scholarly journals Factors Involved in the Functional Motor Recovery of Rats with Cortical Ablation after GH and Rehabilitation Treatment: Cortical Cell Proliferation and Nestin and Actin Expression in the Striatum and Thalamus

2019 ◽  
Vol 20 (22) ◽  
pp. 5770 ◽  
Author(s):  
Margarita Heredia ◽  
Natalia Rodríguez ◽  
Virginia Sánchez Robledo ◽  
José María Criado ◽  
Antonio de la Fuente ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Cortical Cell ◽  
Motor Recovery ◽  
Proliferating Cells ◽  
Post Injury ◽  
Cortical Ablation ◽  
Actin Expression ◽  
Ventral Nucleus ◽  
Contralateral Motor

Previously we demonstrated, in rats, that treatment with growth hormone (GH) and rehabilitation, carried out immediately after a motor cortical ablation, significantly improved the motor affectation produced by the lesion and induced the re-expression of nestin in the contralateral motor cortex. Here we analyze cortical proliferation after ablation of the frontal motor cortex and investigate the re-expression of nestin in the contralateral motor cortex and the role of the striatum and thalamus in motor recovery. The rats were subjected to ablation of the frontal motor cortex in the dominant hemisphere or sham-operated and immediately treated with GH or the vehicle (V), for five days. At 1 dpi (days post-injury), all rats received daily injections (for four days) of bromodeoxyuridine and five rats were sacrificed at 5 dpi. The other 15 rats (n = 5/group) underwent rehabilitation and were sacrificed at 25 dpi. GH induced the greatest number of proliferating cells in the perilesional cortex. GH and rehabilitation produced the functional recovery of the motor lesion and increased the expression of nestin in the striatum. In the thalamic ventral nucleus ipsilateral to the lesion, cells positive for nestin and actin were detected, but this was independent on GH. Our data suggest that GH-induced striatal nestin is involved in motor recovery.

scholarly journals Factors Involved in the Functional Motor Recovery of Rats with Cortical Ablation after GH and Rehabilitation Treatment: Cortical Cell Proliferation and Nestin and Actin Expressions in Striatum and Thalamus

2019 ◽  
Author(s):  
Margarita Heredia ◽  
Natalia Rodríguez ◽  
Virginia Sánchez Robledo ◽  
José María Criado ◽  
Antonio de la Fuente ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Cortical Cell ◽  
Motor Recovery ◽  
The Other ◽  
Dominant Hemisphere ◽  
Proliferating Cells ◽  
Cortical Ablation ◽  
Ventral Nucleus ◽  
Contralateral Motor

Previously we demonstrated, in rats, that the treatment with growth hormone (GH) and rehabilitation, carried out immediately after a motor cortical ablation, significantly improved the motor affectation produced by the lesion and induced the re-expression of nestin in the contralateral motor cortex. Here we analyze cortical proliferation after ablation of the frontal motor cortex and investigate the re-expression of nestin in the contralateral motor cortex and the role of the striatum and thalamus in motor recovery. The rats were subjected to ablation of the frontal motor cortex in the dominant hemisphere or sham-operated and immediately treated with GH or vehicle (V), for five days. At 1 dpi (days after injury), 5 rats received daily injections (4 days) of bromodeoxyuridine and were sacrificed. The other 15 rats (n = 5 / group) underwent treatment and rehabilitation and were sacrificed at 25 dpi. GH induced the greatest number of proliferating cells in the perilesional cortex. GH and rehabilitation produced the functional recovery of the motor lesion and increased the expression of nestin in the striatum. In the thalamic ventral nucleus ipsilateral to the lesion, cells positive for nestin and actin were detected, but this was independent of GH. Our data suggest that GH-induced striatal nestin is involved in motor recovery.

scholarly journals The Role of the Contralesional Motor Cortex for Motor Recovery in the Early Days after Stroke Assessed with Longitudinal fMRI

2010 ◽  
Vol 21 (4) ◽  
pp. 756-768 ◽  
Author(s):  
Anne K. Rehme ◽  
Gereon R. Fink ◽  
D. Yves von Cramon ◽  
Christian Grefkes
Keyword(s):  
Motor Cortex ◽  
Motor Recovery

scholarly journals C.04 Motor cortex electrical stimulation to promote spinal cord injury repair in an animal model

2016 ◽  
Vol 43 (S2) ◽  
pp. S12-S12
Author(s):  
A Jack ◽  
A Nataraj ◽  
K Fouad
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Electrical Stimulation ◽  
Motor Cortex ◽  
Post Injury ◽  
Biphasic Pulse ◽  
Cord Injury ◽  
Axonal Sprouts ◽  
Electrode Insertion

Background: Electrical stimulation (ES) to promote corticospinal tract (CST) repair has been recently examined, though remains under investigated. We examine the role of motor cortex ES on axonal re-growth and functional recovery in a spinal cord injury (SCI) rat model. Methods: A partial transection was performed at C4 in 48 rats. Animal groups included: ES333 rats (n=14; 333Hz, biphasic pulse, 0.2ms every 500ms), ES20 (n=14; 20Hz, biphasic pulse, 0.2ms every 1ms), SCI only (n=10), and sham (n=10; electrode insertion without ES). Rats were trained in stairwell-grasping with subsequent SCI and ES. Post-injury reaching scores were recorded weekly, and histology completed quantifying axonal re-growth. Results: Post-SCI grasping (p<0.01, ANOVA) and well reached were lower than baseline values (p<0.01, ANOVA) for all groups. ES20 animals had lower grasping scores (p=0.03, ANOVA) and farthest well reached scores post-SCI than controls (p=0.03, ANOVA). ES333 rats had more axonal collaterals (axonal sprouts rostral to lesion) compared to control animals (p<0.01, M-W). No difference was found between groups with respect to axonal regeneration into the lesion (p=0.13, ANOVA). Conclusions: Cortical ES of the injured CST results in greater axonal outgrowth, and influences functional outcomes depending on ES parameters. ES is a potentially promising SCI therapy, but further investigation is required.

scholarly journals Motor Improvement of Skilled Forelimb Use Induced by Treatment with Growth Hormone and Rehabilitation Is Dependent on the Onset of the Treatment after Cortical Ablation

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Margarita Heredia ◽  
Jesús Palomero ◽  
Antonio de la Fuente ◽  
José María Criado ◽  
Javier Yajeya ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Brain Injuries ◽  
Time Window ◽  
Brain Plasticity ◽  
Critical Time ◽  
Gh Treatment ◽  
Cortical Ablation ◽  
Severe Motor ◽  
Motor Improvement ◽  
Contralateral Motor

We previously demonstrated that the administration of GH immediately after severe motor cortex injury, in rats, followed by rehabilitation, improved the functionality of the affected limb and reexpressed nestin in the contralateral motor cortex. Here, we analyze whether these GH effects depend on a time window after the injury and on the reexpression of nestin and actin. Injured animals were treated with GH (0.15 mg/kg/day) or vehicle, at days 7, 14, and 35 after cortical ablation. Rehabilitation was applied at short and long term (LTR) after the lesion and then sacrificed. Nestin and actin were analyzed by immunoblotting in the contralateral motor cortex. Giving GH at days 7 or 35 after the lesion, but not 14 days after it, led to a remarkable improvement in the functionality of the affected paw. Contralateral nestin and actin reexpression was clearly higher in GH-treated animals, probably because compensatory brain plasticity was established. GH and immediate rehabilitation are key for repairing brain injuries, with the exception of a critical time period: GH treatment starting 14 days after the lesion. Our data also indicate that there is not a clear plateau in the recovery from a brain injury in agreement with our data in human patients.

scholarly journals Anatomical Plasticity of the Distal Forelimb Projection of the Ventral Premotor Cortex Four weeks After Primary Motor Cortex Injury

2020 ◽  
Author(s):  
David W. McNeal ◽  
Scott Barbay ◽  
Shawn B. Frost ◽  
Michael Taylor ◽  
David J. Guggenmos ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Somatosensory Cortex ◽  
Primary Motor Cortex ◽  
Premotor Cortex ◽  
Early Time ◽  
Fold Increase ◽  
Motor Recovery ◽  
Variable Degree ◽  
Post Injury ◽  
Ventral Premotor Cortex

AbstractBrain injury affecting the isocortical frontal cortex is a common pathological occurrence. Many patients report severe deficits to functions of daily living. However, there is a variable degree of motor recovery that occurs with some individuals recovering astounding degrees of motor recovery while others have not. This variability has led researchers into investigating the possible mechanisms for this variability. Recently, several non-human primate studies have shed light on the possibility of spared, ipsilesional motor area taken over the lost function to the damaged cortex. Unfortunately, these studies have focused on long-term adaption ranging from 5months to one year post injury. In this present study, we are the first use rigorous stereological quantification to show that significant neuroplastic changes in the form of changes to neuroanatomical connections between distant cortical area occurs at a very early time point of 4 weeks post injury. Much like the Dancause study in 2005, we found that ishemic damage to the distal forelimb area (DFL) of the primary motor cortex (M1) induced plastic changes between the DFL of the ventral premotor cortex (PMv) and area 1/2 of the somatosensory cortex. Indeed, we found a nearly 2 fold increase in the number of boutons between PMV and area 1/2. Additionally, labeled fibers from PMv change direction from their normal termination within M1 and traveled in a ventral posterior direction toward the somatosensory cortex. Also of interest, several labeled fibers actually traveled through the glial scar of M1 toward the somatosensory cortex. These data demonstrate that a massive neuroplastic response has occurred following an ischemic insult to the DFL of M1. These data may suggest that the brain may be undergoing an attempt to re-establish a degree of motor and or sensory control to compensate for the lost function due to the injury.

Sports Concussions (TBI), Imbalance, and Dizziness

2015 ◽  
Vol 25 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Steven M. Doettl
Keyword(s):  
Assessment Tools ◽  
Vestibular Evoked Myogenic Potentials ◽  
Post Injury ◽  
Management Tools ◽  
Concussion Management ◽  
Post Concussion Syndrome ◽  
Behavioral Marker ◽  
Valid Assessment ◽  
Injury Assessment

It has been widely accepted that the assessment of balance after concussion plays a large role in determining deficit. Qualitative balance assessments have been an established piece of the post-injury assessment as a clinical behavioral marker of concussion for many years. Recently more specific guidelines outlining the role of balance evaluation in concussion identification and management have been developed as part of concussion management tools. As part of the ongoing development of concussions protocols, quantitative assessment of balance function following concussion has also been identified to have an important role. Frequently imbalance and dizziness reported following concussion is assumed to be associated with post-concussion syndrome (PCS). While imbalance and dizziness are common complaints in PCS, they can also be a sign of additional underlying pathology. In cases of specific dizziness symptoms or limited balance recovery beyond the initial post-concussive period, a quantitative vestibular assessment may also be needed. Electronystagmography and videonystagmography (ENG/VNG), rotary chair testing (RCT), and vestibular evoked myogenic potentials (VEMPs) have all been identified as valid assessment tools for vestibular dysfunction following traumatic brain injury (TBI). The assessment of balance and dizziness following sports-related concussions is an integral piece of the puzzle for removal from play, assessment of severity, and management.

scholarly journals Pre-motor versus motor cerebral cortex neuromodulation for chronic neuropathic pain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Cerebral Cortex ◽  
Motor Cortex ◽  
Initial Assessment ◽  
Motor Cortex Stimulation ◽  
Chronic Neuropathic Pain ◽  
Long Term Effect ◽  
Stimulation Of

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.

Tissue Ki67 proliferative index expression and pathological changes in hemodialysis arteriovenous fistulae: Preliminary single-center results

2021 ◽  
pp. 112972982110154
Author(s):  
Raffaella Mauro ◽  
Cristina Rocchi ◽  
Francesco Vasuri ◽  
Alessia Pini ◽  
Anna Laura Croci Chiocchini ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Hot Spot ◽  
Wall Thickening ◽  
Proliferating Cells ◽  
Ki 67 ◽  
Group A ◽  
The Mean ◽  
Set Up ◽  
Group B

Background: Arteriovenous fistula (AVF) for hemodialysis integrates outward remodeling with vessel wall thickening in response to drastic hemodynamic changes. Aim of this study is to determine the role of Ki67, a well-established proliferative marker, related to AVF, and its relationship with time-dependent histological morphologic changes. Materials and methods: All patients were enrolled in 1 year and stratified in two groups: (A) pre-dialysis patients submitted to first AVF and (B) patients submitted to revision of AVF. Morphological changes: neo-angiogenesis (NAG), myointimal thickening (MIT), inflammatory infiltrate (IT), and aneurysmatic fistula degeneration (AD). The time of AVF creation was recorded. A biopsy of native vein in Group A and of arterialized vein in Group B was submitted to histological and immunohistochemical (IHC) analysis. IHC for Ki67 was automatically performed in all specimens. Ki67 immunoreactivity was assessed as the mean number of positive cells on several high-power fields, counted in the hot spots. Results: A total of 138 patients were enrolled, 69 (50.0%) Group A and 69 (50.0%) Group B. No NAG or MIT were found in Group A. Seven (10.1%) Group A veins showed a mild MIT. Analyzing the Group B, a moderate-to-severe MIT was present in 35 (50.7%), IT in 19 (27.5%), NAG in 37 (53.6%); AD was present in 10 (14.5%). All AVF of Group B with the exception of one (1.4%) showed a positivity for Ki67, with a mean of 12.31 ± 13.79 positive cells/hot spot (range 0–65). Ki67-immunoreactive cells had a subendothelial localization in 23 (33.3%) cases, a myointimal localization in SMC in 35 (50.7%) cases. The number of positive cells was significantly correlated with subendothelial localization of Ki67 ( p = 0.001) and with NA ( p = 0.001). Conclusions: Native veins do not contain cycling cells. In contrast, vascular cell proliferation starts immediately after AVF creation and persists independently of the time the fistula is set up. The amount of proliferating cells is significantly associated with MIT and subendothelial localization of Ki67-immunoreactive cells, thus suggesting a role of Ki-67 index in predicting AVF failure.

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