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PubMed2001

[Optic neuritis as a complication in preventive tetanus-diphtheria-poliomyelitis vaccination: a case report].

BACKGROUND: The preventive value of vaccinations is generally accepted. Public recommended vaccinations are administered frequently and therefore even rare complications may occur. PATIENT: We report on a 56-year-old patient who suffered from an acute unilateral optic neuritis, following ten days after vaccination against diphtheria, tetanus and poliomyelitis. A complete remission occurred within six weeks after intravenous megadose prednisolone. CONCLUSIONS: Neurological and ophthalmological complications following vaccinations are rare, and in most cases reversible.

Diphtheria-Tetanus-Pertussis Vaccine↗
PubMed2004

Acute peripheral facial palsy in Lyme disease -- a distal neuritis at the infection site.

AIM: Children with acute peripheral facial palsy have often suffered tick bites and/or erythema migrans in the head/neck region on the same side. With respect to the pathogenesis of neuroborreliosis this topographical association was investigated in an animal model. METHODS: A Borrelia garinii strain, isolated from the CSF of a child with acute facial palsy, was injected in 9 rats intracutaneously in the right subauricular region. Infected rats were examined for clinical symptoms of Lyme disease, the spread of the spirochetes was investigated by PCR of necropsies (facial nerves, trigeminus nerves, heart, brain, skin) up to 47 days after infection. The nerve tissues were investigated by histology, immunohistochemistry and electron microscopy. RESULTS: None of the rats developed a facial palsy or other symptoms of Lyme disease. Borrelia DNA was found in the heart after 5 days and in the brain after 7 days of infection up to the end of investigation (47 days), as well as in the ipsilateral peripheral nerves after 7 to 33 days. Borrelia was detected by electron microscopy near endoneural vessels of the facial nerve. Peri-, epi-, and endoneural infiltrations of macrophages, plasma cells and B cells characterized an inflammation of the facial and trigeminus nerves ipsilateral to the infection site. CONCLUSION: An infection with Borrelia garinii in the subauricular region induces an ipsilateral neuritis of peripheral nerves. The particular vulnerability of the human facial nerve may be a result of its long intraosseus course. Thus, an inflammatory edema may injure the nerve in the canalis facialis.

Acute Disease↗
PubMed1998

Characterization of the mitochondrial genome in childhood multiple sclerosis. I. Optic neuritis and LHON mutations.

The occurrence of optic neuropathy in patients with MS-like disorders who carry one of the pathogenetically significant LHON mutations as well as the higher incidence of maternal transmission in familial cases of MS support the hypothesis that mitochondrial genes may be implicated in susceptibility to MS. We sequenced the entire mtDNA of six children with MS who developed optic neuritis as early and prominent visual involvement. The analysis revealed a high degree of nucleotide variations relative to the standard mtDNA sequence. After excluding various synonymous nucleotide changes and common neutral polymorphisms, eight discrete novel missense mutations within the protein coding, tRNA or rRNA genes were detected. None of the eight polymorphic sites were found in common between the patients with MS. Of particular interest was the observation that five of six children carried a total of nine secondary LHON mutations at nucleotide positions 4216, 4917 or 13708. We conclude that variation in mtDNA is unlikely to contribute to genetic predisposition for MS. However, secondary LHON mutations may be regarded as additional risk factor for developing prominent optic nerve involvement. The association of individual sets of mtDNA variations with phenotypic presentation in certain subgroups of MS patients remains to be clarified.

Child↗
PubMed1997

Severe irreversible optic neuritis following Mantoux tuberculin skin test in a child with multiple sclerosis--a case report.

A 12-year-old girl was diagnosed as suffering from multiple sclerosis. At age 14, just after recovery from an exacerbation of MS with left-sided optic neuritis, she underwent a Mantoux tuberculin skin test. Within 30 minutes she developed complete irreversible optic neuropathy of the left eye. This case illustrates the urge for caution to perform vaccinations and tuberculin skin tests not only during progressive disease activity of MS, but also in the reconvalescent phase after an acute exacerbation.

Child↗
PubMed1995

[Bilateral posterior ischemic optic neuritis in an adolescent with diabetes mellitus with decompensated blood glucose homeostasis].

BACKGROUND: Diabetogenic loss of visual acuity is very rare in juvenile onset diabetics. PATIENT: A 14-year-old adolescent with type-I diabetes mellitus since 7 years is reported. She experienced an episode of ketoacidotic diabetic coma after one year of very bad glycemic control. Even two weeks before onset of the diabetic coma her visual acuity decreased to 8/200 in both eyes. The perimetry revealed central and paracentral socotomas, the examination of the fundi showed only some microaneurysms and a normal optic disc. Electrophysiological results (normal ERG and EOG, pathologic pattern-VECP) proved irreversible damage of optic nerve or optic tract. RESULTS: Neuritis of optic nerve may not be existent but ischemic damage: the pattern-VECP showed no reproducible answers and the flash-VECP showed normal latency and borderline normal amplitude. There were no pathological findings in neurological and serological tests (like CT, NMR, EEG, cerebrospinal fluid, auto-antibodies or parasites). In the two years after visual loss the visual acuity increased only slightly to 13/200 in the right eye and 20/200 in the left. The optic disc showed temporal pallor in both eyes as sign of descending atrophy of the optic nerve. CONCLUSIONS: The clinical signs in this unusual case of diabetes mellitus point towards the diagnosis of a posterior ischemic optic neuropathy in both eyes caused by the extremely bad diabetic condition.

Adolescent↗
PubMed1989

[Borrelia burgdorferi infection with bilateral optic neuritis and intracerebral demyelinization lesions].

In September, 1987, the authors saw a 25-year-old female patient with retinal perivasculitis, cystoid macular edema and papilledema in her right eye. The left eye was normal. Visual acuity was 0.2 (OD), 1.2 (OS). After conventional infections had been ruled out systemic methylprednisolone therapy was instituted, but the patient's condition deteriorated. In May 1988 she presented with papilledema and a "neuroretinitis"-like finding in her left eye; in her right eye advanced optic nerve atrophy; visual acuity was 0.1 (OD) and 0.07 (OS). The laboratory workup revealed an acute phase of a chronic Borrelia burgdorferi infection, with total immunoglobulins (immunofluorescence test) of 1:1280 and an IgM of 1:650 (normal ranges: total Ig up to 1.80, IgM up to 1:40). MRI showed multiple paraventricular and subcortical demyelinating lesions. However, the cranial CT scan was normal. After 14 days' treatment with doxycycline 200 mg/d, visual fields and acuity improved to sc 0.2 (OD) and sc 0.1 (OS) (July, 1988). This case of intracranial demyelinizating lesions associated with bilateral optic neuritis in a serologically determined Borrelia burgdorferi infection is the first of its kind described in the literature.

Adult↗
PubMed1988

[Role of nuclear magnetic resonance imaging in the diagnosis of monosymptomatic optic neuritis].

34 patients with monosymptomatic optic neuritis were examined ophthalmologically and by magnetic resonance imaging (MRI). In 18 patients subclinical lesions with a high MRI signal intensity were found. The distribution of these lesions was similar to that seen in multiple sclerosis. Neither the severity of the visual impairment nor the course of remission correlated to the MRI findings. Pathologic MRI findings were more common in patients aged over 27 than in younger patients (57% vs. 42%).

Adolescent↗
PubMed1986

[Significance of the flicker test for follow-up and prognosis in optic nerve neuritis].

In 105 eyes with florid optic neuritis (ON) the sensation of brightness lessened when the frequency of flickering light was reduced to between 5 and 10 Hz, but remained stable or increased in 239 healthy eyes, 106 eyes after an ON had subsided, and 117 eyes with other diagnoses. This Aulhorn Flicker Test is highly accurate (98%) and specific. It gives pathologic results only for florid ON, and yields normal results again after the inflammation has subsided, even though other visual functions may remain reduced. The Flicker Test therefore makes it possible to distinguish between acute, recidivous, chronic and subsided ON, a distinction which is clinically often ambiguous and cannot be made on the basis of visually evoked potentials. The fact that the Flicker Test reveals pathologic conditions even in abortive cases or when an Uhthoff phenomenon is present is of great diagnostic value. Five representative cases from the group of patients with ON are described in some detail to show how the test can be used to judge the course of the disease, course, to predict its prognosis and to distinguish various patterns of development.

Evoked Potentials, Visual↗
PubMed1980

[Follow-up study in patients with neuritis retrobulbaris (author's transl)].

In 11 patients with multiple sclerosis (MS) and eight patients in whom MS was not verified visus, computerized perimetry, bipolar flash evoked cortical potential (H-EP) and pattern-reversal evoked cortical response (M-EP) were recorded in the acute stage and convalescent period of neuritis retrobulbaris. In the acute stage visual field deficiencies, diminutions of H-EP and M-EP amplitudes and increases in H-EP latencies were seen in both eyes in all cases. The most severe pathologic changes were found in the worst eyes in the group without MS. In the convalescent period a complete restitution of the electro-ophthalmological parameters was found in neither group of patients by statistical methods. Restitution was more common in patients who were not suffering from MS.

Adult↗
PubMed2001

Vaccination, prevention, and treatment of experimental autoimmune neuritis (EAN) by an oligomerized T cell epitope.

Using a polypeptide oligomer harboring 16 repeats of the neuritogenic epitope (aa 58-73) of myelin P2 protein separated by spacers, enhancement of the immune response to the P2 protein, an important neuritogenic autoantigen in experimental autoimmune neuritis (EAN), was attempted. In contrast to a previous study with PLP-16-mer antigen-specific response of T cells was attenuated at all doses examined to a variable degree. Treatment of Lewis rats with the P2-16-mer up to 2 months before immunization with P2(53-78) (vaccination) or after immunization but before appearance of disease (prevention) had a strong tolerizing effect against the induction of EAN on immunization with P2(53-78). Moreover, rats injected with 200 microg of the P2-16-mer i.v. on day 11 after disease induction, at which time the initial signs of disease had appeared, were almost completely protected against progression of clinical disease, whereas animals treated with the same amount of monomeric control peptide developed severe disease (treatment). Similar results were obtained by i.v. treatment of adoptive-transfer EAN with the P2-16-mer. The lack of clinical signs of disease after 16-mer therapy could be correlated with a reduced proliferative response of P2(53-78)-specific lymph node cells. The frequency of apoptotic T cells in sciatic nerve or in lymph node cells, however, was not increased by the 16-mer treatment, suggesting that induction of anergy or other forms of peripheral tolerance may be responsible for the effect. Thus, the oligomerized P2 peptide antigen was highly effective in all three treatment modalities examined in this specific autoreactive T cell-mediated immune response.

Animals↗
PubMed2006

Abducens nerve palsy and optic neuritis as initial manifestation in brucellosis.

Cranial nerve involvement in brucellosis is rare. We present a case of brucellosis presenting with optic neuritis and abducens nerve palsy on the left side. Cerebrospinal fluid findings indicated Brucella meningitis with high protein count, low sugar level and pleocystosis. In addition, Brucella agglutination test (Wright test) was found to be 1/128 in cerebrospinal fluid. Serum agglutination test for Brucella was also positive at 1/1280. This case was diagnosed as brucellosis involving optic and abducens nerves. The patient was treated by ceftriaxone (intravenous), rifampicin (orally) and doxycycline (orally). Two months later the patient's vision acuity in the left eye had moderately improved and the patient's left abducens palsy had almost disappeared. In conclusion, cranial nerve involvement in brucellosis can have good prognosis if anti-Brucella treatment is undertaken early.

Abducens Nerve Diseases↗
PubMedDate not supplied

Increased expression of phospholipase D1 in the sciatic nerve of rats with experimental autoimmune neuritis.

Phospholipase D1 (PLD1) expression in the sciatic nerve was studied in induced experimental autoimmune neuritis (EAN) in Lewis rats. PLD1 immunoreactivity was seen in some Schwann cells in the sciatic nerves of normal rats. In parallel with the progression of EAN, PLD1-positive Schwann cells significantly increased in number and showed intense immunoreactivity. PLD1 was also detected in some ED1+ macrophages in EAN lesions. These results suggest that PLD1 in macrophages and Schwann cells plays an important role in the activation of these cells in the pathogenesis of EAN, an animal model of human peripheral demyelinating disease.

Amino Acid Sequence↗
PubMed2003

Involvement of cyclooxygenase-1 and -2 in the sciatic nerve of rats with experimental autoimmune neuritis.

The expression of both cyclooxygenase (COX)-1 and COX-2, which are representative enzymes in prostaglandin synthesis, was evaluated in the sciatic nerve of rats with experimental autoimmune neuritis (EAN). Western blot analysis showed that both COX-1 and COX-2 were significantly increased in the sciatic nerve at the peak stage of EAN and declined during the recovery stage. Vascular endothelial cells in normal sciatic nerves immunostained for both COX-1 and COX-2. COX-1 was mainly detected in macrophages, and not in other cell types, while COX-2 was detected in Schwann cells and axons as well as inflammatory macrophages in EAN lesions. This suggests that COXs are involved in the pathogenesis of peripheral demyelinating disease, including EAN, and the major cellular source of both COXs in EAN lesions is inflammatory macrophages. Furthermore, COX-2 is enhanced in some Schwann cells and neural elements, possibly mediating peripheral nervous system inflammation.

Animals↗
PubMed1968

The initial lesion in experimental allergic neuritis. A phase and electron microscopic study.

Experimental allergic neuritis (EAN) was produced in rats by the intradermal injection of an emulsion of peripheral nerve in Freund's adjuvant. Early lesions in perfused sciatic nerves were studied by phase, light, and electron microscopy at intervals up to 15 days following immunization. Circulating lymphocytes attached focally to the inner surface of blood vessels, primarily venules, to initiate parenchymal lesion formation. Attached cells had the hand mirror configuration typical of the motile lymphocyte. They subsequently flattened against the endothelial surface and then traversed the vascular wall by sinking into and passing through the cytoplasm of endothelial cells. The transgressor and transgressed cell membranes were intact and both cells retained their integrity. Lymphocytes began to transform and divide intravascularly; these events accelerated extravascularly. Although the migrating cells became larger and more pleomorphic in the perivascular regions, their essential character was in keeping with an origin from circulating lymphocytes. In many lesions, there was fluid with protein, possibly produced by the transformed extravascular cells. The described cellular events precede tissue damage and are likely instrumental in the myelin destruction which follows

Animals↗
PubMed1995

Experimental autoimmune peripheral neuritis induced in BALB/c mice by myelin basic protein-specific T cell clones.

In vivo adoptive transfer of CD4+ T helper cell type 1 clones reactive with autologous myelin basic protein (MBP) may initiate an inflammatory demyelinating disease of the central nervous system called experimental autoimmune encephalomyelitis. Although MBP is also a component of peripheral nervous system (PNS) myelin, previous studies have failed to demonstrate inflammation in the PNS induced by MBP-reactive T cells. Here, we report on two MBP-specific T cell clones that preferentially initiate inflammatory and demyelinating peripheral neuritis when adoptively transferred to syngeneic recipients. The MBP epitope recognized by these clones spans the junction of exons 6 and 7 and, therefore, is present in the 21- and 18.5-kD but not the 14- and 17-kD MBP isoforms, in which exon 5 is spliced to exon 7. The data suggest that MBP may be processed and presented differently in the central nervous system and PNS, and they provide evidence for MBP as a potential target for autoimmune reactions in the PNS.

Amino Acid Sequence↗
PubMed1997

Insights into Campylobacter jejuni-induced Guillain-Barré syndrome from the Lewis rat model of experimental allergic neuritis.

Experimental allergic neuritis (EAN) is considered the in vivo model of Guillain-Barré syndrome (GBS) and has been extensively studied in the Lewis rat. Both cellular and humoral components of the immune response are implicated in the inflammatory demyelination of peripheral nerves that characterizes EAN. The recognition of Campylobacter jejuni infection as a frequent antecedent event in GBS, and in particular its association with anti-ganglioside antibodies and a primary axonal neuropathy, has raised many questions about the specific disease mechanisms involved. While C. jejuni can produce an acute motor neuropathy in chickens, confirming the relationship between C. jejuni infection and acute neuropathy, no detailed information is available from this animal model. Insights from experimental studies relating to the effector phase of Lewis rat EAN that may be relevant to C. jejuni-induced GBS are discussed.

Animals↗
PubMed1983

Eye movement disorders in multiple sclerosis and optic neuritis.

Horizontal saccadic and smooth pursuit eye movements were studied in 84 patients with multiple sclerosis (MS) and 21 patients with optic neuritis (ON). The MS patients were clinically classified as 'definite', 'probable', or 'possible'; subclinical eye movement disorder was found in 80 per cent of the definite, 74 per cent of the probable and 60 per cent of the possible category. Five of the ON patients (25 per cent) showed a subclinical eye movement deficit; these 5 were young patients with a recent history of ON. In a group of 27 MS patients with symptoms of spinal cord involvement only, 14 showed subclinical oculomotor disorder indicating the involvement of cerebral structures in the demyelination process. A study of the correlation between specific eye movement parameters and results of visual evoked response (VER) tests revealed that saccadic latency or smooth pursuit abnormalities are not correlated with prolonged VER latencies (P-100 peak latency). This indicates that lesions beyond the primary visual pathway contribute substantially to both parameters of oculomotor dysfunction. A significant correlation was found between prolonged saccadic latency and smooth pursuit deficit. An explanation for this finding based on functional aspects of the saccadic and smooth pursuit systems and their mutual interaction is presented. The occurrence of internuclear ophthalmoplegia (INO) is significantly related to an increase of saccadic latency. This finding indicates that demyelination in the patients manifesting INO may not be restricted exclusively to one or both medial longitudinal fasciculi, but may extend to other brainstem structures which are functionally involved in the programming of saccades. The findings confirm the value of standardized objective examination of eye movements in the detection and clarification of subclinical lesions in the central nervous system of patients with an early diagnosis of MS or ON.

Adolescent↗