Selective atrophy of the connected deepest cortical layers following small subcortical infarct

Neurology ◽  
2019 ◽  
Vol 92 (6) ◽  
pp. e567-e575 ◽  
Author(s):  
Eyal Lotan ◽  
Ido Tavor ◽  
Daniel Barazany ◽  
Shani Ben-Amitay ◽  
Chen Hoffmann ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Corticospinal Tract ◽  
Healthy Controls ◽  
Cortical Layers ◽  
Clinical Symptomatology ◽  
Cortical Thinning ◽  
Corticospinal Tracts ◽  
Microstructural Integrity ◽  
Subcortical Infarct

ObjectiveTo explore whether in patients with chronic small subcortical infarct the cortical layers of the connected cortex are differentially affected and whether these differences correlate with clinical symptomatology.MethodsTwenty patients with a history of chronic small subcortical infarct affecting the corticospinal tracts and 15 healthy controls were included. Connected primary motor cortex was identified with tractography starting from infarct. T1-component probability maps were calculated from T1 relaxation 3T MRI, dividing the cortex into 5 laminar gaussian classes.ResultsFocal cortical thinning was observed in the connected cortex and specifically only in its deepest laminar class compared to the nonaffected mirrored cortex (p < 0.001). There was loss of microstructural integrity of the affected corticospinal tract with increased mean diffusivity and decreased fractional anisotropy compared to the contralateral nonaffected tract (p ≤ 0.002). Clinical scores were correlated with microstructural damage of the corticospinal tracts and with thinning of the cortex and specifically only its deepest laminar class (p < 0.001). No differences were found in the laminar thickness pattern of the bilateral primary motor cortices or in the microstructural integrity of the bilateral corticospinal tracts in the healthy controls.ConclusionOur results support the concept of secondary neurodegeneration of connected primary motor cortex after a small subcortical infarct affecting the corticospinal tract, with observations that the main cortical thinning occurs in the deepest cortex and that the clinical symptomatology is correlated with this cortical atrophy pattern. Our findings may contribute to a better understanding of structural reorganization and functional outcomes after stroke.

Corticospinal tract integrity is related to primary motor cortex thinning in relapsing–remitting multiple sclerosis

2015 ◽  
Vol 21 (14) ◽  
pp. 1771-1780 ◽  
Author(s):  
Niels Bergsland ◽  
Maria Marcella Laganà ◽  
Eleonora Tavazzi ◽  
Matteo Caffini ◽  
Paola Tortorella ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Motor Cortex ◽  
Linear Regression ◽  
Multiple Linear Regression ◽  
Primary Motor Cortex ◽  
Corticospinal Tract ◽  
Healthy Controls ◽  
Relapsing Remitting ◽  
Relapsing Remitting Multiple Sclerosis

Background: The relationship between white matter injury and cortical atrophy development in relapsing–remitting multiple sclerosis (RRMS) remains unclear. Objectives: To investigate the associations between corticospinal tract integrity and cortical morphology measures of the primary motor cortex in RRMS patients and healthy controls. Methods: 51 RRMS patients and 30 healthy controls underwent MRI examination for cortical reconstruction and assessment of corticospinal tract integrity. Partial correlation and multiple linear regression analyses were used to investigate the associations of focal and normal appearing white matter (NAWM) injury of the corticospinal tract with thickness and surface area measures of the primary motor cortex. Relationships between MRI measures and clinical disability as assessed by the Expanded Disability Status Scale and disease duration were also investigated. Results: In patients only, decreased cortical thickness was related to increased corticospinal tract NAWM mean, axial and radial diffusivities in addition to corticospinal tract lesion volume. The final multiple linear regression model for PMC thickness retained only NAWM axial diffusivity as a significant predictor (adjusted R2= 0.270, p= 0.001). Clinical measures were associated with NAWM corticospinal tract integrity measures. Conclusions: Primary motor cortex thinning in RRMS is related to alterations in connected white matter and is best explained by decreased NAWM integrity.

Abstract 12: Effect of Corticospinal Tract Injury on Motor Cortex Function and Connectivity After Stroke

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Steven C Cramer ◽  
Jessica M Cassidy ◽  
Morgan Ingemanson ◽  
Ramesh Srinivasan
Keyword(s):  
Motor Cortex ◽  
Frequency Band ◽  
Primary Motor Cortex ◽  
Corticospinal Tract ◽  
Premotor Cortex ◽  
Structural Mri ◽  
Network Activity ◽  
Neural Function ◽  
Lead System ◽  
Hemiparetic Stroke

Background and Purpose: Behavioral outcome after stroke is the product of both neural injury and neural function. Little is known about how injury to the corticospinal tract (CST) affects the function of motor cortex. The purpose of this study was to understand how subcortical injury to the CST affects function and connectivity of motor cortex. Methods: Patients with chronic hemiparetic stroke completed (1) a 3-minute resting-state EEG recording using a dense-array (256-lead) system, (2) a structural MRI scan, and (3) behavioral testing. Motor cortex activity was defined as EEG power within the high beta (20-30 Hz) frequency band commonly associated with motor network activity. Motor cortex connectivity was defined as coherence in the same frequency band. CST injury was defined as % lesion overlap with CST. Results: Of the 39 subjects (56 ± 14 years, 10 females, 15 ± 25 months post-stroke), none had injury to ipsilesional primary motor cortex (M1). Spearman correlation analyses revealed that increased CST injury was significantly related to reduced cortical activity in EEG leads overlying M1 (r= -0.48, p <0.002), dorsal premotor cortex (r= -0.41, p= 0.01), and supplementary motor area (r= -0.41, p= 0.01), but not in any other brain region, bilaterally. However, increased CST injury was not associated with any changes in M1 connectivity. Arm motor status (Fugl-Meyer score) tended to be associated with increased CST injury (r= -0.28, p= 0.08) but had no relationship with M1 connectivity. Conclusions: Increased CST injury after stroke is associated with decreased activity in those motor areas that issue descending fibers via this tract, a finding consistent with prior reports indicating that axonal injury modulates upstream function of surviving cortical elements. Increased CST injury was not associated with changes in M1 connectivity, suggesting a retained capacity for plasticity in support of behavioral recovery.

scholarly journals Corticospinal Tract Anatomy and Functional Connectivity of Primary Motor Cortex in Autism

2015 ◽  
Vol 54 (10) ◽  
pp. 859-867 ◽  
Author(s):  
Ruth A. Carper ◽  
Seraphina Solders ◽  
Jeffrey M. Treiber ◽  
Inna Fishman ◽  
Ralph-Axel Müller
Keyword(s):  
Functional Connectivity ◽  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Corticospinal Tract

scholarly journals Surface-based Map Plasticity of the Sensorimotor Cortex in Hip Disorder at Local and Extensive Levels: A Resting-state fMRI Study

2020 ◽  
Author(s):  
Jie Ma ◽  
Xu-Yun Hua ◽  
Mou-Xiong Zheng ◽  
Jia-Jia Wu ◽  
Bei-Bei Huo ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Cortical Thickness ◽  
Resting State ◽  
Primary Motor Cortex ◽  
Premotor Cortex ◽  
Frontal Eye Field ◽  
Healthy Controls ◽  
Eye Field ◽  
Somatotopic Map ◽  
The Right

Abstract Background: Pain is one of the manifestations of hip disorder and has been proven to lead to the remodeling of somatotopic map plasticity in the cortex. However, it’s not clear whether hip disorder with pain induces somatotopic map plasticity in the cortex. We aimed to evaluate the surface-based map plasticity of the somatotopic cortex in hip disorder at local and extensive levels by resting-state functional magnetic resonance imaging (rs-fMRI).Methods: 20 patients with osteonecrosis of the femoral head (ONFH) (12 males and 8 females, age= 56.80±13.60 years) with Visual Analogue Scale (VAS) scores ≥ 4 and 20 healthy controls (9 males and 11 females, age= 54.56±10.23 years) were enrolled in this study. rs-fMRI data and T1 imaging data were collected, and surface-based regional homogeneity (ReHo), seed-based functional connectivity (FC), cortical thickness and the volume of subcortical gray nuclei were calculated.Results: Compared with the healthy controls, the ONFH patients showed significantly increased surface-based ReHo in areas distributed mainly in the left dorsolateral prefrontal cortex and frontal eye field, the right frontal eye field and the premotor cortex and decreased surface-based ReHo in the right primary motor cortex and primary sensory cortex. When the area with decreased surface-based ReHo in the frontal eye field and right premotor cortex was used as the regions of interest (ROI), compared with the controls, the ONFH patients displayed increased FC in the right middle frontal cortex and right inferior parietal cortex and decreased FC in the right precentral cortex and right middle occipital cortex. ONFH patients also showed significantly decreased cortical thickness in the para-insular area, supplementary motor cortex area and frontal eye field and decreased volume of subcortical gray matter nuclei in the right nucleus accumbens (479.32±88.26 vs 539.44±68.36, P=0.026). Conclusions: Hip disorder patients showed cortical plasticity changes, mainly in sensorimotor and pain-related regions.

scholarly journals Habenula functional resting-state connectivity in pediatric CRPS

2014 ◽  
Vol 111 (2) ◽  
pp. 239-247 ◽  
Author(s):  
Nathalie Erpelding ◽  
Simona Sava ◽  
Laura E. Simons ◽  
Alyssa Lebel ◽  
Paul Serrano ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Resting State ◽  
Primary Motor Cortex ◽  
Premotor Cortex ◽  
Brain Regions ◽  
Healthy Controls ◽  
Resting State Functional Connectivity ◽  
Dorsal Thalamus ◽  
Functional Connections ◽  
Midcingulate Cortex

The habenula (Hb) is a small brain structure located in the posterior end of the medial dorsal thalamus and through medial (MHb) and lateral (LHb) Hb connections, it acts as a conduit of information between forebrain and brainstem structures. The role of the Hb in pain processing is well documented in animals and recently also in acute experimental pain in humans. However, its function remains unknown in chronic pain disorders. Here, we investigated Hb resting-state functional connectivity (rsFC) in patients with complex regional pain syndrome (CRPS) compared with healthy controls. Twelve pediatric patients with unilateral lower-extremity CRPS (9 females; 10–17 yr) and 12 age- and sex-matched healthy controls provided informed consent to participate in the study. In healthy controls, Hb functional connections largely overlapped with previously described anatomical connections in cortical, subcortical, and brainstem structures. Compared with controls, patients exhibited an overall Hb rsFC reduction with the rest of the brain and, specifically, with the anterior midcingulate cortex, dorsolateral prefrontal cortex, supplementary motor cortex, primary motor cortex, and premotor cortex. Our results suggest that Hb rsFC parallels anatomical Hb connections in the healthy state and that overall Hb rsFC is reduced in patients, particularly connections with forebrain areas. Patients' decreased Hb rsFC to brain regions implicated in motor, affective, cognitive, and pain inhibitory/modulatory processes may contribute to their symptomatology.

Reduced Muscle Selectivity During Individuated Finger Movements in Humans After Damage to the Motor Cortex or Corticospinal Tract

2004 ◽  
Vol 91 (4) ◽  
pp. 1722-1733 ◽  
Author(s):  
Catherine E. Lang ◽  
Marc H. Schieber
Keyword(s):  
Motor Cortex ◽  
Muscle Activation ◽  
Primary Motor Cortex ◽  
Corticospinal Tract ◽  
Hand Function ◽  
Descending Pathways ◽  
Finger Movements ◽  
Abductor Pollicis Brevis ◽  
Flexion Extension ◽  
Pure Motor

We investigated how damage to the motor cortex or corticospinal tract affects the selective activation of finger muscles in humans. We hypothesized that damage relatively restricted to the motor cortex or corticospinal tract would result in unselective muscle activations during an individuated finger movement task. People with pure motor hemiparesis attributed to ischemic cerebrovascular accident were tested. Pure motor hemiparetic and control subjects were studied making flexion/extension and then abduction/adduction finger movements. During the abduction/adduction movements, we recorded muscle activity from 3 intrinsic finger muscles: the abductor pollicis brevis, the first dorsal interosseus, and the abductor digit quinti. Each of these muscles acts as an agonist for only one of the abduction/adduction movements and might therefore be expected to be active in a highly selective manner. Motor cortex or corticospinal tract damage in people with pure motor hemiparesis reduced the selectivity of finger muscle activation during individuated abduction/adduction finger movements, resulting in reduced independence of these movements. Abduction/adduction movements showed a nonsignificant trend toward being less independent than flexion/extension movements in the affected hands of hemiparetic subjects. These changes in the selectivity of muscle activation and the consequent decrease in individuation of movement were correlated with decreased hand function. Our findings imply that, in humans, spared cerebral motor areas and descending pathways that remain might activate finger muscles, but cannot fully compensate for the highly selective control provided by the primary motor cortex and the crossed corticospinal system.

scholarly journals Combining tractography and cortical measures to test system-specific hypotheses in multiple sclerosis

2010 ◽  
Vol 16 (5) ◽  
pp. 555-565 ◽  
Author(s):  
Nikos Gorgoraptis ◽  
Claudia AM Wheeler-Kingshott ◽  
Thomas M Jenkins ◽  
Daniel R Altmann ◽  
David H Miller ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Motor Cortex ◽  
Surface Area ◽  
Fractional Anisotropy ◽  
Primary Motor Cortex ◽  
Corticospinal Tract ◽  
Imaging Techniques ◽  
Test System ◽  
Precentral Gyrus ◽  
Multiple Sclerosis Patients

The objective was to test three motor system-specific hypotheses in multiple sclerosis patients: (i) corticospinal tract and primary motor cortex imaging measures differ between multiple sclerosis patients and controls; (ii) in patients, these measures correlate with disability; (iii) in patients, corticospinal tract measures correlate with measures of the ipsilateral primary motor cortex. Eleven multiple sclerosis patients with a history of hemiparesis attributable to a lesion within the contralateral corticospinal tract, and 12 controls were studied. We used two advanced imaging techniques: (i) diffusion-based probabilistic tractography, to obtain connectivity and fractional anisotropy of the corticospinal tract; and (ii) FreeSurfer, to measure volume, thickness, surface area, and curvature of precentral and paracentral cortices. Differences in these measures between patients and controls, and relationships between each other and to clinical scores, were investigated. Patients showed lower corticospinal tract fractional anisotropy and smaller volume and surface area of the precentral gyrus than controls. In patients, corticospinal tract connectivity and paracentral cortical volume, surface area, and curvature were lower with increasing disability; lower connectivity of the affected corticospinal tract was associated with greater surface area of the ipsilateral paracentral cortex. Corticospinal tract connectivity and new measures of the primary motor cortex, such as surface area and curvature, reflect the underlying white and grey matter damage that contributes to disability. The correlation between lower connectivity of the affected corticospinal tract and greater surface area of the ipsilateral paracentral cortex suggests the possibility of cortical adaptation. Combining tractography and cortical measures is a useful approach in testing hypotheses which are specific to clinically relevant functional systems in multiple sclerosis, and can be applied to other neurological diseases.

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