In multiple sclerosis (MS), retinal nerve fiber layer thickness is associated with brain parenchymal fraction and CSF volume. These data suggest that quantification of axonal thickness in the retina by optical coherence tomography (OCT) provides concurrent information about MRI brain abnormality in MS. OCT should be examined in longitudinal studies to determine if it could be used as an outcome measure in clinical trials of neuroprotective drugs.

Retinal nerve fiber layer (RNFL) is significantly decreased in multiple sclerosis (MS) optic neuritis (ON) eyes, unaffected fellow eyes of patients with MS ON, and MS eyes not affected by ON in our cohort. Macular volumes (MV) showed a significant decrease in MS ON eyes. Progressive MS cases showed more marked decreases in RNFL and MV than relapsing-remitting MS. OCT is a promising tool to detect subclinical changes in RNFL and MV in patients with MS and should be examined in longitudinal studies as a potential biomarker of retinal pathology in MS.

To determine whether damage to the optic radiation (OR) in multiple sclerosis (MS) is associated with optic nerve injury and visual dysfunction.

Background-Inflammatory demyelination and axon damage in the corpus callosum are prominent features of multiple sclerosis (MS) and may partially account for impaired performance on complex tasks.

The human spinal cord contains segregated sensory and motor pathways that have been difficult to quantify using conventional magnetic resonance imaging (MRI) techniques. Multiple sclerosis is characterized by both focal and spatially diffuse spinal cord lesions with heterogeneous pathologies that have limited attempts at linking MRI and behaviour. We used a novel magnetization-transfer-weighted imaging approach to quantify damage to spinal white matter columns and tested its association with sensorimotor impairment. We studied 42 participants with multiple sclerosis who each underwent MRI at 3 Tesla and quantitative tests of sensorimotor function. We measured cerebrospinal-fluid-normalized magnetization-transfer signals in the dorsal and lateral columns and grey matter of the cervical cord. We also measured brain lesion volume, cervical spinal cord lesion number and cross-sectional area, vibration sensation, strength, walking velocity and standing balance. We used linear regression to assess the relationship between sensorimotor impairment and MRI abnormalities. We found that the dorsal column cerebrospinal-fluid-normalized magnetization-transfer signal specifically correlated with vibration sensation (R = 0.58, P < 0.001) and the lateral column signal with strength (R = -0.45, P = 0.003). Spinal cord signal measures also correlated with walking and balance dysfunction. A stepwise multiple regression showed that the dorsal column signal and diagnosis subtype alone explained a significant portion of the variance in sensation (R(2) = 0.54, P < 0.001), whereas the lateral column signal and diagnosis subtype explained a significant portion of the variance in strength (R(2) = 0.30, P < 0.001). These results help to understand the anatomic basis of sensorimotor disability in multiple sclerosis and have implications for testing the effects of neuroprotective and reparative interventions.

Q-space analysis is an alternative analysis technique for diffusion-weighted imaging (DWI) data in which the probability density function (PDF) for molecular diffusion is estimated without the need to assume a Gaussian shape. Although used in the human brain, q-space DWI has not yet been applied to study the human spinal cord in vivo. Here we demonstrate the feasibility of performing q-space imaging in the cervical spinal cord of eight healthy volunteers and four patients with multiple sclerosis. The PDF was computed and water displacement and zerodisplacement probability maps were calculated from the width and height of the PDF, respectively. In the dorsal column white matter, q-space contrasts showed a significant (P < 0.01) increase in the width and a decrease in the height of the PDF in lesions, the result of increased diffusion. These q-space contrasts, which are sensitive to the slow diffusion component, exhibited improved detection of abnormal diffusion compared to perpendicular apparent diffusion constant measurements. In white matter (WM) the axonal membrane and myelin sheath present barriers to water displacement, resulting in anisotropic diffusion (1-4). WM damage is known to affect tissue microstructure and diffusion-weighted MRI (DWI) has been used to measure changes in diffusion properties (both parallel and perpendicular to WM fiber bundles) in a number of WM diseases in humans (5) as well as animal models of myelin deficiency (6,7). In general, however, conclusive assignment of diffusion changes observed with DWI to axonal and/or myelin damage is not straightforward, in part because the biophysics of diffusion in vivo is not fully understood and because axonal and myelin loss are histopathologically related. Additionally, the technique selected to analyze diffusion-weighted images (DWIs) is an important consideration and has an impact on the quantitative interpretation of diffusion experiments. DWIs are typically analyzed with a monoexponential tensor model that characterizes the observed signal decay according to the Stejskal-Tanner equation (8):where S/S 0 is the normalized signal intensity, ␥ is the proton gyromagnetic ratio, ␦, G, and ⌬ are the duration, magnitude, and leading edge separation time of the diffusion weighting gradient vector, respectively, and D is the diffusion tensor. Diffusion tensor imaging (DTI) has been applied in the brain (5,9 -12) and spinal cord (10,(13)(14)(15) and is typically performed in the low b-value (Ͻ1500 s/mm 2 ) regime where the signal decay is, to a reasonable approximation, monoexponential. The degree to which diffusion is reduced in the CNS, compared to free water, is the result of microstructural barriers, which generally includes multiple compartments in vivo and the diffusion time that molecules have to explore their environment. If restrictions between compartments are sufficiently large so that exchange is slow on the MR timescale, the signal attenuation will become non-monoexponential. This effect becomes apparent at higher b-values (Ͼ1500 s/mm 2 )...

Multiparametric MRI allows rapid detection, localization, and characterization of tract-specific abnormalities in multiple sclerosis. Tract profiles bridge the gap between whole-brain imaging of neurological disease and the interrogation of individual, functionally relevant subsystems.

Acute flaccid myelitis (AFM) is a disabling, polio-like illness mainly affecting children. Outbreaks of AFM have occurred across multiple global regions since 2012, and the disease appears to be caused by non-polio enterovirus infection, posing a major public health challenge. The clinical presentation of flaccid and often profound muscle weakness (which can invoke respiratory failure and other critical complications) can mimic several other acute neurological illnesses. There is no single sensitive and specific test for AFM, and the diagnosis relies on identification of several important clinical, neuroimaging, and cerebrospinal fluid characteristics. Following the acute phase of AFM, patients typically have substantial residual disability and unique long-term rehabilitation needs. In this Review we describe the epidemiology, clinical features, course, and outcomes of AFM to help to guide diagnosis, management, and rehabilitation. Future research directions include further studies evaluating host and pathogen factors, including investigations into genetic, viral, and immunological features of affected patients, host-virus interactions, and investigations of targeted therapeutic approaches to improve the long-term outcomes in this population.