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At least 451 records · Page 25Linked to original sources
PubMed2002

Cytomegalovirus neuritis in perineal ulcers.

BACKGROUND: Although a range of cytomegalovirus (CMV)-induced cutaneous manifestations is described in AIDS patients, skin involvement in immunocompromised patients is rare, and intraneural CMV inclusions or CMV neuritis has not been documented in skin biopsies. METHODS AND RESULTS: Cutaneous biopsies of CMV lesions were collected prospectively for 12 months. The morphology, sites and symptomatology of the individual lesions, associated systemic illnesses, treatment schedules and disease outcome were recorded. A total of nine biopsies were obtained from three females who presented with extensive painful perineal ulceration and disseminated cutaneous ulcers, nodules and plaques. Clinically, herpes simplex virus (HSV) ulceration was diagnosed and treatment with acyclovir was initiated after biopsies from the natal cleft, perineum and neck were obtained. All were superficial and demonstrated HSV infection. Only the natal cleft biopsy demonstrated coexistent CMV inclusions. Suboptimal healing necessitated two further biopsies from each patient, none of which demonstrated HSV inclusions. Three of four deep perineal biopsies demonstrated CMV inclusions within nerves attended by a lymphocytic infiltrate and architectural disturbances. Two deep cutaneous biopsies of the trunk and abdominal wall confirmed CMV in extraneural locations only. One superficial perineal biopsy did not demonstrate any viral inclusion. CONCLUSIONS: In documenting CMV neuritis in painful perineal ulcers, the histopathological spectrum of perineal CMV ulcers is expanded, a cutaneous neurotropic characteristic of CMV is presented and a direct role for CMV in the pathogenesis of pain is suggested. CMV latency within perineal nerves is also revisited as another potential site of CMV reactivation in immunocompromised patients, and another potential site for possible venereal transmission of CMV infection. The exclusive presence of HSV in initial superficial biopsies highlights the need for optimally biopsied tissue to confirm the coexistence of CMV infection.

AIDS-Related Opportunistic Infections↗
PubMed1999

Multiple sclerosis with extensive lesions left hemiplegia, mental dysfunction and retrobulbar neuritis.

Multiple sclerosis (MS) is usually diagnosed on the basis of the typical clinical course, with remission and exacerbation in multiple parts of the central nervous system (CNS). Recently, magnetic resonance imaging (MRI) has made a large contribution to the diagnosis of patients with MS. But it is difficult to make a definite diagnosis due to clinical variability of the disease and variable MRI findings. We report the case of a 26-year-old woman who developed progressive left hemiplegia, mental dysfunction, and had extensive bilateral cerebral white matter lesions diagnosed by brain MRI. Complete recovery from the left hemiplegia followed the use of corticosteroid, and her brain MRI findings also improved after medication. Early in the clinical course it was difficult to differentiate between multiple sclerosis and granulomatous angiitis of the CNS. After recovery from the first episode of left hemiplegia and mental dysfunction, she developed acute visual disturbance five months after her first admission. Readmission followed and her retrobulbar neuritis was successfully treated by methylpredonisolone pulse therapy. In summary, she experienced two episodes of neurological deficit, had left hemiplegia and mental dysfunction associated with multiple lesions in bilateral cerebral white matter in brain MRI, and the left retrobulbar neuritis with delay of P100 by visual evoked potential study. Due to these two episodes we concluded that she had multiple sclerosis. Though the initial diagnosis was difficult, prompt treatment and close follow-up was important, since multiple sclerosis and granulomatous angiitis of the CNS can both recur.

Adult↗
PubMed1997

[Optic nerve neuritis after 50 years of age: symptom of a previously undiagnosed multiple sclerosis].

BACKGROUND: The onset of multiple sclerosis after the age of 50 years is rare. We report four patients with optic neuritis and oligoclonal bands or increased IgG production in the cerebrospinal fluid. Three of them subsequently developed clinically definite multiple sclerosis. PATIENTS: Four apparently healthy women, 62, 56, 50 and 50 years of age, presented with progressive visual loss, three patients in one eye and one patient in both eyes. The diagnostic work-up revealed no findings indicating an ischemic process, an infectious, systemic inflammatory, or neoplastic disease. Examination of the cerebrospinal fluid revealed oligoclonal bands and/or increased production of IgG. Visual acuity recovered during the following weeks to 8 months. Three of the 4 patients subsequently developed additional neurologic signs compatible with multiple sclerosis. CONCLUSION: Optic neuritis can be the presenting sign of multiple sclerosis even after the age of 50.

Diagnosis, Differential↗
PubMed1995

[Vestibular neuritis: a frequently unrecognized cause of diplopia].

The vestibular function plays an essential role in the stabilization of the image on the retina. In addition, when the head is tilted, it contributes to maintain horizontally the plane of the gaze. Vestibular changes can result in oscillopsia and/or diplopia. The latter is related to occurrence of a skew deviation. The authors emphasize the frequent occurrence of diplopia following disorders of the vestibular nerve, specially after vestibular neuritis. In clinical practice, the causal relationship between vestibular neuritis and diplopia is often unrecognized.

Adult↗
PubMed1990

[Changes in visual evoked potential latencies following retrobulbar neuritis].

After unilateral retrobulbar neuritis, VEP latency time does not remain stable: in 7 out of 9 patients, significant changes in latency time were recorded after intervals of 15 to 35 months. In 6 of the 9 cases a reduction in latency time was observed, in 2 of them complete normalization. In one patient it increased further as compared to the initial examination. One conclusion from these findings is that optic neuritis in remission cannot be ruled out by normal VEPs.

Adult↗
PubMed1984

[Pattern ERG and VECP following optic neuritis in childhood].

Pattern ERGs and pattern VECPs were recorded in 12 patients who had suffered from optic neuritis in childhood. When each individual's eyes were compared, the eye with the longer P100-latency in pattern VECP was found to have the smaller amplitude in pattern ERG. The latency differences correlated with the amplitude differences. These findings confirm that after optic neuritis the amplitude of pattern ERG is reduced.

Adolescent↗
PubMed1981

[Follow-up of retrobulbar neuritis with the octopus computer perimeter (author's transl)].

Methodological possibilities of quantifying the visual field course in retrobulbar neuritis were studied. In nine patients suffering from this condition the visual field had been examined repeatedly using the Octopus computer perimeter (program 31, stimulus size 3). Total loss of sensitivity and the number of test points with pathologic results had been chosen to correlate to recovery of visual function. These parameters, as well as visual acuity, were compared with the cumulative steroid dose. It is concluded that rapid recovery of visual function with initial steroid therapy may have a starter effect for spontaneous further improvement of sensitivity in the central visual field. However, a prospective, controlled clinical trial would be required to provide definite proof of the usefulness of steroid therapy in retrobulbar neuritis.

Follow-Up Studies↗
PubMed1997

Antigen therapy eliminates T cell inflammation by apoptosis: effective treatment of experimental autoimmune neuritis with recombinant myelin protein P2.

Exposure of T cells to their specific antigen normally results in proliferation, but in the presence of high and repeatedly administered doses of antigen, T cells may undergo apoptosis. Here we demonstrate that i.v. administration of as little as 100 microg of recombinant P2 protein twice daily completely prevents experimental autoimmune neuritis induced by adoptive transfer of neuritogenic P2-specific T cells or by immunization with the neuritogenic P2-peptide-spanning amino acids 53-78. Antigen treatment started after disease onset markedly ameliorated experimental autoimmune neuritis. The mechanism of action may be through programmed T cell death; a profound increase of the rate of apoptosis was seen in inflammatory foci of peripheral nerves and in the spleen. There was no cytokine switch by our Th1 cells after exposure to their specific antigen, but increased secretion of interferon gamma and tumor necrosis factor alpha was demonstrated. High antigen dose therapy using recombinant, pathogen-free protein may prove useful for the treatment of autoimmune inflammatory disorders of the nervous system.

Adoptive Transfer↗
PubMed2002

Treatment of acute demyelinating optic neuritis.

Patients with typical acute monosymptomatic demyelinating optic neuritis should receive gadolinium-enhanced magnetic resonance imaging (MRI) of the brain and orbits to determine if they are at high risk for the subsequent development of clinically definite multiple sclerosis (CDMS). The presence of >or=2 white matter lesions (>or=3 mm in diameter, at least 1 lesion periventricular or ovoid) indicates high risk for CDMS; the following treatment should be considered for such patients: 1. Intravenous methylprednisolone sodium succinate (1 gram IV/day for 3 days) followed by oral prednisone (1 mg/kg/day for 11 days) with 4-day taper (20 mg on day 1, 10 mg on days 2 and 4); 2. Interferon beta 1-a (Avonex 30microg intramuscularly [IM] weekly, or Rebif 22 microg subcutaneously [SQ] weekly). These two drugs have been shown to reduce the short-term risk of CDMS in high risk monosymptomatic patients. In monosymptomatic patients with <2 white matter lesions, and in patients for whom CDMS has been established, IV methylprednisolone treatment followed by oral prednisone should be considered on an individual basis. Treatment in these patients may hasten visual recovery, but does not affect long-term visual outcome. Oral prednisone alone, without prior treatment with IV methylprednisolone, may increase the risk for recurrent optic neuritis and should be avoided.

Acute Disease↗
PubMed2003

Correlation between morphological and functional retinal impairment in patients affected by ocular hypertension, glaucoma, demyelinating optic neuritis and Alzheimer's disease.

In this article the correlations between the morphological evaluation of the nerve fiber layer (NFL) thickness (by OCT) and retinal functional assessment (by Pattern ERG recordings) performed in patients affected by ocular hypertension (OHT), glaucoma (OAG), demyelinating optic neuritis (MSON), and Alzheimer's disease (AD) are reported. In OHT eyes with ocular hypertension we observed that the inter-individual variation in NFL thickness is correlated with the variability of the PERG responses (the thinner the layer, the worse the visual function). In our OAG, MSON and AD eyes we observed a significant reduction in NFL thickness when compared with controls. In OHT, OAG, MSON and AD eyes abnormal PERG responses with delayed implicit times and reduced amplitudes were found. The impairment in the PERG parameters was significantly correlated to the reduction in NFL thickness. Our results suggest that in patients affected by ocular hypertension, glaucoma, demyelinating optic neuritis, and Alzheimer's Disease there is a reduction of NFL thickness evaluated "in vivo" by OCT, and this morphological involvement is correlated with electrophysiological responses assumed to be originating from the innermost retinal layers.

Alzheimer Disease↗
PubMed1981

Autonomic neuropathy in experimental allergic neuritis: an electrophysiological and histological study.

Electrophysiological and histological studies have been performed on the vagus and splanchnic nerves of guinea pigs with experimental allergic neuritis. Slowing of conduction and dispersion of the compound action potential were consistent with the pathological changes of demyelination. In teased single fibre preparations, axonal degeneration was found more frequently than was expected and in the splanchnic nerves, the unmyelinated fibres appeared to have been indirectly involved. These findings in experimental allergic neuritis are relevant to the pathogenesis of autonomic dysfunction in the Landry-Guillain-Barré syndrome.

Animals↗
PubMed1996

Vestibular neuritis spares the inferior division of the vestibular nerve.

Acute unilateral vestibulopathy, or vestibular neuritis, is the second most common cause of vertigo. To quantify the involvement of the different semicircular canal (SCC) afferents in this disease, we studied the three-dimensional (3D) properties of the vestibuloocular reflex (VOR) in 16 patients 3-10 days after onset of symptoms. Using 3D magnetic search coil eye movement recordings, we measured the speed and axis of eye rotation during spontaneous nystagmus and during rotation in the planes of the different SCCs. In all patients, spontaneous nystagmus axes clustered between the direction expected with involvement of just one horizontal SCC and the direction expected with combined involvement of the horizontal and anterior SCC on one side. Likewise, dynamic asymmetries were found only during rotations about axes which stimulated the ipsilesional horizontal or ipsilesional anterior SCCs. No asymmetry was found when the ipsilesional posterior SCC was stimulated. Thus, both measurements suggest that vestibular neuritis is a partial and not a complete unilateral vestibular lesion and that this partial lesion affects the superior division of the vestibular nerve which includes the afferents from the horizontal and anterior SCCs.

Adult↗
PubMed1976

Impaired temporal resolution of vision after acute retrobulbar neuritis.

Following retrobulbar neuritis patients need a greater interval between two flashes of light in order to see them as double. The abnormality is large and easily detectable; the values lie well outside the normal 99 per cent tolerance limits. The abnormality sometimes occurs in localized retinal areas but can cover the whole visual field. The abnormality is a persistent one, remaining up to five years after visual acuity has returned to normal. It can occur in the absence of optic atrophy and with normal visual fields. There is also a delay in visual perception following retrobulbar neuritis but when this and double flash discrimination are both measured at the same retinal sites, the areas of abnormality do not correlate for the two tests. This indicates that the two tests monitor different aspects of visual damage. Double flash threshold can be a more sensitive indication of visual damage due to demyelination than conventional clinical tests including critical flicker fusion frequency. It provides an absolute measurement of local damage in the visual field and has advantages over the recording of perceptual delay and of evoked potentials.

Acute Disease↗
PubMed2004

Serial magnetization transfer imaging in acute optic neuritis.

In serial studies of multiple sclerosis lesions, reductions in magnetization transfer ratio (MTR) are thought to be due to demyelination and axonal loss, with later rises due to remyelination. This study followed serial changes in MTR in acute optic neuritis in combination with clinical and electrophysiological measurements to determine if the MTR changes over time mirror the picture in multiple sclerosis lesions, further validating MTR as a marker of tissue integrity. Twenty-nine patients were recruited who had acute optic neuritis for a median of 13 days (range 7-24 days) since the onset of visual symptoms. A clinical examination and measurement of visual evoked potentials (VEP) was performed on each patient. Their optic nerves were imaged with a fat-saturated fast spin echo (FSE) sequence and a magnetization transfer sequence. Twenty-one had multiple subsequent examinations over the course of 1 year. In addition, 27 control subjects had their optic nerves imaged up to three times over 1 year. A blinded observer segmented the optic nerves from the MTR maps. Lesions were defined on the acute FSE images and, from the coordinates, the ratio of mean lesion MTR : healthy nerve MTR (lesion ratio) was calculated for each dataset. The time-averaged mean MTR in control optic nerves was 47.7 per cent units (pu). In diseased optic nerves, baseline mean MTR was 47.3 pu, with a mean lesion ratio of 0.98. The diseased optic nerve MTR and lesion ratio declined over time with a nadir at about 240 days at a mean MTR value of 44.2 pu and mean lesion ratio of 0.91. Subsequently, diseased optic nerve MTR appeared to rise; after 1 year the diseased optic nerve mean MTR was 45.1 pu (mean lesion ratio 0.93), although the difference was not significant compared with the nadir value. For each 0.01 increase in time-averaged lesion ratio logMAR visual acuity recovery improved by 0.03 (95% CI, 0.002, 0.08, P = 0.02). Time-averaged VEP central field latency was shorter by 6.1 ms (95% CI 1.5, 10.7, P = 0.012) per 1 pu rise in time-averaged diseased optic nerve MTR. The early fall in diseased optic nerve MTR is consistent with demyelination and Wallerian degeneration of transected axons. The late nadir compared with studies of multiple sclerosis lesions may have been due to slow clearance of myelin debris. Remyelination may have influenced subsequent MTR changes. The observations support using MTR to monitor symptomatic demyelinating lesions.

Acute Disease↗
PubMed1994

Retrobulbar neuritis complicating acute Epstein-Barr virus infection.

A 19-year-old man presented with retrobulbar neuritis and was initially suspected to have neurosyphilis because of a positive microhemagglutination assay for Treponema pallidum (MHA-TP). However, a Venereal Disease Research Laboratory assay was negative, and the patient was subsequently diagnosed with infection due to Epstein-Barr virus (EBV) by heterophile antibody assay and serology for EBV. A biological false-positive MHA-TP has been reported in association with EBV infection. Physicians need to be aware that both retrobulbar neuritis and a biological false-positive MHA-TP can be seen in association with EBV infection.

Adult↗
PubMed1994

Postinfectious hepatitis B optic neuritis.

A 41-year-old female nurse's aide presented with a recent history of viral hepatitis B. Approximately 1 month after her liver functions had normalized she developed symptoms of optic neuritis with painful loss of vision and optic disc edema. Her laboratory studies revealed evidence of systemic vasculitis and glomerulonephritis. A discussion is presented of the patient's clinical course and a brief history of the systemic effects of acute hepatitis B infection (HBV); the pathophysiology for HBV-induced autoimmune optic neuritis (ON), management guidelines, and differential diagnoses are discussed.

Acute Disease↗
PubMedDate not supplied

Failure of corticosteroid therapy to prevent diphtheritic myocarditis or neuritis.

The efficacy of corticosteroid therapy for the prevention of diphtheritic myocarditis and neuritis was studied. Sixty-six patients with diphtheria were divided into two groups. Steroid therapy was given in addition to specific treatment for diphtheria in one group, while the other group was given only specific treatment. The groups were comparable regarding age, duration of illness and extent of exudate. The result shows that steroid therapy does not prevent the occurrence of electrocardiographic changes and of neuritis in the patient with diphtheria.

Adrenal Cortex Hormones↗
PubMed1996

Optic neuritis in a child.

A previously healthy four-year-old girl developed bilateral loss of vision over one day. Her course of optic nerve abnormalities, a related neurologic episode, and the response to corticosteroid therapy is presented. The diagnosis of optic neuritis in a child is made infrequently in an emergency department, but it must be considered in any patient presenting with an acute nontraumatic loss of vision. The characteristic findings associated with optic neuritis, and a review of childhood cases, are discussed.

Acute Disease↗