Sensory Tracts Research Articles

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B cell rich meningeal inflammation associates with increased spinal cord pathology in multiple sclerosis.

Increased inflammation in the cerebral meninges is associated with extensive subpial cortical grey matter pathology in the forebrain and a more severe disease course in a substantial proportion of secondary progressive multiple sclerosis (SPMS) cases. It is not known whether this relationship extends to spinal cord pathology. We assessed the contribution of meningeal and parenchymal immune infiltrates to spinal cord pathology in SPMS cases characterized in the presence (F+) or absence (F−) of lymphoid‐like structures in the forebrain meninges. Transverse cryosections of cervical, thoracic and lumbar cord of 22 SPMS and five control cases were analyzed for CD20+ B cells, CD4+ and CD8+ T cells, microglia/macrophages (IBA‐1+), demyelination (myelin oligodendrocyte glycoprotein+) and axon density (neurofilament‐H+). Lymphoid‐like structures containing follicular dendritic cell networks and dividing B cells were seen in the spinal meninges of 3 out of 11 F+ SPMS cases. CD4+ and CD20+ cell counts were increased in F+ SPMS compared to F− SPMS and controls, whilst axon loss was greatest in motor and sensory tracts of the F+ SPMS cases (P < 0.01). The density of CD20+ B cells of the spinal leptomeninges correlated with CD4+ T cells and total B and T cells of the meninges; with the density of white matter perivascular CD20+ and CD4+ lymphocytes (P < 0.05); with white matter lesion area (P < 0.05); and the extent of axon loss (P < 0.05) in F+ SPMS cases only. We show that the presence of lymphoid‐like structures in the forebrain is associated with a profound spinal cord pathology and local B cell rich meningeal inflammation associates with the extent of cord pathology. Our work supports a principal role for B cells in sustaining inflammation and tissue injury throughout the CNS in the progressive disease stage.

White matter characteristics of motor, sensory and interhemispheric tracts underlying impaired upper limb function in children with unilateral cerebral palsy.

This study explored the role of lesion timing (periventricular white matter versus cortical and deep grey matter lesions) and type of corticospinal tract (CST) wiring pattern (contralateral, bilateral, ipsilateral) on white matter characteristics of the CST, medial lemniscus, superior thalamic radiations and sensorimotor transcallosal fibers in children with unilateral cerebral palsy (CP), and examined theassociation with upper limb function. Thirty-four children (mean age 10 years 7 months ± 2 years 3 months) with unilateral CP underwent a comprehensive upper limb evaluation and diffusion weighted imaging (75 directions, b value 2800). Streamline count, fractional anisotropy and mean diffusivity were extracted from the targeted tracts and asymmetry indices were additionally calculated. Transcranial magnetic stimulation was applied to assess the CST wiring pattern. Results showed a more damaged CST in children with cortical and deep grey matter lesions (N = 10) and ipsilateral CST projections (N = 11) compared to children with periventricular white matter lesions (N = 24; p < 0.02) and contralateral CST projections (N = 9; p < 0.025), respectively. Moderate to high correlations were found between diffusion metrics of the targeted tracts and upper limb function (r = 0.45-0.72; p < 0.01). Asymmetry indices of the CST and sensory tracts could best explain bimanual performance (74%, p < 0.0001) and unimanual capacity (50%, p = 0.004). Adding lesion timing and CST wiring pattern did not further improve the model of bimanual performance, while for unimanual capacity lesion timing was additionally retained (58%, p = 0.0002). These results contribute to a better understanding of the underlying neuropathology of upper limb function in children with unilateral CP and point towards a clinical potential of tractography.

척추 수술의 수술중신경계감시를 위한 기본 해부학: 운동신경로와 감각신경로

척추 수술의 수술중신경계감시를 위한 기본 해부학: 운동신경로와 감각신경로

An AARS variant as the likely cause of Swedish type hereditary diffuse leukoencephalopathy with spheroids

Swedish type Hereditary Diffuse Leukoencephalopathy with Spheroids (HDLS-S) is a severe adult-onset leukoencephalopathy with the histopathological hallmark of neuraxonal degeneration with spheroids, described in a large family with a dominant inheritance pattern. The initial stage of the disease is dominated by frontal lobe symptoms that develop into a rapidly advancing encephalopathy with pyramidal, deep sensory, extrapyramidal and optic tract symptoms. Median survival is less than 10 years. Recently, pathogenic mutations in CSF1R were reported in a clinically and histologically similar leukoencephalopathy segregating in several families. Still, the cause of HDLS-S remained elusive since its initial description in 1984, with no CSF1R mutations identified in the family. Here we update the original findings associated with HDLS-S after a systematic and recent assessment of several family members. We also report the results from exome sequencing analyses indicating the p.Cys152Phe variant in the alanyl tRNA synthetase (AARS) gene as the probable cause of this disease. The variant affects an amino acid located in the aminoacylation domain of the protein and does not cause differences in splicing or expression in the brain. Brain pathology in one case after 10 years of disease duration showed the end stage of the disease to be characterized by widespread liquefaction of the white matter leaving only some macrophages and glial cells behind the centrifugally progressing front. These results point to AARS as a candidate gene for rapidly progressing adult-onset CSF1R-negative leukoencephalopathies.

Childhood-onset autosomal recessive ataxias: a cross-sectional study from Turkey.

Autosomal recessive ataxias (ARAs) are a heterogeneous group of inherited neurodegenerative disorders that affect the cerebellum, the spinocerebellar tract, and/or the sensory tracts of the spinal cord. This study is aimed at establishing molecular classification and phenotypic correlation of childhood-onset ARAs in Southeast Anatolia of Turkey. Sixty-five children (aged 0 to 18) from 40 unrelated families who were analyzed through hereditary ataxia NGS panel between the years of 2015-2018 were selected for the study. Seventeen different, clinically significant ARA-related pathogenic variants were detected in 33 of 40 families (82.5%), 12 of which were noted to be unreported variants. Among these 33 families, 24 had ATM-related (72.72%), four had SACS-related (12.12%), three had COQ8A-related (9.09%), and two had APTX-related (6.06%) pathogenic variants. The c.3576G>A (p.K1192=) was the most common homozygous pathogenic ATM variant (33.33%) that was associated with milder phenotype of ataxia telangiectasia (AT) with the onset of age of 3. Patients with SACS variants demonstrated developmental delay and progressive ataxia before the age of 3. Slowly progressive ataxia and intellectual disability were the common clinical manifestations of the patients with homozygous c.1396delG (p. E466Rfs*11) pathogenic variant in COQ8A. Homozygous APTX c.689T>G (p.V230G) pathogenic variant was identified in two patients who had chief complaint of ataxic gait onset after puberty. The most common types of ARAs in this region are AT- and Charlevoix-Saguenay-type spastic ataxia. ATM gene analysis should be performed foremost on children presenting early-onset ataxia from Southeastern Anatolia. If there is a concomitant peripheral neuron involvement, SACS gene analysis should be preferred. This valuable data will be a guide for the first step molecular diagnostic approach before requesting the NGS panel for ARA.

POLR3A-related spastic ataxia: new mutations and a look into the phenotype.

Adolescent-onset spastic ataxia is a proposed novel phenotype in compound heterozygous carriers of an intronic mutation (c.1909 + 22G > A) in the POLR3A gene. Here, we present ten new cases of POLR3A-related spastic ataxia and discuss the genetic, clinical and imaging findings. Patients belonged to six pedigrees with hereditary spastic paraplegia or cerebellar ataxia of unknown origin. All affected subjects presented with compound heterozygous variants, comprising c.1909 + 22G > A in combination in each pedigree with one of the following novel mutations (Thr596Met, Tyr665LeufsTer11, Glu198Ter, c.646-687_1185 + 844del). The new mutations segregated with the phenotype in all families. The phenotype combined variable cerebellar ataxia, gait and lower limb spasticity, involvement of central sensory tracts and in some cases also intention tremor. The reportedly characteristic hyperintensity along the superior cerebellar peduncle on MRI was observed in ~ 80% of the cases. Our study extends the clinical and molecular phenotype further supporting the pathogenic role of the c.1909 + 22G4A intronic mutation and identifying four novel causative mutations in POLR3A-related spastic ataxia. Certain characteristic MRI features may be useful to guide genetic diagnosis.

Clinical Study of Thirteen Patients with Spinal Cord Infarction

BackgroundA concept of sensory tracts in the spinal cord has been established in relation to a dorsolateral pathway which is located in the posterior part of the lateral column and conveys the deep sense. MethodsThe clinical status at onset, neurological symptoms, and magnetic resonance imaging (MRI) findings in 13 patients of spinal cord infarction were studied. ResultsThe clinical status was acute in 11 patients and subacute in 2 patients. Palsy of the extremities was noted in 11 patients. Segmental sensory disturbance was shown in all patients. One patient showed disturbance of all senses and paraplegia, which indicated transverse myelopathy. In the other 12 patients, 11 patients showed impairment of pain sense although joint position sense was preserved, excluding 1 patient whose sensory disturbance showed dysesthesia alone. In these 11 patients, soft touch and vibration senses were impaired in 7 patients. Abnormality of spinal cord MRI was detected 7 patients. The lesions were located in the cervical cord in 3 patients, cervical to thoracic cord in 1 patient, and thoracic cord in 3 patients. ConclusionsIn the 11 patients in whom pain sense was impaired and joint position sense was preserved, involvement of the anterior spinal cord artery (ASCA) was the mainstay. Impairment of vibration sense was accompanied in 7 patients in patients of ASCA infarction. It was speculated that impairment of vibration sense can occur in patients with ASCA infarction whose ischemia spread to the dorsolateral pathway in the posterior part of the lateral column.

Nutritive sucking abnormalities and brain microstructural abnormalities in infants with established brain injury: a pilot study.

To determine the relationship between nutritive sucking and microstructural integrity of sensorimotor tracts in newborns with brain injury. Diffusion imaging was performed in ten newborns with brain injury. Nutritive sucking was assessed using Nfant®. The motor, sensory, and corpus callosum tracts were reconstructed via tractography. Fractional anisotropy, radial, axial, and mean diffusivity were estimated for these tracts. Multiple regression models were developed to test the association between sucking features and diffusion parameters. Low-sucking smoothness correlated with low-fractional anisotropy of motor tracts (p = 0.0096). High-sucking irregularity correlated with high-mean diffusivity of motor (p = 0.030) and corpus callosum tracts (p = 0.032). For sensory tracts, high-sucking irregularity (p = 0.018) and low-smoothness variability (p = 0.002) correlated with high-mean diffusivity. We show a correlation between neuroimaging-demonstrated microstructural brain abnormalities and variations in sucking patterns of newborns. The consistency of this relationship should be shown on larger cohorts.

Neural Correlates of Passive Position Finger Sense After Stroke

Background. Proprioception of fingers is essential for motor control. Reduced proprioception is common after stroke and is associated with longer hospitalization and reduced quality of life. Neural correlates of proprioception deficits after stroke remain incompletely understood, partly because of weaknesses of clinical proprioception assessments. Objective. To examine the neural basis of finger proprioception deficits after stroke. We hypothesized that a model incorporating both neural injury and neural function of the somatosensory system is necessary for delineating proprioception deficits poststroke. Methods. Finger proprioception was measured using a robot in 27 individuals with chronic unilateral stroke; measures of neural injury (damage to gray and white matter, including corticospinal and thalamocortical sensory tracts), neural function (activation of and connectivity of cortical sensorimotor areas), and clinical status (demographics and behavioral measures) were also assessed. Results. Impairment in finger proprioception was present contralesionally in 67% and bilaterally in 56%. Robotic measures of proprioception deficits were more sensitive than standard scales and were specific to proprioception. Multivariable modeling found that contralesional proprioception deficits were best explained (r2 = 0.63; P = .0006) by a combination of neural function (connectivity between ipsilesional secondary somatosensory cortex and ipsilesional primary motor cortex) and neural injury (total sensory system injury). Conclusions. Impairment of finger proprioception occurs frequently after stroke and is best measured using a quantitative device such as a robot. A model containing a measure of neural function plus a measure of neural injury best explained proprioception performance. These measurements might be useful in the development of novel neurorehabilitation therapies.

062 Alcohol associated toxic myelopathy with normal hepatic function

IntroductionAlcohol related neurological dysfunction affects the central and peripheral nervous system. We present a rare consequence of excessive alcohol consumption. A 42-year-old female consuming 2 bottles of wine daily for the preceding 5 years presented with 12 months of progressive gait disturbance. Examination revealed a spastic paraparesis with prominent dorsal column signs. Extensive work up found no alternate cause for her presentation. The final diagnosis was direct alcohol mediated toxic myelopathy. We reviewed the current literature on this rare condition.MethodsWe searched PubMED/OVID databases with the terms ‘alcohol AND myelopathy’.ResultsThere is a paucity of research on this clinical entity. Sage et al.1 described 5 well-nourished alcoholics presenting with a progressive myelopathy. As with our patient, routine laboratory tests, including nutritional screen, were normal. CT Myelogram revealed no structural cause. CSF was normal. In contrast, a myelopathic syndrome can occur in alcoholic hepatic failure, attributed to portosystemic shunting of blood, with resultant hyper-ammonaemia and demyelination of corticospinal tracts.2–4ConclusionAlcohol associated toxic myelopathy is a rare entity, distinct from hepatic myelopathy. It is thought to result from direct toxic effects of ethanol on corticospinal and large myelinated sensory tracts. The sensory involvement is unique for this entity, which distinguishes it from hepatic myelopathy, where corticospinal involvement predominates. It is prudent to look for other potentially treatable secondary causes of myelopathy. Abstinence from alcohol results in modest improvement in symptoms. Minimal literature exists on this clinical entity and further research is required.ReferencesSage JI, et al. Alcoholic myelopathy without substantial liver disease. A syndrome of progressive dorsal and lateral column dysfunction. Arch Neurol. 1984 Sep;41(9):999–1001.Premkumar M, et al. Hepatic Myelopathy in a Patient with Decompensated Alcoholic Cirrhosis and Portal Colopathy. Volume 2012, Article ID 735906, 4 pages.Koo JE, et al. Hepatic myelopathy as a presenting neurological complication in patients with cirrhosis and spontaneous splenorenal shunt. Korean J Hepatol. 2008 Mar;14(1):89–96.Kori P, et al. Hepatic myelopathy: an unusual neurological complication of chronic liver disease presenting as quadriparesis. BMJ Case Rep. 2013; 2013: bcr2013009078.

Microstructural integrity of corticospinal and medial lemniscus tracts: insights from diffusion tensor tractography of right-hand amputees

Reductions in sensory and motor activity following unilateral upper limb amputation during adulthood are associated with widespread, activity-dependent reorganization of the gray matter and white matter through the central nervous system. Likewise, in cases of congenital limb absence there is evidence that limited afferent or efferent activity affects the structural integrity of white matter pathways serving the affected side. Evidence that the structural integrity of mature sensory and motor tracts controlling the lost upper limb exhibits similar activity dependence is, however, sparse and inconsistent. Here we used diffusion tensor tractography to test whether amputation of the dominant right hand during adulthood (n = 16) alters the microstructural integrity of the major sensory (medial lemniscus, ML) and motor (corticospinal tract, CST) pathways controlling missing hand function. Consistent with prior findings, healthy control subjects (n = 27) exhibited higher fractional anisotropy (FA), an index of white matter microstructural integrity, within dominant left CST and nondominant right ML. Critically, in contrast to what might be expected if the microstructural organization of these tracts is activity dependent, these asymmetries persisted in amputees. Moreover, we failed to detect any differences in dominant left ML or CST between healthy control subjects and amputees. Our results are consistent with these white matter tracts being robust to changes in activity once mature or that continued use of the residual limb (in a compensatory fashion or with prosthesis) provides stimulation sufficient to maintain tract integrity. NEW & NOTEWORTHY We report that unilateral hand amputation in adults has no significant effects on the structure of major sensory or motor pathways contralateral to the amputation. Our results are consistent with the organization of these white matter tracts being robust to changes in activity once mature or that continued use of the residual limb (with or without a prosthesis) provides stimulation sufficient to maintain tract integrity.

Diffusiontensor MRI tractography in patients with children’s cerebral palsy: assessment of structural lesions of conduction tracts

Introduction. The application of diffusion-tensor (DT)-MRI tractography in patients with children S cerebral palsy (CP) allows to establish pathophysiological mechanisms of the development of motor and sensory impairments, to perform a clinical and neuroimaging comparison, as well as to determine correlations between lesions of the conduction tracts and neurological deficits. Aim. For the determination of changes in fractional anisotropy (FA) and mean diffusivity coefficient (MDC), obtained with DT-MRI in the corticospinal and sensory tracts, structures of the corpus callosum in spastic forms of CP. Materials and methods. There were examined 105 children with spastic forms of CP (spastic tetraparesis - 47, spastic diplegia - 38, hemiparetic form - 20) and 50 children without neurological deficit, at the age of 2-18 years. In all CP patients the severity of motor deficit was evaluated according to Gross Motor Function Classification System (GMFCS). DT-MRI was performed in all cases with the use of devices of General Electric (US), under magnetic field strength of 1.5T and 3T, with the calculation of the FA and the MDC in areas of interest - cerebral peduncles the brain stem, the posterior limb of the internal capsule, the genu and splenium of the corpus callosum, posterior thalamic radiation, postcentral gyrus, the thalamus. Results. There was established the distribution of children according to the GMFCS scale: I - 14 (13,4%), II - 19 (18,1%), III - 20 (19%), IV- 10 (9,5%), V- 42 (40%) cases. The severity of motor impairment on the GMFCS scale closely correlated with the values of FA and ADC in cerebral peduncles, posterior limb of the internal capsule, posterior thalamic radiance, genu of the corpus callosum. Conclusion. DT-MRI enables to assess adequately the changes in the white matter of the brain, structural andfunctional state of the motor and sensory conduction tracts, gives a possibility to predict the development of a child with CP.

Proprioception and motor performance after stroke: An examination of diffusion properties in sensory and motor pathways.

Proprioceptive and motor impairments commonly occur after stroke. Relationships between corticospinal tract (CST) fractional anisotropy (FA) and motor recovery have been identified. However, the relationship between sensory tract microstructure and proprioceptive recovery remains unexplored. Using probabilistic tractography, we examined the relationship between diffusion metrics in three tracts known to contain proprioceptive information (a) dorsal-column medial-lemniscal (DCML), (b) postcentral gyrus to supramarginal gyrus (POCG-SMG), (c) postcentral gyrus to Heschl's gyrus (POCG-HG) and proprioception at 1 (n = 26) and 6 months (n = 19) poststroke. Proprioception was assessed using two robotic tasks. Motor performance was also assessed robotically and compared to CST diffusion metrics. At 1-month poststroke, a nonsignificant relationship (r = -0.43, p = 0.05) was observed between DCML-FA and proprioceptive impairment. A moderate relationship was identified between POCG-SMG FA and POCG-HG FA and proprioceptive impairment (r = -0.47, p = 0.001 and r = -0.51, p = 0.008, respectively). No relationships were significant at 6 months poststroke. Similar to previous studies, lower CST-FA correlated with motor impairment at 1 month poststroke (r = -0.58, p = 0.002). While CST-FA is considered a predictor of motor impairment, our findings suggest that the relationship between FA and tracts containing proprioceptive information is not as straightforward and highlights the importance of sensory association areas in proprioception.

Multisensory integration in rodent tactile but not visual thalamus

Behavioural performance requires a coherent perception of environmental features that address multiple senses. These diverse sensory inputs are integrated in primary sensory cortices, yet it is still largely unknown whether their convergence occurs even earlier along the sensory tract. Here we investigate the role of putatively modality-specific first-order (FO) thalamic nuclei (ventral posteromedial nucleus (VPM), dorsal lateral geniculate nucleus (dLGN)) and their interactions with primary sensory cortices (S1, V1) for multisensory integration in pigmented rats in vivo. We show that bimodal stimulation (i.e. simultaneous light flash and whisker deflection) enhances sensory evoked activity in VPM, but not dLGN. Moreover, cross-modal stimuli reset the phase of thalamic network oscillations and strengthen the coupling efficiency between VPM and S1, but not between dLGN and V1. Finally, the information flow from VPM to S1 is enhanced. Thus, FO tactile, but not visual, thalamus processes and relays sensory inputs from multiple senses, revealing a functional difference between sensory thalamic nuclei during multisensory integration.

Diffusion Tensor Imaging Assessment of Regional White Matter Changes in the Cervical and Thoracic Spinal Cord in Pediatric Subjects.

There are no studies to date,describing changes in the diffusion tensor imaging (DTI) metrics of the white matter (WM) regions of the entire cervical and thoracic spinal cord (SC) remote from the lesion in pediatric spinal cord injury (SCI) subjects. The purpose of this study was to determine whether DTI at sites cephalad and caudal to a lesion provides measures of cord abnormalities in children with chronic SCI. A retrospective study included 10 typically developing subjects (TD) and 10 subjects with chronic SCI who underwent SC imaging in 2014-2017. Axial diffusion tensor images using an inner field of view DTI sequence were acquired to cover the entire cervical and thoracic SC. Regions of interest were drawn on the SC WM: right and left lateral (motor), ventral (motor), and dorsal (sensory) tracts. To detect differences in DTI metrics between TD and SCI of the cord, a one way analysis of variance with pooled t test was performed. A stepwise regression analysis was performed to assess the correlation between DTI metrics and clinical scores. In motor and sensory tracts, fractional anisotropy (FA) and axial diffusivity (AD) were significantly decreased in the proximal segments of the caudal cord. In motor tracts cephalad to the lesion, FA was significantly decreased whereas AD was significantly increased in the proximal segment; however, AD was decreased in the distal and middle segments. International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) total score was significantly correlated with FA and AD of the motor and sensory tracts cephalad to the lesion. This study demonstrates that FA and AD have the potential to be sensitive biomarkers of the full extent of cord injury and might be useful in detecting remote injuries to the SC and in guiding new treatments.

Maturation of sensory and motor tracts in children with congenital hemiplegia using diffusion tensor imaging

Maturation of sensory and motor tracts in children with congenital hemiplegia using diffusion tensor imaging

Dorsal Root Ganglion Maintains Stemness of Bone Marrow Mesenchymal Stem Cells by Enhancing Autophagy through the AMPK/mTOR Pathway in a Coculture System.

Our previous studies found that sensory nerve tracts implanted in tissue-engineered bone (TEB) could result in better osteogenesis. To explore the mechanism of the sensory nerve promoting osteogenesis in TEB in vitro, a transwell coculture experiment was designed between dorsal root ganglion (DRG) cells and bone marrow mesenchymal stem cells (BMSCs). BMSC proliferation was determined by CCK8 assay, and osteo-, chondro-, and adipogenic differentiation were assessed by alizarin red, alcian blue, and oil red staining. We found that the proliferation and multipotent differentiation of BMSCs were all enhanced in the coculture group compared to the BMSCs group. Crystal violet staining showed that the clone-forming ability of BMSCs in the coculture group was also enhanced and mRNA levels of Sox2, Nanog, and Oct4 were significantly upregulated in the coculture group. Moreover, the autophagy level of BMSCs, regulating their stemness, was promoted in the coculture group, mediated by the AMPK/mTOR pathway. In addition, AMPK inhibitor compound C could significantly downregulate the protein expression of LC3 and the mRNA level of stemness genes in the coculture group. Finally, we found that the NK1 receptor antagonist, aprepitant, could partly block this effect, which indicated that substance P played an important role in the effect. Together, we conclude that DRG could maintain the stemness of BMSCs by enhancing autophagy through the AMPK/mTOR pathway in a transwell coculture system, which may help explain the better osteogenesis after implantation of the sensory nerve into TEB.

Cerebellar peduncle injury predicts motor impairments in preterm infants: A quantitative tractography study at term-equivalent age

PurposeCerebellar injury is well established as an important finding in preterm infants with cerebral palsy (CP). In this study, we investigated associations between injury to the cerebellar peduncles and motor impairments in preterm infants using quantitative tractography at term-equivalent age, which represents an early phase before the onset of motor impairments. MethodsWe studied 64 preterm infants who were born at <33 weeks gestational age. These infants were divided into three groups: CP, Non-CP (defined as infants with periventricular leukomalacia but having normal motor function), and a Normal group. Diffusion tensor imaging was performed at term-equivalent age and motor function was assessed no earlier than a corrected age of 2 years. Using tractography, we measured fractional anisotropy (FA) and apparent diffusion coefficient (ADC) of the superior cerebellar peduncles (SCP) and middle cerebellar peduncles (MCP), as well as the motor/sensory tracts. ResultsThe infants in the CP group had significantly lower FA of the SCP and sensory tract than those in the other groups. There was no significant difference in FA and ADC of the motor tract among the three groups. Severity of CP had a significant correlation with FA of the MCP, but not with the FA of other white matter tracts. ConclusionOur results suggested that the infants with CP had injuries of the ascending tracts (e.g. the SCP and sensory tract), and that additional MCP injury might increase the severity of CP. Quantitative tractography assessment at term-equivalent age may be useful for screening preterm infants for prediction of future motor impairments.

Axonal regeneration of different tracts following transplants of human glial restricted progenitors into the injured spinal cord in rats

The goal of this study was to compare the efficacy of human glial restricted progenitors (hGRPs) in promoting axonal growth of different tracts. We examined the potential of hGRPs grafted into a cervical (C4) dorsal column lesion to test sensory axons, and into a C4 hemisection to test motor tracts. The hGRPs, thawed from frozen stocks, were suspended in a PureCol matrix and grafted acutely into a C4 dorsal column or hemisection lesion. Control rats received PureCol only. Five weeks after transplantation, all transplanted cells survived in rats with the dorsal column lesion but only about half of the grafts in the hemisection. In the dorsal column lesion group, few sensory axons grew short distances into the lesion site of control animals. The presence of hGRPs transplants enhanced axonal growth significantly farther into the transplants. In the hemisection group, coerulospinal axons extended similarly into both control and transplant groups with no enhancement by the presence of hGRPs. Rubrospinal axons did not grow into the lesion even in the presence of hGRPs. However, reticulospinal and raphespinal axons grew for a significantly longer distance into the transplants. These results demonstrate the differential capacity of axonal growth/regeneration of the motor and sensory tracts based on their intrinsic abilities as well as their response to the modified environment induced by the hGRPs transplants. We conclude that hGRP transplants can modify the injury site for axon growth of sensory and some motor tracts, and suggest they could be combined with other interventions to restore connectivity.