Somatosensory Deficits After Stroke: Insights From MRI Studies
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SUBMITTER: Lv Q
PROVIDER: S-EPMC9328992 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The aim of this study was to investigate the relationship between stroke lesion location and the resulting somatosensory deficit. We studied exteroceptive and proprioceptive somatosensory symptoms and stroke lesions in 38 patients with first-ever acute stroke. The Erasmus modified Nottingham Sensory Assessment was used to clinically evaluate somatosensory functioning in the arm and hand within the first week after stroke onset. Additionally, more objective measures such as the perceptual threshold of touch and somatosensory evoked potentials were recorded. Non-parametric voxel-based lesion-symptom mapping was performed to investigate lesion contribution to different somatosensory deficits in the upper limb. Additionally, structural connectivity of brain areas that demonstrated the strongest association with somatosensory symptoms was determined, using probabilistic fiber tracking based on diffusion tensor imaging data from a healthy age-matched sample. Voxels with a significant association to somatosensory deficits were clustered in two core brain regions: the central parietal white matter, also referred to as the sensory component of the superior thalamic radiation, and the parietal operculum close to the insular cortex, representing the secondary somatosensory cortex. Our objective recordings confirmed findings from clinical assessments. Probabilistic tracking connected the first region to thalamus, internal capsule, brain stem, postcentral gyrus, cerebellum, and frontal pathways, while the second region demonstrated structural connections to thalamus, insular and primary somatosensory cortex. This study reveals that stroke lesions in the sensory fibers of the superior thalamocortical radiation and the parietal operculum are significantly associated with multiple exteroceptive and proprioceptive deficits in the arm and hand.
| S-EPMC4724038 | biostudies-literature
Project description:Schizophrenia is often accompanied by disturbances in motor behavior thought to result from abnormalities in the brain's timing mechanisms. Virtually all behavior has a motor component, and proper regulation of motor behavior is often dependent upon accurate registration of somatosensory input. This study uses the steady-state evoked response (SSR) to quantify the accuracy of timing of the neocortical response to rapidly presented tactile somatosensory stimuli in patients with schizophrenia compared to control subjects. We used magnetic evoked fields and source space projection to estimate the time course of equivalent current sources in somatosensory cortex. Wavelet-based time-frequency analysis was used to compute intertrial timing consistency and amplitudes. SSRs in schizophrenic subjects demonstrated decreased performance in both metrics to contralateral 25-Hz tactile stimulation. Previous studies have reported similar abnormalities in the SSR in both auditory and visual domains. The magnetic SSR to tactile stimuli is thought to reflect activation of layer 3 pyramidal cells in primary sensory cortex. Thus, these findings, as in other sensory domains, are suggestive of impaired GABAergic inhibitory interneuronal control of the timing of pyramidal cell activity. This deficit may be intrinsic to neocortex, or might reflect as well impairment of cerebellar and/or thalamic involvement. These findings reinforce the notion that abnormalities in the brain's timing mechanisms are a central component of the schizophrenia syndrome.
| S-EPMC3604058 | biostudies-literature
Project description:Recovery from stroke is rarely complete as humans and experimental animals typically show lingering deficits in sensory function. One explanation for limited recovery could be that rewired cortical networks do not process sensory stimuli with the same temporal precision as they normally would. To examine how well peri-infarct and more distant cortical networks process successive vibro-tactile stimulations of the affected forepaw (a measure of temporal fidelity), we imaged cortical depolarizations with millisecond temporal resolution using voltage-sensitive dyes. In control mice, paired forepaw stimulations (ranging from 50 to 200 milliseconds apart) induced temporally distinct depolarizations in primary forelimb somatosensory (FLS1) cortex, and to a lesser extent in secondary FLS (FLS2) cortex. For mice imaged 3 months after stroke, the first forepaw stimulus reliably evoked a strong depolarization in the surviving region of FLS1 and FLS2 cortex. However, depolarizations to subsequent forepaw stimuli were significantly reduced or completely absent (for stimuli ?100 milliseconds apart) in the FLS1 cortex, whereas FLS2 responses were relatively unaffected. Our data reveal that stroke induces long-lasting impairments in how well the rewired FLS1 cortex processes temporal aspects of sensory stimuli. Future therapies directed at enhancing the temporal fidelity of cortical circuits may be necessary for achieving full recovery of sensory functions.
| S-EPMC3597364 | biostudies-literature
Project description:Somatosensory dysfunction is associated with a high incidence of functional impairment and safety in patients with stroke. With developments in brain mapping techniques, many studies have addressed the recovery of various functions in such patients. However, relatively little is known about the mechanisms of recovery of somatosensory function. Based on the previous human studies, a review of 11 relevant studies on the mechanisms underlying the recovery of somatosensory function in stroke patients was conducted based on the following topics: (1) recovery of an injured somatosensory pathway, (2) peri-lesional reorganization, (3) contribution of the unaffected somatosensory cortex, (4) contribution of the secondary somatosensory cortex, and (5) mechanisms of recovery in patients with thalamic lesions. We believe that further studies in this field using combinations of diffusion tensor imaging, functional neuroimaging, and magnetoencephalography are needed. In addition, the clinical significance, critical period, and facilitatory strategies for each recovery mechanism should be clarified.
| S-EPMC5561841 | biostudies-other
Project description:Neutrophils have key roles in ischemic brain injury, thrombosis, and atherosclerosis. As such, neutrophils are of great interest as targets to treat and prevent ischemic stroke. After stroke, neutrophils respond rapidly promoting blood-brain barrier disruption, cerebral edema, and brain injury. A surge of neutrophil-derived reactive oxygen species, proteases, and cytokines are released as neutrophils interact with cerebral endothelium. Neutrophils also are linked to the major processes that cause ischemic stroke, thrombosis, and atherosclerosis. Thrombosis is promoted through interactions with platelets, clotting factors, and release of prothrombotic molecules. In atherosclerosis, neutrophils promote plaque formation and rupture by generating oxidized-low density lipoprotein, enhancing monocyte infiltration, and degrading the fibrous cap. In experimental studies targeting neutrophils can improve stroke. However, early human studies have been met with challenges, and suggest that selective targeting of neutrophils may be required. Several properties of neutrophil are beneficial and thus may important to preserve in patients with stroke including antimicrobial, antiinflammatory, and neuroprotective functions.
| S-EPMC4640255 | biostudies-other
Project description:BackgroundClinical and neuroimaging measures incompletely explain behavioral deficits in the acute stroke setting. We hypothesized that electroencephalography (EEG)-based measures of neural function would significantly improve prediction of acute stroke deficits.MethodsPatients with acute stroke (n=50) seen in the emergency department of a university hospital from 2017 to 2018 underwent standard evaluation followed by a 3-minute recording of EEG at rest using a wireless, 17-electrode, dry-lead system. Artifacts in EEG recordings were removed offline and then spectral power was calculated for each lead pair. A primary EEG metric was DTABR, which is calculated as a ratio of spectral power: [(Delta*Theta)/(Alpha*Beta)]. Bivariate analyses and least absolute shrinkage and selection operator (LASSO) regression identified clinical and neuroimaging measures that best predicted initial National Institutes of Health Stroke Scale (NIHSS) score. Multivariable linear regression was then performed before versus after adding EEG findings to these measures, using initial NIHSS score as the dependent measure.ResultsAge, diabetes status, and infarct volume were the best predictors of initial NIHSS score in bivariate analyses, confirmed using LASSO regression. Combined in a multivariate model, these 3 explained initial NIHSS score (adjusted r2=0.47). Adding any of several different EEG measures to this clinical model significantly improved prediction; the greatest amount of additional variance was explained by adding contralesional DTABR (adjusted r2=0.60, P<0.001).ConclusionsEEG measures of neural function significantly add to clinical and neuroimaging for explaining initial NIHSS score in the acute stroke emergency department setting. A dry-lead EEG system can be rapidly and easily implemented. EEG contains information that may be useful early after stroke.
| S-EPMC9881885 | biostudies-literature
Project description:AimTo synthetize studies assessing somatosensory deficits and alterations in cerebral responses evoked by somatosensory stimulation in individuals with cerebral palsy (CP) compared to typically developing individuals.MethodA scoping review of the literature was performed in the MEDLINE, Embase, PsycInfo, CINAHL, Evidence-Based Medicine Reviews, and Web of Science databases (last search carried out on 6th and 7th August 2020) with a combination of keywords related to CP and somatosensory functions. Somatosensory deficits were measured with clinical tests and alterations in cerebral responses were measured with functional magnetic resonance imaging, electroencephalography, and magnetoencephalography.ResultsForty-eight articles were included. Overall, 1463 participants with CP (mean [SD] age 13y 1mo [4y 11mo], range 1-55y; 416 males, 319 females, sex not identified for the remaining participants) and 1478 controls (mean [SD] age 13y 1mo [5y 8mo], range 1-42y; 362 males, 334 females, sex not identified for the remaining participants) were included in the scoping review. For tactile function, most studies reported registration (8 out of 13) or perception (21 out of 21) deficits in participants with CP. For proprioception, most studies also reported registration (6 out of 8) or perception (10 out of 15) deficits. Pain function has not been studied as much, but most studies reported registration (2 out of 3) or perception (3 out of 3) alterations. Neuroimaging findings (18 studies) showed alterations in the somatotopy, morphology, latency, or amplitude of cortical responses evoked by somatosensory stimuli.InterpretationDespite the heterogeneity in the methods employed, most studies reported somatosensory deficits. The focus has been mainly on tactile and proprioceptive function, whereas pain has received little attention. Future research should rigorously define the methods employed and include a sample that is more representative of the population with CP. What this paper adds Most of the papers reviewed found tactile registration and perception deficits in the upper limbs. Proprioceptive deficits were generally observed in cerebral palsy but results were heterogeneous. Pain has received little attention compared to tactile and proprioceptive functions. Neuroimaging studies supported behavioral observations. Alterations were observed for both the most and least affected limb.
| S-EPMC9290873 | biostudies-literature
Project description:Carpal tunnel syndrome, a median nerve entrapment neuropathy, is characterized by sensorimotor deficits. Recent reports have shown that this syndrome is also characterized by functional and structural neuroplasticity in the primary somatosensory cortex of the brain. However, the linkage between this neuroplasticity and the functional deficits in carpal tunnel syndrome is unknown. Sixty-three subjects with carpal tunnel syndrome aged 20-60 years and 28 age- and sex-matched healthy control subjects were evaluated with event-related functional magnetic resonance imaging at 3 T while vibrotactile stimulation was delivered to median nerve innervated (second and third) and ulnar nerve innervated (fifth) digits. For each subject, the interdigit cortical separation distance for each digit's contralateral primary somatosensory cortex representation was assessed. We also evaluated fine motor skill performance using a previously validated psychomotor performance test (maximum voluntary contraction and visuomotor pinch/release testing) and tactile discrimination capacity using a four-finger forced choice response test. These biobehavioural and clinical metrics were evaluated and correlated with the second/third interdigit cortical separation distance. Compared with healthy control subjects, subjects with carpal tunnel syndrome demonstrated reduced second/third interdigit cortical separation distance (P < 0.05) in contralateral primary somatosensory cortex, corroborating our previous preliminary multi-modal neuroimaging findings. For psychomotor performance testing, subjects with carpal tunnel syndrome demonstrated reduced maximum voluntary contraction pinch strength (P < 0.01) and a reduced number of pinch/release cycles per second (P < 0.05). Additionally, for four-finger forced-choice testing, subjects with carpal tunnel syndrome demonstrated greater response time (P < 0.05), and reduced sensory discrimination accuracy (P < 0.001) for median nerve, but not ulnar nerve, innervated digits. Moreover, the second/third interdigit cortical separation distance was negatively correlated with paraesthesia severity (r = -0.31, P < 0.05), and number of pinch/release cycles (r = -0.31, P < 0.05), and positively correlated with the second and third digit sensory discrimination accuracy (r = 0.50, P < 0.05). Therefore, reduced second/third interdigit cortical separation distance in contralateral primary somatosensory cortex was associated with worse symptomatology (particularly paraesthesia), reduced fine motor skill performance, and worse sensory discrimination accuracy for median nerve innervated digits. In conclusion, primary somatosensory cortex neuroplasticity for median nerve innervated digits in carpal tunnel syndrome is indeed maladaptive and underlies the functional deficits seen in these patients.
| S-EPMC4032104 | biostudies-literature
Project description:Background: Somatosensory function plays an important role in motor learning. More than half of the stroke patients have somatosensory impairments in the upper limb, which could hamper recovery. Question: Is sensorimotor upper limb (UL) therapy of more benefit for motor and somatosensory outcome than motor therapy? Design: Randomized assessor- blinded multicenter controlled trial with block randomization stratified for neglect, severity of motor impairment, and type of stroke. Participants: 40 first-ever stroke patients with UL sensorimotor impairments admitted to the rehabilitation center. Intervention: Both groups received 16 h of additional therapy over 4 weeks consisting of sensorimotor (N = 22) or motor (N = 18) UL therapy. Outcome measures: Action Research Arm test (ARAT) as primary outcome, and other motor and somatosensory measures were assessed at baseline, post-intervention and after 4 weeks follow-up. Results: No significant between-group differences were found for change scores in ARAT or any somatosensory measure between the three time points. For UL impairment (Fugl-Meyer assessment), a significant greater improvement was found for the motor group compared to the sensorimotor group from baseline to post-intervention [mean (SD) improvement 14.65 (2.19) vs. 5.99 (2.06); p = 0.01] and from baseline to follow-up [17.38 (2.37) vs. 6.75 (2.29); p = 0.003]. Conclusion: UL motor therapy may improve motor impairment more than UL sensorimotor therapy in patients with sensorimotor impairments in the early rehabilitation phase post stroke. For these patients, integrated sensorimotor therapy may not improve somatosensory function and may be less effective for motor recovery. Clinical Trial Registration: www.ClinicalTrials.gov, identifier NCT03236376.
| S-EPMC7746814 | biostudies-literature
Project description:Although clinical neuroscience and the neuroscience of consciousness have long sought mechanistic explanations of tactile-awareness disorders, mechanistic insights are rare, mainly because of the difficulty of depicting the fine-grained neural dynamics underlying somatosensory processes. Here, we combined the stereo-EEG responses to somatosensory stimulation with the lesion mapping of patients with a tactile-awareness disorder, namely tactile extinction. Whereas stereo-EEG responses present different temporal patterns, including early/phasic and long-lasting/tonic activities, tactile-extinction lesion mapping co-localizes only with the latter. Overlaps are limited to the posterior part of the perisylvian regions, suggesting that tonic activities may play a role in sustaining tactile awareness. To assess this hypothesis further, we correlated the prevalence of tonic responses with the tactile-extinction lesion mapping, showing that they follow the same topographical gradient. Finally, in parallel with the notion that visuotactile stimulation improves detection in tactile-extinction patients, we demonstrated an enhancement of tonic responses to visuotactile stimuli, with a strong voxel-wise correlation with the lesion mapping. The combination of these results establishes tonic responses in the parietal operculum as the ideal neural correlate of tactile awareness.
| S-EPMC8719842 | biostudies-literature