Optic neuritis. Medical search

Optic Neuritis: Inflammation of the optic nerve. Commonly associated conditions include autoimmune disorders such as MULTIPLE SCLEROSIS, infections, and granulomatous diseases. Clinical features include retro-orbital pain that is aggravated by eye movement, loss of color vision, and contrast sensitivity that may progress to severe visual loss, an afferent pupillary defect (Marcus-Gunn pupil), and in some instances optic disc hyperemia and swelling. Inflammation may occur in the portion of the nerve within the globe (neuropapillitis or anterior optic neuritis) or the portion behind the globe (retrobulbar neuritis or posterior optic neuritis).Neuritis: A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include PAIN; PARESTHESIAS; PARESIS; or HYPESTHESIA.Neuritis, Autoimmune, Experimental: An experimental animal model for the demyelinating disease of GUILLAINE-BARRE SYNDROME. In the most frequently used protocol, animals are injected with a peripheral nerve tissue protein homogenate. After approximately 2 weeks the animals develop a neuropathy secondary to a T cell-mediated autoimmune response directed towards the MYELIN P2 PROTEIN in peripheral nerves. Pathologic findings include a perivascular accumulation of macrophages and T lymphocytes in the peripheral nervous system, similar to that seen in the Guillaine-Barre syndrome. (From Adams et al., Principles of Neurology, 6th ed, p1314; J Neuroimmunol 1998 Apr 1;84(1):40-52)Optic Nerve: The 2nd cranial nerve which conveys visual information from the RETINA to the brain. The nerve carries the axons of the RETINAL GANGLION CELLS which sort at the OPTIC CHIASM and continue via the OPTIC TRACTS to the brain. The largest projection is to the lateral geniculate nuclei; other targets include the SUPERIOR COLLICULI and the SUPRACHIASMATIC NUCLEI. Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM.Neuromyelitis Optica: A syndrome characterized by acute OPTIC NEURITIS; MYELITIS, TRANSVERSE; demyelinating and/or necrotizing lesions in the OPTIC NERVES and SPINAL CORD; and presence of specific autoantibodies to AQUAPORIN 4.Multiple Sclerosis: An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)Optic Disk: The portion of the optic nerve seen in the fundus with the ophthalmoscope. It is formed by the meeting of all the retinal ganglion cell axons as they enter the optic nerve.Evoked Potentials, Visual: The electric response evoked in the cerebral cortex by visual stimulation or stimulation of the visual pathways.Visual Acuity: Clarity or sharpness of OCULAR VISION or the ability of the eye to see fine details. Visual acuity depends on the functions of RETINA, neuronal transmission, and the interpretative ability of the brain. Normal visual acuity is expressed as 20/20 indicating that one can see at 20 feet what should normally be seen at that distance. Visual acuity can also be influenced by brightness, color, and contrast.Vestibular Neuronitis: Idiopathic inflammation of the VESTIBULAR NERVE, characterized clinically by the acute or subacute onset of VERTIGO; NAUSEA; and imbalance. The COCHLEAR NERVE is typically spared and HEARING LOSS and TINNITUS do not usually occur. Symptoms usually resolve over a period of days to weeks. (Adams et al., Principles of Neurology, 6th ed, p304)Optic Atrophy: Atrophy of the optic disk which may be congenital or acquired. This condition indicates a deficiency in the number of nerve fibers which arise in the RETINA and converge to form the OPTIC DISK; OPTIC NERVE; OPTIC CHIASM; and optic tracts. GLAUCOMA; ISCHEMIA; inflammation, a chronic elevation of intracranial pressure, toxins, optic nerve compression, and inherited conditions (see OPTIC ATROPHIES, HEREDITARY) are relatively common causes of this condition.Retinal Ganglion Cells: Neurons of the innermost layer of the retina, the internal plexiform layer. They are of variable sizes and shapes, and their axons project via the OPTIC NERVE to the brain. A small subset of these cells act as photoreceptors with projections to the SUPRACHIASMATIC NUCLEUS, the center for regulating CIRCADIAN RHYTHM.Scotoma: A localized defect in the visual field bordered by an area of normal vision. This occurs with a variety of EYE DISEASES (e.g., RETINAL DISEASES and GLAUCOMA); OPTIC NERVE DISEASES, and other conditions.Aquaporin 4: Aquaporin 4 is the major water-selective channel in the CENTRAL NERVOUS SYSTEM of mammals.Vision Disorders: Visual impairments limiting one or more of the basic functions of the eye: visual acuity, dark adaptation, color vision, or peripheral vision. These may result from EYE DISEASES; OPTIC NERVE DISEASES; VISUAL PATHWAY diseases; OCCIPITAL LOBE diseases; OCULAR MOTILITY DISORDERS; and other conditions (From Newell, Ophthalmology: Principles and Concepts, 7th ed, p132).Methylprednisolone: A PREDNISOLONE derivative with similar anti-inflammatory action.Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes.Optic Neuropathy, Ischemic: Ischemic injury to the OPTIC NERVE which usually affects the OPTIC DISK (optic neuropathy, anterior ischemic) and less frequently the retrobulbar portion of the nerve (optic neuropathy, posterior ischemic). The injury results from occlusion of arterial blood supply which may result from TEMPORAL ARTERITIS; ATHEROSCLEROSIS; COLLAGEN DISEASES; EMBOLISM; DIABETES MELLITUS; and other conditions. The disease primarily occurs in the sixth decade or later and presents with the sudden onset of painless and usually severe monocular visual loss. Anterior ischemic optic neuropathy also features optic disk edema with microhemorrhages. The optic disk appears normal in posterior ischemic optic neuropathy. (Glaser, Neuro-Ophthalmology, 2nd ed, p135)Color Perception Tests: Type of vision test used to determine COLOR VISION DEFECTS.Papilledema: Swelling of the OPTIC DISK, usually in association with increased intracranial pressure, characterized by hyperemia, blurring of the disk margins, microhemorrhages, blind spot enlargement, and engorgement of retinal veins. Chronic papilledema may cause OPTIC ATROPHY and visual loss. (Miller et al., Clinical Neuro-Ophthalmology, 4th ed, p175)Visual Fields: The total area or space visible in a person's peripheral vision with the eye looking straightforward.Demyelinating Diseases: Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.Brachial Plexus Neuritis: A syndrome associated with inflammation of the BRACHIAL PLEXUS. Clinical features include severe pain in the shoulder region which may be accompanied by MUSCLE WEAKNESS and loss of sensation in the upper extremity. This condition may be associated with VIRUS DISEASES; IMMUNIZATION; SURGERY; heroin use (see HEROIN DEPENDENCE); and other conditions. The term brachial neuralgia generally refers to pain associated with brachial plexus injury. (From Adams et al., Principles of Neurology, 6th ed, pp1355-6)Color Vision Defects: Defects of color vision are mainly hereditary traits but can be secondary to acquired or developmental abnormalities in the CONES (RETINA). Severity of hereditary defects of color vision depends on the degree of mutation of the ROD OPSINS genes (on X CHROMOSOME and CHROMOSOME 3) that code the photopigments for red, green and blue.Myelitis, Transverse: Inflammation of a transverse portion of the spinal cord characterized by acute or subacute segmental demyelination or necrosis. The condition may occur sporadically, follow an infection or vaccination, or present as a paraneoplastic syndrome (see also ENCEPHALOMYELITIS, ACUTE DISSEMINATED). Clinical manifestations include motor weakness, sensory loss, and incontinence. (Adams et al., Principles of Neurology, 6th ed, pp1242-6)Optic Nerve Injuries: Injuries to the optic nerve induced by a trauma to the face or head. These may occur with closed or penetrating injuries. Relatively minor compression of the superior aspect of orbit may also result in trauma to the optic nerve. Clinical manifestations may include visual loss, PAPILLEDEMA, and an afferent pupillary defect.Nerve Fibers: Slender processes of NEURONS, including the AXONS and their glial envelopes (MYELIN SHEATH). Nerve fibers conduct nerve impulses to and from the CENTRAL NERVOUS SYSTEM.Tomography, Optical Coherence: An imaging method using LASERS that is used for mapping subsurface structure. When a reflective site in the sample is at the same optical path length (coherence) as the reference mirror, the detector observes interference fringes.Reflex, Pupillary: Constriction of the pupil in response to light stimulation of the retina. It refers also to any reflex involving the iris, with resultant alteration of the diameter of the pupil. (Cline et al., Dictionary of Visual Science, 4th ed)Encephalomyelitis, Autoimmune, Experimental: An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the OPTIC NERVE and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the CHOROID and the inner surface with the VITREOUS BODY. The outer-most layer is pigmented, whereas the inner nine layers are transparent.Visual Field Tests: Method of measuring and mapping the scope of vision, from central to peripheral of each eye.Ophthalmology: A surgical specialty concerned with the structure and function of the eye and the medical and surgical treatment of its defects and diseases.Acute Disease: Disease having a short and relatively severe course.Myelin-Oligodendrocyte Glycoprotein: A transmembrane protein present in the MYELIN SHEATH of the CENTRAL NERVOUS SYSTEM. It is one of the main autoantigens implicated in the pathogenesis of MULTIPLE SCLEROSIS.Myelin Proteins: MYELIN-specific proteins that play a structural or regulatory role in the genesis and maintenance of the lamellar MYELIN SHEATH structure.Ophthalmoscopy: Examination of the interior of the eye with an ophthalmoscope.Myelitis: Inflammation of the spinal cord. Relatively common etiologies include infections; AUTOIMMUNE DISEASES; SPINAL CORD; and ischemia (see also SPINAL CORD VASCULAR DISEASES). Clinical features generally include weakness, sensory loss, localized pain, incontinence, and other signs of autonomic dysfunction.Color Perception: Mental processing of chromatic signals (COLOR VISION) from the eye by the VISUAL CORTEX where they are converted into symbolic representations. Color perception involves numerous neurons, and is influenced not only by the distribution of wavelengths from the viewed object, but also by its background color and brightness contrast at its boundary.Visual Pathways: Set of cell bodies and nerve fibers conducting impulses from the eyes to the cerebral cortex. It includes the RETINA; OPTIC NERVE; optic tract; and geniculocalcarine tract.Retinal Neurons: Nerve cells of the RETINA in the pathway of transmitting light signals to the CENTRAL NERVOUS SYSTEM. They include the outer layer of PHOTORECEPTOR CELLS, the intermediate layer of RETINAL BIPOLAR CELLS and AMACRINE CELLS, and the internal layer of RETINAL GANGLION CELLS.Optic Lobe, Nonmammalian: In invertebrate zoology, a lateral lobe of the FOREBRAIN in certain ARTHROPODS. In vertebrate zoology, either of the corpora bigemina of non-mammalian VERTEBRATES. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1329)Stilbamidines: STILBENES with AMIDINES attached.Color Vision: Function of the human eye that is used in bright illumination or in daylight (at photopic intensities). Photopic vision is performed by the three types of RETINAL CONE PHOTORECEPTORS with varied peak absorption wavelengths in the color spectrum (from violet to red, 400 - 700 nm).Vision Tests: A series of tests used to assess various functions of the eyes.Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.Optic Flow: The continuous visual field seen by a subject through space and time.Neurology: A medical specialty concerned with the study of the structures, functions, and diseases of the nervous system.Diagnostic Techniques, Ophthalmological: Methods and procedures for the diagnosis of diseases of the eye or of vision disorders.Myelin Sheath: The lipid-rich sheath surrounding AXONS in both the CENTRAL NERVOUS SYSTEMS and PERIPHERAL NERVOUS SYSTEM. The myelin sheath is an electrical insulator and allows faster and more energetically efficient conduction of impulses. The sheath is formed by the cell membranes of glial cells (SCHWANN CELLS in the peripheral and OLIGODENDROGLIA in the central nervous system). Deterioration of the sheath in DEMYELINATING DISEASES is a serious clinical problem.

mtDNA haplogroup J: a contributing factor of optic neuritis. (1/359)

Optic neuritis frequently occurs in multiple sclerosis (MS), and shares several similarities with the optic neuritis of Leber's hereditary optic neuropathy (LHON), which is mainly due to maternally transmitted mitochondrial DNA (mtDNA) mutations. Our report shows for the first time that a mitochondrial DNA background could influence the clinical expression of MS. One European mtDNA haplogroup was found only in MS patients with optic neuritis but not in MS patients without visual symptoms. Therefore, we hypothesize that mtDNA haplogroup J might constitute a risk factor for optic neuritis occurrence when it is coincidentally associated with MS, but not be a risk factor for developing MS per se as suggested previously. (+info)

Correlation between morphological and functional retinal impairment in multiple sclerosis patients. (2/359)

PURPOSE: To assess whether a correlation exists between optic nerve fiber layer (NFL) thickness and the retinal or visual pathway function in multiple sclerosis (MS) patients previously affected by optic neuritis. METHODS: Fourteen patients with a diagnosis of definite MS were examined. All had been affected by optic neuritis (MSON) with complete recovery of visual acuity (14 eyes included in study). These were compared with 14 eyes from 14 age-matched control subjects. NFL thickness was measured by optical coherence tomography (OCT). Three different measurements in each quadrant (superior, inferior, nasal, and temporal) were taken and averaged. The data in all quadrants (12 values averaged) were identified as NFL Overall, whereas the data obtained in the temporal quadrant only (3 values averaged) were identified as NFL Temporal. Retinal and visual pathway function was assessed by simultaneously recording pattern electroretinograms (PERGs) and visual evoked potentials (VEPs) using high-contrast (80%) checkerboard stimuli subtending 15 minutes and 60 minutes of the visual arc (min arc) and reversed at the rate of two reversals per second. RESULTS: In MSON eyes there was a significant (P < 0.01) reduction in NFL thickness in both NFL Overall and NFL Temporal evaluations compared with the values observed in control eyes. PERG, (15-min arc checks) and VEP (15-min arc and 60-min arc checks), showed a significant (P < 0.01) delay in latency and reduction in amplitude. NFL Overall and NFL Temporal values were significantly correlated (P < 0.01) to the PERG P50 latency and P50 to N95 amplitude recorded with 15-min arc checks. No correlations (P > 0.01) between NFL values and the other electrophysiological data (PERG recorded with 60-min arc checks and VEP recorded with 15-min arc and 60-min arc checks) were found. CONCLUSIONS: There is a correlation between PERG changes and NFL thickness in MS patients previously affected by optic neuritis, but there is no correlation between VEP changes and NFL thickness. (+info)

Lack of restriction of T cell receptor beta variable gene usage in cerebrospinal fluid lymphocytes in acute optic neuritis. (3/359)

OBJECTIVES: There have been many studies reporting restricted patterns of T cell receptor usage in established multiple sclerosis and these have led to clinical trials of immunomodulation directed at deleting clonal T cell populations. The present study aims to test the hypothesis that highly restricted T cell populations are also present in the CSF in the earliest clinical stages of acute demyelinating disease of the CNS. METHODS: T cell receptor Vbeta (TCRBV) gene expression was studied in CSF and blood in nine patients with acute optic neuritis within 7 days of onset of symptoms, six patients with an acute relapse of multiple sclerosis, and 13 control subjects. RNA was extracted and cDNA synthesised from unstimulated CSF and blood lymphocytes, and TCRBV gene segments were amplified from the cDNA by polymerase chain reaction (PCR) using 21 family specific primers. PCR products were separated by polyacrylamide gel electrophoresis and detected via a labelled oligonucleotide probe. A semiquantitative analysis of band intensity was performed by laser densitometry. RESULTS: TCRBV mRNA was detected in the CSF of eight of nine patients with optic neuritis, six of six patients with multiple sclerosis, and five of 13 controls, and was closely correlated with the presence of oligoclonal IgG. Usage of a single TCRBV family was demonstrated in two of nine patients with optic neuritis and two of six patients with multiple sclerosis. The number of TCRBV families expressed in the other patients ranged between 5 and 15 (optic neuritis) and 4 and 17 (multiple sclerosis). CONCLUSIONS: There is a relative lack of restriction of TCRBV usage by CSF lymphocytes in the very earliest stages (<7 days) of acute optic neuritis. This may imply either that multiple sclerosis is not a monoclonal disease even at onset, or that the autoimmune response has widened before the disease becomes clinically evident. This may have important consequences for the design of immune therapies in multiple sclerosis. Further studies are required to determine whether the CSF T cell repertoire at presentation has prognostic importance. Longitudinal studies are required to follow the CSF T cell repertoire from the time of presentation and to determine whether it may have prognostic significance. (+info)

Demonstration of Bartonella grahamii DNA in ocular fluids of a patient with neuroretinitis. (4/359)

We describe the clinical and laboratory features of a 55-year-old human immunodeficiency virus-negative female patient who presented with bilateral intraocular inflammatory disease (neuroretinitis type) and behavioral changes caused by a Bartonella grahamii infection. Diagnosis was based on the PCR analysis of DNA extracted from the intraocular fluids. DNA analysis of the PCR product revealed a 100% identity with the 16S rRNA gene sequence of B. grahamii. The patient was successfully treated with doxycycline (200 mg/day) and rifampin (600 mg/day) for 4 weeks. This is the first report that demonstrates the presence of a Bartonella species in the intraocular fluids of a nonimmunocompromised patient and that indicates that B. grahamii is pathogenic for humans. (+info)

Combined fat- and water-suppressed MR imaging of orbital tumors. (5/359)

BACKGROUND AND PURPOSE: The use of a high-resolution T2-weighted MR sequence, which suppresses signal from both fat and water, has been shown to be highly effective for depicting areas of inflammatory damage within the optic nerve. The ability of this sequence to show neoplastic and inflammatory orbital lesions, which may mimic neuritis, is unknown. This study was designed to examine the characteristics of such a sequence for the investigation of orbital mass lesions. METHODS: Twenty-eight patients with known or suspected mass lesions of the orbit and six healthy volunteers were recruited for study. Imaging was performed with a 1.5-T MR unit. Participants were examined by selective partial inversion recovery (SPIR) sequences with T2-weighted fast spin-echo acquisition, selective partial inversion recovery/fluid attenuated inversion recovery (SPIR/FLAIR) sequences with fast spin-echo acquisition, short tau inversion recovery (STIR) sequences with fast spin-echo acquisition, and SPIR sequences with contrast-enhanced T1-weighted fast spin-echo acquisition. Two neuroradiologists, using a randomised, blinded method, scored images for lesion presence and extent. Lesion extent was defined as the number of images with visible abnormality, and was compared with the standard of reference established at a later date by consensus review of all imaging sequences. The ability of the sequences to show the presence and extent of pathologic lesions was compared. RESULTS: The SPIR/FLAIR sequence showed both the presence and extent of orbital masses significantly better than did either STIR or T2-weighted SPIR sequences (P<.01 and P<.001, respectively). Contrast-enhanced T1-weighted SPIR images ranked better than SPIR/FLAIR images, although the difference failed to reach statistical significance. In the orbital apex, the SPIR/FLAIR technique was superior to all other techniques used. This reflected its ability to distinguish enhancing, pathologic lesions from enhancing, normal anatomy. CONCLUSION: SPIR/FLAIR is an appropriate screening technique for orbital masses and offers significant advantages over currently used fat-suppressed sequences for the investigation of orbital disease. (+info)

Multiple sclerosis: the disease and its manifestations. (6/359)

Multiple sclerosis is an immune-mediated inflammatory demyelinating disease of the central nervous system clinically characterized by relapses and remissions of neurological disturbance. A typical relapse, exemplified by optic neuritis, increases in severity over a week or two and after approximately one month begins to remit. Resolution takes place over the course of two to three months. In the early stages, clinical recovery is virtually complete, though persistent abnormalities of conduction can usually be detected by evoked potential techniques and persistent structural abnormalities can be detected by magnetic resonance imaging (MRI). These techniques, together with cerebrospinal fluid examination for oligoclonal IgG, provide supporting evidence for the diagnosis which, in the absence of a specific test, nevertheless remains primarily clinical. The course of the disease is very variable, but after a number of years neurological deficit begins to accumulate after each relapse. In most patients, the relapsing and remitting phase of the disease is followed by a phase of continuous progression of disability. Cognitive disturbances can be detected in many patients even quite early in the course of the illness. Deficits in attention, memory and executive skills may be prominent and tend to become increasingly prominent as neurological deficit increases, although this is not always the case. There is some correlation between the extent of MRI abnormalities in the cerebral white matter and the severity of cognitive deficit. Depression and anxiety are commonly experienced but are poorly correlated to the lesion load seen on MRI. In contrast, the much rarer psychotic symptoms, euphoria and emotional lability are closely linked to the severity of white matter disease. (+info)

Response variability in the visual field: comparison of optic neuritis, glaucoma, ocular hypertension, and normal eyes. (7/359)

PURPOSE: To compare the relationship between sensitivity and response variability in the visual field of normal eyes and eyes with optic neuritis (ON), glaucoma (POAG), and ocular hypertension (OHT). METHODS: Frequency-of-seeing (FOS) data were collected from four visual field locations in one eye of 71 subjects (12 ON, 25 POAG, 11 OHT, and 23 normal), using a constant stimulus method on an Henson 4000 perimeter (Tinsley Instruments, Croydon, UK). At each location, at least 20 stimuli (subtending 0.5 degrees) were presented for 200 ms at six or more intensities above and below the estimated threshold. The mean and SD of the probit fitted cumulative Normal function were used to estimate sensitivity and response variability. Cluster regression analysis was carried out to determine whether there were differences in the sensitivity-log (variability) relationship between the four groups. RESULTS: Variability was found to increase with decreased sensitivity for all four groups. The combined data from the four groups was well represented (R2 = 0.57) by the function log(e)(SD) = A.sensitivity (dB) + B, where the constants A and B were -0.081 (SE, +/-0.005) and 3.27 (SE, +/-0.15), respectively. Including other statistically significant covariates (false-negative errors, P = 0.004) and factors (diagnosis, P = 0.005) into the model increased the proportion of explained variance to 62% (R2 = 0.62). Stimulus eccentricity (P = 0.34), patient age (P = 0.33), fixation loss rate (P = 0.10), and false-positive rate (P = 0.66) did not reach statistical significance as additional predictors of response variability. CONCLUSIONS: The relationship between response variability and sensitivity is similar for ON, POAG, OHT, and normal eyes. These results provide supporting evidence for the hypothesis that response variability is dependent on functional ganglion cell density. (+info)

Recovery from optic neuritis is associated with a change in the distribution of cerebral response to visual stimulation: a functional magnetic resonance imaging study. (8/359)

OBJECTIVES: Recovery to normal or near normal visual acuity is usual after acute demyelinating optic neuritis, despite the frequent persistence of conduction abnormalities as evidenced by the visual evoked potential (VEP). This raises the possibility that cortical adaptation to a persistently abnormal input contributes to the recovery process. The objective of this study was to investigate the pattern of cerebral response to a simple visual stimulus in recovered patients in comparison to normal subjects. METHODS: Functional magnetic resonance imaging (fMRI) was used to study the brain activation pattern induced by a periodic monocular 8Hz photic stimulus in seven patients who had recovered from a single episode of acute unilateral optic neuritis, and in seven normal controls. VEPs and structural optic nerve MRI were performed on patients. RESULTS: Stimulation of either eye in controls activated only the occipital visual cortex. However, in patients, stimulation of the recovered eye also induced extensive activation in other areas including the insula-claustrum, lateral temporal and posterior parietal cortices, and thalamus; stimulation of the clinically unaffected eye activated visual cortex and right insula-claustrum only. The volume of extraoccipital activation in patients was strongly correlated with VEP latency (r = 0.71, p = 0.005). CONCLUSIONS: The extraoccipital areas that were activated in patients all have extensive visual connections, and some have been proposed as sites of multimodal sensory integration. The results indicate a functional reorganisation of the cerebral response to simple visual stimuli after optic neuritis that may represent an adaptive response to a persistently abnormal input. Whether this is a necessary part of the recovery process remains to be determined. (+info)