Optic Nerve MRI Research Articles

Value of Optic Nerve MRI in Multiple Sclerosis Clinical Management: A MAGNIMS Position Paper and Future Perspectives.

The optic nerve is frequently involved in multiple sclerosis (MS). However, MRI of the optic nerve is considered optional in the differential diagnosis of optic neuropathy symptoms either at presentation or in established MS. In addition, unlike spinal cord imaging in comparable scenarios, no role is currently recommended for optic nerve MRI in patients presenting with optic neuritis for its confirmation, to plan therapeutic strategy, within the MS diagnostic framework, nor for the detection of subclinical activity in established MS. In this article, evidence related to these 3 aspects will be summarized and gaps in knowledge will be highlighted, including (1) the acquisition challenges and novel sequences that assess pathologic changes within the anterior visual pathways; (2) the clinical implications of quantitative magnetic resonance studies of the optic nerve, focusing on atrophy measures, magnetization transfer, and diffusion tensor imaging; and (3) the relevant clinical studies performed to date. Finally, an algorithm for the application of optic nerve MRI will be proposed to guide future studies aimed at addressing our knowledge gaps.

Improved optic nerve visualization and treatment planning through a dedicated optic nerve MRI protocol.

This study describes an innovative optic nerve MRI protocol for better delineating optic nerve anatomy from neighboring pathology. Twenty-two patients undergoing MRI examination of the optic nerve with the dedicated protocol were identified and included for analysis of imaging, surgical strategy, and outcomes. T2-weighted and fat-suppressed T1-weighted gadolinium-enhanced images were acquired perpendicular and parallel to the long axis of the optic nerve to achieve en face and in-line views along the course of the nerve. Dedicated optic nerve MRI sequences provided enhanced visualization of the nerve, CSF within the nerve sheath, and local pathology. Optic nerve sequences leveraged the "CSF ring" within the optic nerve sheath to create contrast between pathology and normal tissue, highlighting areas of compression. Tumor was readily tracked along the longitudinal axis of the nerve by images obtained parallel to the nerve. The findings augmented treatment planning. The authors present a dedicated optic nerve MRI protocol that is simple to use and affords improved cross-sectional and longitudinal visualization of the nerve, surrounding CSF, and pathology. This improved visualization enhances radiological evaluation and treatment planning for optic nerve lesions.

Optic Neuropathy AFG3L2 Related in a Patient Affected by Congenital Stationary Night Blindness

Objective: We describe a patient affected by congenital stationary night blindness (CSNB) secondary to CACNA1F and optic neuropathy associated with an AFG3L2 variant.Methods: We performed comprehensive neuro‐ophthalmologic examinations, retinal imaging, complete ocular electrophysiology, and brain and optic nerve MRI. Genomic DNA was extracted from the peripheral blood. The patient’s DNA was then investigated by next‐generation sequencing (NGS) with a panel including 32 genes associated with retinal dystrophy and therefore with a panel including seven genes associated with genetic forms of optic atrophy.Results: The genetic analysis identified a pathogenetic CACNA1F variant causing CSNB and a heterozygous variant in AFG3L2 that alters OPA1 processing and is known to be associated with OPA1‐like optic neuropathy.Conclusion: Optic disc atrophy has been previously described as an atypical feature in the phenotype of CSNB CACNA1F‐related. In this patient, we found a variant of the AFG3L2 gene that presumably explains the presence of optic atrophy in a subject affected by CSNB.Clinical Relevance: The clinical evidence of optic atrophy, which is atypical in CSNB, should raise the suspicion of concomitant hereditary optic neuropathy and emphasize the importance of broad genetic diagnostic testing to better define the genotype–phenotype correlation.

Asymptomatic MRI lesions in pediatric-onset AQP4-IgG positive NMOSD

Background and purposeAround 5% of all Neuromyelitis Optica Spectrum Disorders (NMOSD) cases start before 18 years of age. Clinical and radiological manifestations of AQP4-IgG positive NMOSD were revised in 2015, and the importance of neuroimaging in the diagnosis is well recognized. Neuroimaging findings in pediatric-onset NMOSD were scarcely described, and longitudinal evaluation of NMOSD lesions was only accessed in a few adult-onset cohorts. MethodsThis study evaluated brain, spinal cord, and optic nerve MRI of sixteen pediatric-onset AQP4-IgG positive NMOSD through a qualitative evaluation of lesion evolution. Lesions were classified as symptomatic or asymptomatic in acute or chronic phase (> 30 days from last attack) MRI. ResultsSeventy MRI scans and 54 subsequent exams were evaluated. Most NMOSD lesions (74.5%) reduced, remained stable, or developed atrophy/cavitation. New brain lesions or enlargement of existing brain lesions were found in two patients (12.5%) without any clinical symptom and in five patients (31.2%) in the course of an attack from other topography (optic neuritis or acute myelitis). One patient (6.3%) presented an asymptomatic spinal cord lesion irrespective of clinical manifestation. No asymptomatic lesion was described in optic nerve MRI. In acute phase exams, longitudinally extensive transverse myelitis (13/19 vs 8/24; p = 0.033), cervical myelitis (15/19 vs 10/24, p = 0.028), lumbar myelitis (5/19 vs 0/24; p = 0.012), and a higher number of segments [median 8 (range 4–17) vs 3.5 (range 1–14); p = 0.003] were affected. ConclusionsAsymptomatic brain and spinal cord lesions can occur in pediatric-onset NMOSD, especially in the course of acute optic neuritis or myelitis. More longitudinal studies are necessary to guide recommendations on neuroimaging frequency in pediatric patients with AQP4-IgG NMOSD.

Differentiating Multiple Sclerosis From AQP4-Neuromyelitis Optica Spectrum Disorder and MOG-Antibody Disease With Imaging.

Relapsing-remitting multiple sclerosis (RRMS), aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) may have overlapping clinical features. There is an unmet need for imaging markers that differentiate between them when serologic testing is unavailable or ambiguous. We assessed whether imaging characteristics typical of MS discriminate RRMS from AQP4-NMOSD and MOGAD, alone and in combination. Adult, nonacute patients with RRMS, APQ4-NMOSD, and MOGAD and healthy controls were prospectively recruited at the National Hospital for Neurology and Neurosurgery (London, United Kingdom) and the Walton Centre (Liverpool, United Kingdom) between 2014 and 2019. They underwent conventional and advanced brain, cord, and optic nerve MRI and optical coherence tomography (OCT). A total of 91 consecutive patients (31 RRMS, 30 APQ4-NMOSD, and 30 MOGAD) and 34 healthy controls were recruited. The most accurate measures differentiating RRMS from AQP4-NMOSD were the proportion of lesions with the central vein sign (CVS) (84% vs 33%, accuracy/specificity/sensitivity: 91/88/93%, p < 0.001), followed by cortical lesions (median: 2 [range: 1-14] vs 1 [0-1], accuracy/specificity/sensitivity: 84/90/77%, p = 0.002) and white matter lesions (mean: 39.07 [±25.8] vs 9.5 [±14], accuracy/specificity/sensitivity: 78/84/73%, p = 0.001). The combination of higher proportion of CVS, cortical lesions, and optic nerve magnetization transfer ratio reached the highest accuracy in distinguishing RRMS from AQP4-NMOSD (accuracy/specificity/sensitivity: 95/92/97%, p < 0.001). The most accurate measures favoring RRMS over MOGAD were white matter lesions (39.07 [±25.8] vs 1 [±2.3], accuracy/specificity/sensitivity: 94/94/93%, p = 0.006), followed by cortical lesions (2 [1-14] vs 1 [0-1], accuracy/specificity/sensitivity: 84/97/71%, p = 0.004), and retinal nerve fiber layer thickness (RNFL) (mean: 87.54 [±13.83] vs 75.54 [±20.33], accuracy/specificity/sensitivity: 80/79/81%, p = 0.009). Higher cortical lesion number combined with higher RNFL thickness best differentiated RRMS from MOGAD (accuracy/specificity/sensitivity: 84/92/77%, p < 0.001). Cortical lesions, CVS, and optic nerve markers achieve a high accuracy in distinguishing RRMS from APQ4-NMOSD and MOGAD. This information may be useful in clinical practice, especially outside the acute phase and when serologic testing is ambiguous or not promptly available. This study provides Class II evidence that selected conventional and advanced brain, cord, and optic nerve MRI and OCT markers distinguish adult patients with RRMS from AQP4-NMOSD and MOGAD.

A Comparative Analysis of Clinical and Imaging Features of Aquaporin 4 (AQP4) Antibody Positive, Myelin Oligodendrocyte Glycoprotein (MOG) Antibody Positive and Double Seronegative Subtypes of Neuro Myelitis Optica Spectrum Disorder (NMOSD).

Objectives:Study was conducted with aim of comparing subtypes types of NMOSD based on serology.Methods:In this retrospective study, patients ≥18 years were included satisfying IPND 2015 criteria. Three groups were created based on seropositivity for AQP4 antibody, MOG antibody or double seronegative. Demographic, clinical and imaging were compared using regression analysis.Results:Forty-six patients, 28 (60.9%) AQP4+, 11 (23.9%) MOG + and remaining 7 (15.2%) double seronegative were included. Thirty-seven patients (80.4%) had presenting symptoms localized to optic nerve and/or cord [AQP4 + 22 (78.5%), MOG + 9 (81.8%) and double seronegative 6 (85.7%)]. Presentation with bilateral optic neuritis was more common in AQP4- patients. Twenty (86.8%) out of the 23 patients who had relapsing disease localized to optic nerve and/or spinal cord [AQP4 + 13/14 (92.8%), MOG + 3/5 (60%) and double seronegative 4/4 (100%)]. Relapses were more common in AQP4+ (77% vs 12% vs10%). In AQP4 negative group disability (EDSS 4.2 vs 3.3) and progression index was relatively less (1.6 vs 1.1). CSF pleocytosis (38.8% vs 17.9%) and raised proteins (66.6% vs 32.1%) were also more common. Optic nerve MRI (>50% optic nerve and chiasma involvement) was more commonly abnormal in AQP4 negative (52.9% vs 31.2%). Regression analysis revealed females to be significantly higher in AQP4 positive NMOSD (89.3%) when compared to MOG positive (36.4%) and double seronegative (42.9%).Conclusion:Gender was the only significant difference between the three groups. There was trend towards greater disability and more relapses in AQP4 + groups.

Motion degradation in optic nerve MRI: A randomized intraindividual comparison study of eye states

PurposeMRI is a powerful tool for optic nerve assessment, but image quality can be degraded by artifacts related to ocular motion. The purpose of this investigation was to evaluate the effect of undergoing MRI with eyes open versus closed on the degree of motion degradation affecting the optic nerves. MethodPatients undergoing 3 Tesla orbital MRI were randomized to undergo the coronal STIR sequence with eyes open and focused on a standardized fixation point, blinking as needed, or with eyes closed. The sequence was then performed again with the other instruction set. Two neuroradiologists rated the intraorbital optic nerves for motion artifact on a 5-point scale (higher numbers reflecting greater motion artifact) in 2 locations of each nerve. Differences were evaluated by the clustered Wilcoxon signed rank test. ResultsSeventy-seven orbits were included. Interrater reliability was high (weighted kappa = 0.78). The anterior intraorbital optic nerves were rated with less motion artifact when eyes were open and focused during acquisition than when closed (p = 0.006), but this was not the case for the posterior intraorbital optic nerve (p = 0.69). For example, at the anterior intraorbital optic nerve, motion artifact of mean grade better than 2 was seen in 60% of eyes-open vs. 32% of eyes-closed acquisitions, while mean grade 4 or worse was seen in 4% of eyes-open vs. 12% of eyes-closed acquisitions. ConclusionUndergoing orbital MRI with eyes open and focused rather than closed reduces motion artifact at the anterior intraorbital segment of the optic nerve.

Editor Response: Asymptomatic Optic Nerve Lesions: An Underestimated Cause of Silent Retinal Atrophy in MS.

Davion et al.1 examined the frequency of asymptomatic optic nerve MRI signal in patients with multiple sclerosis (MS) on natalizumab. All patients were seronegative or had low antibody titers for JC virus (<1.50). The authors found that 60 or 73 (82.2%) eyes with a history of symptomatic optic neuritis (ON) had high signal on MRI of the orbits using 3D double inversion recovery (DIR). There were 123 asymptomatic eyes with no history of ON; nearly 50% of these eyes also showed high signal using DIR MRI. The DIR MRI findings were examined in the context of optical coherence tomography (OCT) findings and low-contrast letter acuity (LCLA) performance. This publication is of significance for several reasons. First, it shows the rate of high signal abnormality in a chronic cohort of symptomatic optic neuritis eyes. The case series also demonstrates a high rate of DIR-identified high signal change in asymptomatic eyes; the association of this finding with reduced OCT-measured retinal thickness values and impaired monocular LCLA scores is also highlighted. Results from DIR imaging of the asymptomatic eyes are notable since the most recent 2017 McDonald Criteria for MS diagnosis do not include optic nerve lesions as part of the criteria for dissemination in space by MRI.2 Thus, OCT imaging and DIR MRI may be valuable to detect subtle symptomatic or asymptomatic optic nerve abnormalities.1,3 Ongoing investigations will need to confirm the value of DIR imaging to define potential false-positive rates for identifying optic nerve disease vs changes in imaging without functional impairment. This study and others that document OCT-measured intereye differences should lead to further investigation into the role of the optic nerve as a lesion site for MS diagnosis.

The clinical analysis of optic neuropathy relative to Behcet's disease with clinical manifestation of anterior ischemic optic neuropathy

Objective: To summarize the clinical manifestation, treatment and prognosis of anterior ischemic optic neuropathy(AION) which was the manifestation of optic neuropathy related with Behcet's disease (BD). Methods: Retrospective series of case studies. The clinical data of 6 cases (9 eyes) of AION associated with BD who were hospitalized at the neurology ward of Beijing Tongren Hospital from February to June in 2016 were collected, the clinical characteristics of these patients were summarized, visual acuity were compared by using Wingerchuk visual grade before and after treatment. Results: Among the 6 patients with AION associated with BD, there were 4 males and 2 female, aged 38-60 years. All patients were acute onset, 3 cases had the onset of one eye, 2 cases with the onset of both eyes and 1 case with successively onset of both eyes. Optic nerve was damaged in 6 cases (9 eyes), only 1 case felt pain of eyes, the best corrected visual acuity of 4 eyes were less than 0.1, optic disk edema and linear bleeding around optic disk were oberved in all patients, the lower half visual field defect was the most common damage type (5 eyes), P100 latency of visual evoked potential prolonged in all patients, optic nerve MRI showed abnormal signal of optic nerve involvement in 2 patients. All patients were treated with corticosteroids and followed for 3 months, there was significant improvement in 1 eye of which the vision improved above 3 grade, and improvement in 6 eyes of which vision improved for 1-2 grade, while there has been no change in 2 eyes. Conclusions: BD may be the etiology of AION. Visual impairment of this kind of patients is relatively serious, visual function is expected to improve with early treatment. (Chin J Ophthalmol, 2019, 55:203-207).

Evaluation of optic nerve functions in subacute combined degeneration using visual evoked potential and diffusion tensor imaging-a pilot study.

To evaluate optic nerve involvement in subacute combined degeneration (SACD) using diffusion tensor imaging (DTI) and visual evoked potential (VEP) studies, and their changes following cobalamine treatment. Six patients with SACD and six healthy matched controls were included. Visual acuity, fieldof vision, and color vision were tested. Pattern shift VEP was done, and P100 latency and amplitude were measured. Optic nerve MRI, and DTI of optic nerve to muscle ratio were measured, and fractional anisotropy ratio (FAR), axial diffusivity ratio (ADR), radial diffusivity ratio (RDR), and mean diffusivity ratio (MDR) were calculated. The patients received hydroxyl cobalamine 1000 µg intramuscularly and their clinical examination, VEP and DTI studies were repeated at 3 months. The age of the patients ranged between 16 and 60 years and two were females. Their visual acuity, fieldof vision, and color vision were normal. P100 latency was prolonged in five patients (10 eyes) and amplitude was reduced in one (1 eye). The SACD patients had reduced FAR (1.94 ± 0.55 vs 2.81 ± 0.42; p = 0.01) and increased MDR (1.00 ± 0.04 vs 0.95 ± 0.01; p = 0.01) and RDR (0.96 ± 0.03 vs 0.89 ± 0.01; p = 0.002) compared to the controls. The FAR value correlated with P100 latency (r = -0.88). At 3 months, FAR value increased which was associated with improvement in P100 latency. In SACD patients, optic nerve FAR is reduced and correlates with P100 latency. Both these parameters improve on cobalamine treatment. Subclinical VEP abnormalities are common in SACD but conventional MRI sequence of optic nerve is normal. DTI of optic nerve reveals reduced fractional anisotropy (FA) values which improve after cobalamine treatment. FA values correlate with prolongation of P100 latency. DTI and VEP abnormalities suggest subclinical optic nerve myelin dysfunction.

Demyelinating disease with antibodies to myelin oligodendrocyte glycoprotein (mog) presenting as nmo

Objectives To describe 2 cases of anti-MOG demyelinating disease presenting as NMO. Methods We reviewed the medical records of 2 patients seen at Nelson Hospital with bilateral optic neuritis, one with transverse myelitis. Cases A 23 years old man developed truncal paraesthesias followed 24 hours later by bilateral visual loss, sphincter disturbance, saddle anaesthesia and imbalance. Treatment with methylprednisolone (MP) resulted in minimal improvement followed by therapeutic plasma exchange with return to normal. CSF showed 50 white cells with normal protein, negative OCB’s and normal IgG index. Brain and optic nerve MRI was reported as normal but there was longitudinally extensive, non-enhancing thoracic cord T2 hyperintensity. IgG antibodies to aquaporin-4 (NMO-IgG) were negative but MOG antibodies were positive. A 54 years old woman developed bilateral severe visual loss and paraesthesias in the right foot which rapidly resolved with MP but recurred one month later, again successfully treated with MP. CSF showed 10 white cells with normal protein, negative OCB’s and normal IgG index. MRI showed bilateral optic nerve enhancement and an enhancing pontine lesion. Cord MRI done a month later was normal. NMO-IgG was negative but MOG antibodies were positive. Conclusions Simultaneous or sequential bilateral optic neuritis and transverse myelitis is the characteristic phenotype of NMO. About 75% of such patients have NMO-IgG. The remainder are seronegative but meet clinical and MRI criteria for the disease and are classified as NMO-spectrum disorder (NMO-SD). We describe two patients who presented with a characteristic clinical phenotype who were seronegative for NMO-IgG but had antibodies to MOG. It has been suggested that this constitutes a unique disorder and should not be classified as part of NMO-SD. This distinction is of practical importance since CNS demyelinating patients with antibodies to MOG has a better prognosis than typical NMO and treatment may be different.

Parallel changes in structural and functional measures of optic nerve myelination after optic neuritis.

IntroductionVisual evoked potential (VEP) latency prolongation and optic nerve lesion length after acute optic neuritis (ON) corresponds to the degree of demyelination, while subsequent recovery of latency may represent optic nerve remyelination. We aimed to investigate the relationship between multifocal VEP (mfVEP) latency and optic nerve lesion length after acute ON.MethodsThirty acute ON patients were studied at 1,3,6 and 12 months using mfVEP and at 1 and 12 months with optic nerve MRI. LogMAR and low contrast visual acuity were documented. By one month, the mfVEP amplitude had recovered sufficiently for latency to be measured in 23 (76.7%) patients with seven patients having no recordable mfVEP in more than 66% of segments in at least one test. Only data from these 23 patients was analysed further.ResultsBoth latency and lesion length showed significant recovery during the follow-up period. Lesion length and mfVEP latency were highly correlated at 1 (r = 0.94, p = <0.0001) and 12 months (r = 0.75, p < 0.001). Both measures demonstrated a similar trend of recovery. Speed of latency recovery was faster in the early follow-up period while lesion length shortening remained relatively constant. At 1 month, latency delay was worse by 1.76ms for additional 1mm of lesion length while at 12 months, 1mm of lesion length accounted for 1.94ms of latency delay.ConclusionA strong association between two putative measures of demyelination in early and chronic ON was found. Parallel recovery of both measures could reflect optic nerve remyelination.

Contribution of imaging to the diagnosis of optic neuropathies

Magnetic resonance imaging is the modality of choice to investigate patients with central nervous system diseases. In patients with optic neuritis, early MRI allows positive and differential diagnosis, and gives arguments for prognosis. The technique should be adapted for the exploration of visual pathways. Inflammatory optic neuritis is characterized by an early signal abnormality within the optic nerve, whereas optic nerve MRI is normal in the early phase of ischemic optic neuropathy. MRI also detects compressive and infiltrative lesions. Meningiomas are characterized by abnormalities within the peri-optical spaces, whereas a global increase in the size of the optic nerve is in favor of a glioma.

Relationship of optic nerve and brain conventional and non-conventional MRI measures and retinal nerve fiber layer thickness, as assessed by OCT and GDx: A pilot study

Background Measurement of retinal nerve fiber layer (RNFL) thickness in multiple sclerosis (MS) is gaining increasing attention. Objectives To explore the relationship between RNFL thickness as measured by optical coherence tomography (OCT) and scanning laser polarimetry with variable corneal compensation (GDx), and conventional and non-conventional optic nerve and brain MRI measures. Methods Twelve relapsing–remitting (RR) MS patients (12 affected and 12 unaffected eyes) and 4 age- and sex-matched normal controls (NC) (8 unaffected eyes) were enrolled. Four MS patients had a history of bilateral optic neuritis (ON), four had a history of unilateral ON, and 4 had no history of ON. Optic nerve MRI measurements included the length of T2 lesions, measurement of optic nerve atrophy, magnetization transfer ratio (MTR) and diffusion tensor imaging (DTI) measures. Optic nerve atrophy was measured by a novel method with high reproducibility. Brain MRI measurements included T1 and T2 lesion volumes (LVs) and their relative MTRs, and tissue class specific atrophy, MTR and DTI measures. Measures of RNFL were evaluated with OCT and GDx. We also evaluated both high and low contrast letter acuities (LCLA) in order to determine the relationship between vision, MRI metrics, and retinal structural architecture. Results LCLA, RNFL-OCT and optic nerve radius measures showed more robust differences between NC and MS patients, and between MS patients with affected and unaffected eyes. T2-LV and T1-LV, as well as gray matter atrophy, DTI and MTR measures were related to LCLA and RNFL thickness. Unique additive variance regression models showed that both brain and optic nerve MRI measures independently accounted for about 50% of the variance in LCLA and RNFL thickness. In reverse models, about 20% of the additional independent variance was explained by optic nerve or brain MRI metrics. Conclusions Measurement of RNFL thickness and radius of the optic nerve should be preferred to the other optic nerve MRI measures in clinical studies. Whole brain lesion and GM measures are predictive of impaired visual function with corresponding structural concomitants.

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.

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.

Proton beam irradiation of pituitary adenomas

Proton beam irradiation of pituitary adenomas

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

OBJECTIVESRecovery 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)....

MRI of optic nerve and postchiasmal visual pathways and visual evoked potentials in secondary progressive multiple sclerosis.

We studied the relationship between abnormalities shown by MRI and functional disturbances in the visual pathway as assessed by the visual evoked potential (VEP) in 25 patients with established multiple sclerosis (MS); only 4 of whom had a history of acute optic neuritis. Optic nerve MRI was abnormal in 19 (76%) and is thus useful in detecting subclinical disease. Optic nerve total lesion length and area on the STIR sequence was found to correlate significantly with prolongation of the VEP latency. This may reflect a predominantly demyelinating rather than inflammatory origin for the signal change in the optic nerve.

Lesion discrimination in optic neuritis using high-resolution fat-suppressed fast spin-echo MRI.

Fast spin-echo (FSE) is a new sequence with acquisition times currently down to one-sixteenth of those obtained with conventional spin-echo sequences, which allows high-resolution (512 x 512 matrix) images to be acquired in an acceptable time. We compared the higher resolution of FSE with the medium resolution of a short inversion-time inversion-recovery (STIR) sequence in depicting the optic nerves of healthy controls and patients with optic neuritis. Optic nerve MRI examinations were performed in 18 patients with optic neuritis and 10 normal controls. Two sequences were obtained coronally: fat-suppressed FSE (FSE TR 3250 ms/TEef 68 ms, echo-train length 16, 4 excitations, 24 cm rectangular field of view, 3 mm interleaved contiguous slices, in-plane resolution 0.5 x 0.5 mm) and STIR (TR 2000 ms/TE 50 ms/TI 175 ms, in-plane resolution 0.8 x 0.8 mm, slice thickness 5 mm). FSE demonstrated much more anatomical detail than STIR, e.g. distinction of optic nerve and sheath. Lesions were seen in 20 of 21 symptomatic nerves using FSE and in 18 of 21 using STIR. Nerve swelling or partial cross-sectional lesions of the optic nerve were each seen only on FSE in 3 cases. Fat-suppressed FSE imaging of the optic nerve improves anatomical definition and increases lesion detection in optic neuritis.