and chiasm and central demyelination of the right optic nerve. No tumor cells were seen. These findings were consistent with a diagnosis of paraneoplastic optic neuritis and paraneoplastic encephalomyelitis. The present case confirms the existence of paraneoplastic optic neuritis and illustrates the clinical course of the disease.

Encephalomyelitis↗
PubMed1999

Incidence of optic neuritis in Stockholm, Sweden, 1990-1995: II. Time and space patterns.

OBJECTIVES: To describe the time and space patterns of patients with monosymptomatic optic neuritis (MON) in Stockholm County, Sweden, and to explore the role of environmental factors in the etiology of MON and multiple sclerosis. DESIGN: Population-based and prospective incidence survey. SETTING: Census based on referrals from 1.68 million inhabitants of Stockholm County. PATIENTS: One hundred forty-seven new patients with MON were consecutively referred by ophthalmologists and neurologists from January 1, 1990, through December 31, 1995. A standardized questionnaire was used for data collection. MAIN OUTCOME MEASURES: Evaluations consisted of annual incidence, statistical significance of temporal aggregation, Knox test, likelihood score test applied to the ratio of the highest to lowest seasonal proportion of registered events, and standardized morbidity ratio for municipalities. RESULTS: We observed a seasonal pattern of MON incidence, with the highest incidence (31%) in the spring and the lowest (17%) in the winter (ratio of highest to lowest seasonal proportion, 1.84; 95% confidence interval, 1.13-3.01; P = .007). The seasonal monthly incidences were correlated with the average number of sunny hours and the temperature. The presence of positive immune activity markers (i.e., mononuclear pleocytosis and oligoclonal IgG bands in the cerebrospinal fluid) seemed to be linked to the onset of MON in winter. No aggregation by time, space, or month of birth was detected. CONCLUSIONS: Monosymptomatic optic neuritis in Stockholm County occurred at an uneven frequency across the seasons, with the highest incidence in spring and the lowest in winter. This seasonal pattern is compatible with that described in most previous reports. Environmental and probable infectious factors unevenly distributed by season may play a role in the etiology and early clinical course of MON.

Adult↗
PubMed1984

Optic neuritis secondary to sinus disease.

Sinus disease is an infrequent, but treatable, cause of optic neuritis. We treated three patients in whom optic neuritis was caused by sinus disease. Treatment of the underlying sinus condition resulted in the improvement of vision.

Child, Preschool↗
PubMed1996

Hypertrophic neuritis due to chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): a postmortem pathological study.

A postmortem pathological study of a 65-year-old woman with hypertrophic neuritis associated with hand tremor and limb ataxia is described. There were many onion bulbs and loss of myelinated nerve fibers in the peripheral nerves, including the facial and subserosal visceral nerves. The hypertrophic neuritis was caused by chronic inflammatory demyelinating neuropathy (CIDP), in which interstitial amorphous substances in the endoneurium and onion bulb formation might contribute to nerve swelling. We speculate that visceral autonomic nerves as well as somatic peripheral nerves are involved in patients with a long clinical CIDP course and that peripheral nerve pathology in this disorder shows more heterogeneous changes than previously recognized.

Aged↗
PubMed1988

Retrobulbar neuritis in a patient treated with intraarterial cisplatin for head and neck cancer.

A case of retrobulbar neuritis which developed in association with intraarterial continuous infusion cisplatin is presented. A 67-year-old man with squamous cell carcinoma of the left tonsillar fossa was treated with induction chemotherapy through the left lingual artery; the regimen consisted of cisplatin and 5-fluoro-deoxyuridine as continuous infusion. He developed some transient mental status changes and then left eye blindness. Ophthalmologic examination was compatible with retrobulbar neuritis. A brief review of reported cases of ophthalmologic toxicity in association with cisplatin is presented, and the likelihood that the toxicity is due to the drug itself rather than the method of administration is discussed.

Aged↗
PubMed1999

Distribution of herpes simplex virus type 1 in human geniculate and vestibular ganglia: implications for vestibular neuritis.

Vestibular neuritis is a common cause of partial unilateral vestibular paralysis, which usually spares posterior semicircular canal function. The cause is assumed to be a viral reactivation of latent herpes simplex virus type 1 (HSV-1) in human vestibular ganglia. The existence of an anastomosis between the intermediate nerve and the superior vestibular nerve suggests the question of whether selective affliction of the superior vestibular nerve is the result of migration of HSV-1 from the geniculate ganglion along this faciovestibular anastomosis. We determined the distribution of HSV-1 among geniculate ganglia, vestibular ganglia, and within Scarpa's ganglion by examining 35 human temporal bones by polymerase chain reaction. HSV-1 was found in 66% of geniculate ganglia and 60% of vestibular ganglia; all examined parts of vestibular ganglia were almost equally HSV-1 infected. Our data provided no support for viral migration along this anastomosis or for a preferential latency of HSV-1 in the superior vestibular nerve. We suggest that the common double innervation of the posterior ampulla by two nerves running in two separate bony canals could offer an alternative explanation for the regular sparing of posterior canal function in vestibular neuritis.

Adolescent↗
PubMed2005

Adaptive cortical plasticity in higher visual areas after acute optic neuritis.

The ability to distinguish adaptive cortical reorganization may help to target future therapeutic strategies after neurological insult. We investigated cortical plasticity by prospectively applying visual functional magnetic resonance imaging (fMRI) and optic nerve MRI to 20 patients with acute optic neuritis at baseline, 1, 3, 6, and 12 months. We performed three types of correlation analyses to investigate the relationships between fMRI activity, clinical function, and optic nerve structure. The first analysis directly correlated the fMRI response to clinical function or optic nerve structure and found dynamic relations especially within the first 3 months. The second analysis used a novel technique that modeled the fMRI response and optic nerve structure together with clinical function, to determine the contribution fMRI made to clinical function after accounting for structural factors. Significant effects were found at baseline only, within the right peristriate cortex, and bilaterally in the lateral occipital complexes, which are normally involved in higher order visual processing. The third analysis investigated the relation between the modeled visual recovery rate and fMRI response but found no significant effects. The key findings of this study are from the second analysis and suggest a genuine adaptive role for cortical reorganization within extrastriate visual areas early after optic neuritis.

Adaptation, Physiological↗
PubMed1988

The role of macrophages in experimental autoimmune neuritis induced by a P2-specific T-cell line.

A P2-specific T-cell line with a helper/inducer phenotype (W3/25+) mediates experimental autoimmune neuritis in the Lewis rat after adoptive transfer to naive recipients. Moderately severe disease was induced in these experiments by the injection of 1 x 10(7) T cells. Motor and mixed afferent nerve conduction, F responses, H reflexes, and lumbar somatosensory evoked potentials were monitored, and morphological alterations were scored semiquantitatively at the end of the experiments. The role of macrophages and macrophage-derived inflammatory mediators in the effector phase of the disease was investigated by administering different inhibitors of macrophage metabolism, including silica, dexamethasone, and a variety of cyclooxygenase and lipoxygenase blockers. Silica and dexamethasone suppressed the clinical, electrophysiological, and morphological manifestations of the disease almost completely, indicating that macrophages are essential for the generation of inflammatory lesions. The inhibitors of arachidonic acid conversion failed to mitigate the severity of the disease. This is in contrast to observations in actively induced experimental autoimmune neuritis in which eicosanoid biosynthesis seems to play a decisive role in the pathogenesis of the disease.

Animals↗
PubMed1991

Impaired critical flicker frequency in recovered optic neuritis.

Thirteen patients with optic neuritis who recovered normal visual acuity and kinetic perimetry all showed impairment of foveal critical flicker frequency, a psychophysical test of visual temporal resolution. Because the magnocellular visual system demonstrates higher temporal resolution than the parvocellular system, this finding implicates involvement of axonal projections of magnocellular retinal ganglion cells in recovered optic neuritis.

Adolescent↗