Gray Matter Lesions Research Articles

Diagnosis of demyelinating brain lesion simulating brain tumors on fast imaging employing steady-state acquisition magnetic resonance imaging.

Background:A single inflammatory demyelinating brain lesion sometimes mimics a brain tumor on conventional magnetic resonance imaging (MRI), and thus poses a considerable diagnostic challenge. We assessed the usefulness of a new MRI technique, fast imaging employing steady-state acquisition (FIESTA), for the diagnosis of inflammatory demyelinating disease (IDD).Methods:Three patients (2 males, 1 female) with a histopathologically proven inflammatory demyelinating brain lesion which mimicked a brain tumor on MRI were evaluated with a post-contrast three-dimensional FIESTA sequence before biopsy and treatment. Those images were compared with the images of intra-axial brain tumors (n = 147).Results:Preoperative FIESTA showed an iso- or slightly hyperintense distinct intralesional structure that appeared reticulate or broad-line in patients with IDD. These structures traversed a hyperintense demyelinating lesion in the deep grey matter (DGM) and were connected to the surrounding extralesional area, which appeared to be dense fibers between DGM. Such distinct intralesional structures were not observed in most brain tumors.Conclusion:Reticulate or broad-line-like intralesional structures on FIESTA may, therefore, be suggestive of IDD rather than indicate a brain tumor.

Small cortical grey matter lesions show no persistent infarction in transient ischaemic attack? A prospective cohort study

ObjectivesTo find determining factors for persistent infarction signs in patients with transient ischaemic attack (TIA), herein initial diffusion lesion size, visibility on apparent diffusion coefficient (ADC) or fluid-attenuated inversion recovery...

Structural Brain Damage and Upper Limb Kinematics in Children with Unilateral Cerebral Palsy.

Background: In children with unilateral cerebral palsy (uCP) virtually nothing is known on the relation between structural brain damage and upper limb (UL) kinematics quantified with three-dimensional movement analysis (3DMA). This explorative study aimed to (1) investigate differences in UL kinematics between children with different lesion timings, i.e., periventricular white matter (PWM) vs. cortical and deep gray matter (CDGM) lesions and (2) to explore the relation between UL kinematics and lesion location and extent within each lesion timing group.Methods: Forty-eight children (age 10.4 ± 2.7 year; 29 boys; 21 right-sided; 33 PWM; 15 CDGM) underwent an UL 3DMA during a reach-to-grasp task. Spatiotemporal parameters [movement duration, (timing of) maximum velocity, trajectory straightness], the Arm Profile Score (APS) and Arm Variable Scores (AVS) were extracted. The APS and AVS refer to the total amount of movement pathology and movement deviations of the wrist, elbow, shoulder, scapula and trunk respectively. Brain lesion location and extent were scored based on FLAIR-images using a semi-quantitative MRI-scale.Results: Children with CDGM lesions showed more aberrant spatiotemporal parameters (p < 0.03) and more movement pathology (APS, p = 0.003) compared to the PWM group, mostly characterized by increased wrist flexion (p = 0.01). In the CDGM group, moderate to high correlations were found between lesion location and extent and duration, timing of maximum velocity and trajectory straightness (r = 0.53–0.90). Lesion location and extent were further moderately correlated with distal UL movement pathology (wrist flexion/extension, elbow pronation/supination, elbow flexion/extension; r = 0.50–0.65) and with the APS (r = 0.51–0.63). In the PWM group, only a few and low correlations were observed, mostly between damage to the PLIC and higher AVS of elbow flexion/extension, shoulder elevation and trunk rotation (r = 0.35–0.42). Regression analysis revealed damage to the temporal lobe with lesion timing as interactor (27%, p = 0.002) and the posterior limb of the internal capsule (PLIC) (7%, p = 0.04) as the strongest predictors, explaining 34% of the variance in APS.Conclusion: UL kinematic deviations are more influenced by lesion location and extent in children with later (CDGM) versus earlier lesions (PWM), except for proximal movement pathology. Damage to the PLIC is a significant predictor for UL movement pathology irrespective of lesion timing.

Lesions in deep gray nuclei after severe traumatic brain injury predict neurologic outcome.

PurposeThis study evaluates the correlation between injuries to deep gray matter nuclei, as quantitated by lesions in these nuclei on MR T2 Fast Spin Echo (T2 FSE) images, with 6-month neurological outcome after severe traumatic brain injury (TBI).Materials and methodsNinety-five patients (80 males, mean age = 36.7y) with severe TBI were prospectively enrolled. All patients underwent a MR scan within the 45 days after the trauma that included a T2 FSE acquisition. A 3D deformable atlas of the deep gray matter was registered to this sequence; deep gray matter lesions (DGML) were evaluated using a semi-quantitative classification scheme. The 6-month outcome was dichotomized into unfavorable (death, vegetative or minimally conscious state) or favorable (minimal or no neurologic deficit) outcome.ResultsSixty-six percent of the patients (63/95) had both satisfactory registration of the 3D atlas on T2 FSE and available clinical follow-up. Patients without DGML had an 89% chance (P = 0.0016) of favorable outcome while those with bilateral DGML had an 80% risk of unfavorable outcome (P = 0.00008). Multivariate analysis based on DGML accurately classified patients with unfavorable neurological outcome in 90.5% of the cases.ConclusionLesions in deep gray matter nuclei may predict long-term outcome after severe TBI with high sensitivity and specificity.

Metabolic counterparts of sodium accumulation in multiple sclerosis: A whole brain 23Na-MRI and fast 1H-MRSI study

Background: Increase of brain total sodium concentrations (TSC) is present in multiple sclerosis (MS), but its pathological involvement has not been assessed yet. Objective: To determine in vivo the metabolic counterpart of brain sodium accumulation. Materials/methods: Whole brain 23Na-MR imaging and 3D-1H-EPSI data were collected in 21 relapsing-remitting multiple sclerosis (RRMS) patients and 20 volunteers. Metabolites and sodium levels were extracted from several regions of grey matter (GM), normal-appearing white matter (NAWM) and white matter (WM) T2 lesions. Metabolic and ionic levels expressed as Z-scores have been averaged over the different compartments and used to explain sodium accumulations through stepwise regression models. Results: MS patients showed significant 23Na accumulations with lower choline and glutamate–glutamine (Glx) levels in GM; 23Na accumulations with lower N-acetyl aspartate (NAA), Glx levels and higher Myo-Inositol (m-Ins) in NAWM; and higher 23Na, m-Ins levels with lower NAA in WM T2 lesions. Regression models showed associations of TSC increase with reduced NAA in GM, NAWM and T2 lesions, as well as higher total-creatine, and smaller decrease of m-Ins in T2 lesions. GM Glx levels were associated with clinical scores. Conclusion: Increase of TSC in RRMS is mainly related to neuronal mitochondrial dysfunction while dysfunction of neuro-glial interactions within GM is linked to clinical scores.

Common brain networks for distinct deficits in visual neglect. A combined structural and tractography MRI approach

Visual neglect is a heterogeneous, multi-component syndrome resulting from right hemisphere damage. Neglect patients do not pay attention to events occurring on their left side, and have a poor functional outcome. The intra-hemispheric location of lesions producing neglect is debated, because studies using different methods reported different locations in the grey matter and in the white matter of the right hemisphere. These reported locations show various patterns of overlapping with the fronto-parietal attention networks demonstrated by functional neuroimaging. We explored the anatomical correlates of neglect patients' performance on distinct tests of neglect. For the first time in neglect anatomy studies, we individually assessed 25 patients with subacute strokes in the right hemisphere, by using a combined structural and diffusion tensor deterministic tractography approach, with separate analyses for each neglect test. The results revealed that lesions in nodes of the ventral attention network (angular and supramarginal gyri) were selectively associated with deficits in performance on all the tests used; damage to other structures correlated with impaired performance on specific tests, such as the bells test (middle and inferior frontal gyri), or the reading test (temporal regions). Importantly, however, white matter damage proved crucial in producing neglect-related deficits. Voxel-based lesion-symptom mapping (VLSM) and tractography consistently revealed that damage to the ventral branch of the superior longitudinal fasciculus (SLF III) and to the inferior fronto-occipital fasciculus (IFOF) predicted pathological scores on line bisection/drawing copy and on the bells test, respectively. Moreover, damage to distinct sectors of SLF III, or combined SLF/IFOF damage, gave rise to different performance profiles. Our results indicate that both grey and white matter lesion analysis must be taken into account to determine the neural correlates of neglect-related deficits. They also suggest that damage to distinct portions of white matter tracts may give rise to distinct clinical signs of neglect, presumably by inducing dysfunction of partly overlapping, but distinct networks.

Clinical Features of Acute Flaccid Myelitis Temporally Associated With an Enterovirus D68 Outbreak: Results of a Nationwide Survey of Acute Flaccid Paralysis in Japan, August-December 2015.

Acute flaccid myelitis (AFM) is an acute flaccid paralysis syndrome with spinal motor neuron involvement of unknown etiology. We investigated the characteristics and prognostic factors of AFM clusters coincident with an enterovirus D68 (EV-D68) outbreak in Japan during autumn 2015. An AFM case series study was conducted following a nationwide survey from August to December 2015. Radiographic and neurophysiologic data were subjected to centralized review, and virology studies were conducted for available specimens. Fifty-nine AFM cases (58 definite, 1 probable) were identified, including 55 children and 4 adults (median age, 4.4 years). The AFM epidemic curve showed strong temporal correlation with EV-D68 detection from pathogen surveillance, but not with other pathogens. EV-D68 was detected in 9 patients: 5 in nasopharyngeal, 2 in stool, 1 in cerebrospinal fluid (adult case), and 1 in tracheal aspiration, nasopharyngeal, and serum samples (a pediatric case with preceding steroid usage). Cases exhibited heterogeneous paralysis patterns from 1- to 4-limb involvement, but all definite cases had longitudinal spinal gray matter lesions on magnetic resonance imaging (median, 20 spinal segments). Cerebrospinal fluid pleocytosis was observed in 50 of 59 cases (85%), and 8 of 29 (28%) were positive for antiganglioside antibodies, as frequently observed in Guillain-Barré syndrome. Fifty-two patients showed variable residual weakness at follow-up. Good prognostic factors included a pretreatment manual muscle strength test unit score >3, normal F-wave persistence, and EV-D68-negative status. EV-D68 may be one of the causative agents for AFM, while host susceptibility factors such as immune response could contribute to AFM development.

TSPO-PET Imaging to Assess Cerebral Microglial Activation in Multiple Sclerosis.

AbstractThe adaptive immune system, particularly T cells and more recently B cells, is considered to play a major role in the pathogenesis of multiple sclerosis (MS). In addition to adaptive immune mechanisms, innate central nervous system (CNS) immunity, particularly mediated by microglia, may play a key role in MS pathogenesis. Microglial activation has been demonstrated throughout the MS disease course and at various locations in the CNS, including white and gray matter lesions as well as normal appearing white and gray matter. Activated microglia overexpress an 18 kilodalton mitochondrial translocator protein (TSPO), which is otherwise expressed at low levels during the resting state. Several positron emission tomography (PET) ligands targeting TSPO have been developed to enable the assessment of microglial activation. In this article, we review the biological basis, methodological aspects, and current status of TSPO-PET imaging in MS and discuss future research directions.

Neuropsychology of Multiple Sclerosis: Looking Back and Moving Forward.

The neuropsychological aspects of multiple sclerosis (MS) have evolved over the past three decades. What was once thought to be a rare occurrence, cognitive dysfunction is now viewed as one of the most disabling symptoms of the disease, with devastating effects on patients' quality of life. This selective review will highlight major innovations and scientific discoveries in the areas of neuropathology, neuroimaging, diagnosis, and treatment that pertain to our understanding of the neuropsychological aspects of MS. Specifically, we focus on the recent discovery that MS produces pathogical lesions of gray matter (GM) that have consequences for cognitive functions. Methods for imaging these GM lesions in MS are discussed along with multimodal imaging studies that integrate structural and functional imaging methods to provide a better understanding of the relationship between cognitive test performance and functional reserve. Innovations in the screening and comprehensive assessment of cognitive disorders are presented along with recent research that examines cognitive dysfunction in pediatric MS. Results of innovative outcome studies in cognitive rehabilitation are discussed. Finally, we highlight trends for potential future innovations over the next decade. (JINS, 2017, 23, 832-842).

Quantitative neuroimaging in mucopolysaccharidoses clinical trials.

The mucopolysaccharidosis (MPS) disorders are rare lysosomal storage disorders caused by mutations in lysosomal enzymes involved in glycosaminoglycan (GAG) degradation. The resulting intracellular accumulation of GAGs leads to widespread tissue and organ dysfunction. In addition to somatic signs and symptoms, patients with MPS can present with neurological manifestations such as cognitive decline, behavioral problems (e.g. hyperactivity and aggressiveness), sleep disturbances, and/or epilepsy. These are associated with significant abnormalities of the central nervous system (CNS), including white and gray matter lesions, brain atrophy, ventriculomegaly, and spinal cord compression. In order to effectively manage and develop therapies for MPS that target neurological disease, it is important to visualize and quantify these CNS abnormalities. This review describes optimal approaches for conducting magnetic resonance imaging assessments in multi-center clinical studies, and summarizes current knowledge from neuroimaging studies in MPS disorders. The content of the review is based on presentations and discussions on these topics that were held during a meeting of an international group of experts.

Cerebral Manifestations of Mitochondrial Disorders.

This review aims at summarizing and discussing previous and recent findings concerning the cerebral manifestations of mitochondrial disorders (MIDs). MIDs frequently present as mitochondrial multiorgan disorder syndrome (MIMODS) either already at onset or later in the course. After the muscle, the brain is the organ second most frequently affected in MIMODS. Cerebral manifestations of MIDs are variable and may present with or without a lesion on imaging or functional studies, but there can be imaging/functional lesions without clinical manifestations. The most well-known cerebral manifestations of MIDs include stroke-like episodes, epilepsy, headache, ataxia, movement disorders, hypopituitarism, muscle weakness, psychiatric abnormalities, nystagmus, white and gray matter lesions, atrophy, basal ganglia calcification, and hypometabolism on 2-deoxy-2-[fluorine-18]fluoro-D-glucose positron-emission tomography. For most MIDs, only symptomatic therapy is currently available. Symptomatic treatment should be supplemented by vitamins, cofactors, and antioxidants. In conclusion, cerebral manifestations of MIDs need to be recognized and appropriately managed because they strongly determine the outcome of MID patients.

Identifying relevant biomarkers of brain injury from structural MRI: Validation using automated approaches in children with unilateral cerebral palsy.

Previous studies have proposed that the early elucidation of brain injury from structural Magnetic Resonance Images (sMRI) is critical for the clinical assessment of children with cerebral palsy (CP). Although distinct aetiologies, including cortical maldevelopments, white and grey matter lesions and ventricular enlargement, have been categorised, these injuries are commonly only assessed in a qualitative fashion. As a result, sMRI remains relatively underexploited for clinical assessments, despite its widespread use. In this study, several automated and validated techniques to automatically quantify these three classes of injury were generated in a large cohort of children (n = 139) aged 5–17, including 95 children diagnosed with unilateral CP. Using a feature selection approach on a training data set (n = 97) to find severity of injury biomarkers predictive of clinical function (motor, cognitive, communicative and visual function), cortical shape and regional lesion burden were most often chosen associated with clinical function. Validating the best models on the unseen test data (n = 42), correlation values ranged between 0.545 and 0.795 (p<0.008), indicating significant associations with clinical function. The measured prevalence of injury, including ventricular enlargement (70%), white and grey matter lesions (55%) and cortical malformations (30%), were similar to the prevalence observed in other cohorts of children with unilateral CP. These findings support the early characterisation of injury from sMRI into previously defined aetiologies as part of standard clinical assessment. Furthermore, the strong and significant association between quantifications of injury observed on structural MRI and multiple clinical scores accord with empirically established structure-function relationships.

Tissue microarray methodology identifies complement pathway activation and dysregulation in progressive multiple sclerosis.

The complement pathway has potential contributions to both white (WM) and grey matter (GM) pathology in Multiple Sclerosis (MS). A quantitative assessment of complement involvement is lacking. Here we describe the use of Tissue MicroArray (TMA) methodology in conjunction with immunohistochemistry to investigate the localization of complement pathway proteins in progressive MS cortical GM and subcortical WM. Antibodies targeting complement proteins C1q, C3b, regulatory proteins C1 inhibitor (C1INH, complement receptor 1 (CR1), clusterin, factor H (FH) and the C5a anaphylatoxin receptor (C5aR) were utilised alongside standard markers of tissue pathology. All stained slides were digitised for quantitative analysis. We found that numbers of cells immunolabelled for HLA-DR, GFAP, C5aR, C1q and C3b were increased in WM lesions (WML) and GM lesions (GML) compared to normal appearing WM (NAWM) and GM (NAGM), respectively. The complement regulators C1INH, CR1, FH and clusterin were more abundant in WM lesions, while the number of C1q+ neurons were increased and the number of C1INH+, clusterin+, FH+ and CR1+ neurons decreased in GM lesions. The number of complement component positive cells (C1q, C3b) correlated with complement regulator expression in WM, but there was no statistical association between complement activation and regulator expression in the GM. We conclude that TMA methodology and quantitative analysis provides evidence of complement dysregulation in MS GML, including an association of the numerical density of C1q+ cells with tissue lesions. Our work confirms that complement activation and dysregulation occur in all cases of progressive MS and suggest that complement may provide potential biomarkers of the disease.

Correlation of clinical findings and brain volume data in multiple sclerosis

Brain volume measurements are becoming an important tool for assessing success in controlling multiple sclerosis (MS) activity. MSmetrix (icometrix) is an easy-to-use platform, specific for MS magnetic resonance imaging (MRI) of the brain. It provides data on total brain volume, grey matter volume and lesion load volume. The objective of the present study was to assess whether disability and the number of relapses during the previous year correlated with brain volume measurements from MSmetrix. Data on 185 icometrix reports from patients with MS were used to evaluate the potential correlation between brain volume measurements and clinical parameters. There was a significant correlation between higher disability and decreased brain volume (total and grey matter). Increased lesion load in the brain and higher number of relapses in the previous year were also independently correlated with decreased brain tissue volume and with increased disability. This is the first study with real-world data to show that icometrix is a relevant tool for the study of brain volume loss in MS.

Impact of Neuronal Membrane Damage on the Local Field Potential in a Large-Scale Simulation of Cerebral Cortex.

Within multiscale brain dynamics, the structure–function relationship between cellular changes at a lower scale and coordinated oscillations at a higher scale is not well understood. This relationship may be particularly relevant for understanding functional impairments after a mild traumatic brain injury (mTBI) when current neuroimaging methods do not reveal morphological changes to the brain common in moderate to severe TBI such as diffuse axonal injury or gray matter lesions. Here, we created a physiology-based model of cerebral cortex using a publicly released modeling framework (GEneral NEural SImulation System) to explore the possibility that performance deficits characteristic of blast-induced mTBI may reflect dysfunctional, local network activity influenced by microscale neuronal damage at the cellular level. We operationalized microscale damage to neurons as the formation of pores on the neuronal membrane based on research using blast paradigms, and in our model, pores were simulated by a change in membrane conductance. We then tracked changes in simulated electrical activity. Our model contained 585 simulated neurons, comprised of 14 types of cortical and thalamic neurons each with its own compartmental morphology and electrophysiological properties. Comparing the functional activity of neurons before and after simulated damage, we found that simulated pores in the membrane reduced both action potential generation and local field potential (LFP) power in the 1–40 Hz range of the power spectrum. Furthermore, the location of damage modulated the strength of these effects: pore formation on simulated axons reduced LFP power more strongly than did pore formation on the soma and the dendrites. These results indicate that even small amounts of cellular damage can negatively impact functional activity of larger scale oscillations, and our findings suggest that multiscale modeling provides a promising avenue to elucidate these relationships.

How does the interaction of presumed timing, location and extent of the underlying brain lesion relate to upper limb function in children with unilateral cerebral palsy?

Upper limb (UL) function in children with unilateral cerebral palsy (CP) vary largely depending on presumed timing, location and extent of brain lesions. These factors might exhibit a complex interaction and the combined prognostic value warrants further investigation. This study aimed to map lesion location and extent and assessed whether these differ according to presumed lesion timing and to determine the impact of structural brain damage on UL function within different lesion timing groups. Seventy-three children with unilateral CP (mean age 10 years 2 months) were classified according to lesion timing: malformations (N=2), periventricular white matter (PWM, N=42) and cortical and deep grey matter (CDGM, N=29) lesions. Neuroanatomical damage was scored using a semi-quantitative MRI scale. UL function was assessed at body function and activity level. CDGM lesions were more pronounced compared to PWM lesions (p=0.0003). Neuroanatomical scores were correlated with a higher degree to UL function in the CDGM group (rs=-0.39 to rs=-0.84) compared to the PWM group (rrb=-0.42 to rs=-0.61). Regression analysis found lesion location and extent to explain 75% and 65% (p<0.02) respectively, of the variance in AHA performance in the CDGM group, but only 24% and 12% (p<0.03) in the PWM group. In the CDGM group, lesion location and extent seems to impact more on UL function compared to the PWM group. In children with PWM lesions, other factors like corticospinal tract (re)organization and structural connectivity may play an additional role.

Language Development and Brain Magnetic Resonance Imaging Characteristics in Preschool Children With Cerebral Palsy.

The purpose of this study was to investigate characteristics of language development in relation to brain magnetic resonance imaging (MRI) characteristics and the other contributing factors to language development in children with cerebral palsy (CP). The study included 172 children with CP who underwent brain MRI and language assessments between 3 and 7 years of age. The MRI characteristics were categorized as normal, malformation, periventricular white matter lesion (PVWL), deep gray matter lesion, focal infarct, cortical/subcortical lesion, and others. Neurodevelopmental outcomes such as ambulatory status, manual ability, cognitive function, and accompanying impairments were assessed. Both receptive and expressive language development quotients (DQs) were significantly related to PVWL or deep gray matter lesion severity. In multivariable analysis, only cognitive function was significantly related to receptive language development, whereas ambulatory status and cognitive function were significantly associated with expressive language development. More than one third of the children had a language developmental discrepancy between receptive and expressive DQs. Children with cortical/subcortical lesions were at high risk for this discrepancy. Cognitive function is a key factor for both receptive and expressive language development. In children with PVWL or deep gray matter lesion, lesion severity seems to be useful to predict language development.

Dynamic MRI follow-up of radiation encephalopathy in the temporal lobe following nasopharyngeal carcinoma radiotherapy.

The natural course of radiation encephalopathy following nasopharyngeal carcinoma (NPC) radiotherapy remains poorly understood. The present study aimed to investigate the magnetic resonance imaging (MRI) characteristics and evolution of radiation encephalopathy. A series of 162 follow-up MRI examinations from 68 NPC patients with radiation encephalopathy in the temporal lobes were analyzed retrospectively. Each component of radiation encephalopathy was defined as follows: i) contrast enhanced lesions were enhanced lesions on contrast enhanced T1-weighted images (T1WI); ii) white matter lesions were lesions of homogeneous hyperintensity on T2-weighted images (T2WI) and hypointensity on T1WI; iii) cysts were round or oval well-defined lesions of hyperintensity on T2WI; iv) hemosiderin deposition were nodular or annular hypointense lesions with lower hypointense than normal white matter on both T1WI and T2WI; v) gray matter lesions were defined as disruption or erosion of hyperintensity in the cortex on T2WI. Contrast enhanced lesions, white matter lesions, gray matter lesions, cysts and hemosiderin deposition were detected in 105 (100.0%), 98 (93.3%), 94 (89.5%), 2 (1.7%) and 2 (1.7%) cases of the 105 initial diagnosed temporal lobe lesions. Contrast enhanced lesions were the most commonly observed, followed by white matter lesions, gray matter lesions, temporal lobe atrophy, cysts and hemosiderin deposition. In addition, 12 new lesions were identified during the follow-up, 4 of which presented as solid enhanced nodular lesions. Importantly, in 11 of the 117 (9.4%) affected temporal lobes, solid enhanced nodular lesions were observed to be the only initial abnormalities to occur. For those enhanced nodular lesions measuring <0.8 cm, no necrosis could be detected. On the contrary, all the contrast enhanced lesions measuring >2.0 cm exhibited a necrotic core. To the best of our knowledge, the present study revealed for the first time solid enhanced nodular lesions as the earliest MRI abnormalities of radiation encephalopathy following NPC radiotherapy.

Lethal high: acute disseminated encephalomyelitis (ADEM) triggered by toxic effect of synthetic cannabinoid black mamba

A previously well 25-year-old man presented with agitation, double incontinence and left-sided incoordination. His symptoms started after smoking a synthetic cannabinoid (black mamba) 5 days earlier. Over 48 hours, he...

Localized over expression of FGF9 in the rat motor cortex reproduces the pathological features of grey matter lesions in progressive multiple sclerosis. (P2.364)

Localized over expression of FGF9 in the rat motor cortex reproduces the pathological features of grey matter lesions in progressive multiple sclerosis. (P2.364)