The anticonvulsant drug vigabatrin has not been found to be detrimental to the recovery process when administered following focal cortical insult. This finding is in contrast to the negative ...postinjury consequences of other anticonvulsant drugs (e.g., phenobarbital and diazepam) with more direct activation of the GABA/benzodiazepine receptor complex. Moreover, phenobarbital directed against kindled seizures affects functional recovery more adversely than either the drug or subconvulsive seizures alone. The purpose of the present study was to determine whether vigabatrin (150, 200, and 250 mg/kg) directed against kindled seizures would impact recovery from lesion-induced somatosensory deficits. Vigabatrin was coupled with daily electrical kindling of the amygdala during the first week after a unilateral anteromedial cortex (AMC) lesion. Somatosensory recovery was assessed using bilateral tactile stimulation tests. Animals receiving the highest dose of vigabatrin prior to electrical kindling (250 mg/kg vigabatrin/kindled) remained significantly impaired even after two months of testing relative to vehicle/kindled, kindled/250 mg/kg vigabatrin, which received vigabatrin after electrical kindling, and the 150, 200, and 250 mg/kg vigabatrin/nonkindled groups (p < 0.0001). In contrast, neither vigabatrin (at any of the doses tested) nor subconvulsive kindled seizures impacted the recovery process (p > 0.05) when administered alone (i.e., without the drug + seizure interaction). These data add to the accumulating experimental and clinical evidence suggesting that the neurobehavioral consequences of the interaction between anticonvulsant drugs and subclinical seizures after brain insult are detrimental to functional recovery.
Provider: - Institution: - Data provided by Europeana Collections- All metadata published by Europeana are available free of restriction under the Creative Commons CC0 1.0 Universal Public Domain ...Dedication. However, Europeana requests that you actively acknowledge and give attribution to all metadata sources including Europeana
Somatosensory deficits are frequently seen in acute stroke patients and may recover over time and affect functional outcome. However, the underlying mechanism of function recovery remains poorly ...understood. In the present study, progressive function alteration of the secondary somatosensory cortex (S2) and its relationship with regional perfusion and neurological outcome were examined using a monkey model of stroke.
Rhesus monkeys (n = 4) were induced with permanent middle cerebral artery occlusion (pMCAo). Resting-state functional MRI, dynamic susceptibility contrast perfusion MRI, diffusion-weighted, T1 and T2 weighted images were collected before surgery and at 4–6, 48, and 96 h post stroke on a 3T scanner. Progressive changes of relative functional connectivity (FC), cerebral blood flow (CBF), and CBF/Tmax (Time to Maximum) of affected S2 regions were evaluated. Neurological deficits were assessed using the Spetzler approach.
Ischemic lesion was evidently seen in the MCA territory including S2 in each monkey. Relative FC of injured S2 regions decreased substantially following stroke. Spetzler scores dropped substantially at 24 h post stroke but slightly recovered from Day 2 to Day 4. Relative FC progressively increased from 6 to 48 and 96 h post stroke and correlated significantly with relative CBFand CBF/Tmax changes.
The present study revealed the progressive alteration of function connectivity in S2 during acute stroke. The preliminary results suggested the function recovery might start couple days post occlusion and collateral circulation might play a key role in the recovery of somatosensory function after stroke insult. The relative function connectivity in S2 may provide additional information for prediction of functional outcome in stroke patients.
Display omitted
•Progressive function connectivity alteration in the secondary somatosensory cortex (S2) of monkeys following ischemic stroke was examined.•Function recovery in S2 may start couple days after stroke insult and associated with regional perfusion and motor deficit.•Collateral circulation may play a key role in the recovery of somatosensory function after stroke.•Relative function connectivity in S2 may provide additional information for prediction of stroke outcome.
Abstract
One of the most prevalent deficits in autism spectrum disorder (ASD) are sensitivities to sensory stimuli. Despite the prevalence of sensory deficits in autism, there are few paradigms ...capable of easily assessing sensory behaviors in ASD-like mouse models. We addressed this need by creating the Somatosensory Nose-poke Adapted Paradigm (SNAP), which consists of an elevated platform with 6 holes in the center, half of which are lined with sandpaper and half are smooth, requiring mice to use their whiskers to sense the texture. The SNAP paradigm assesses tactile sensory preferences as well as stereotypy, anxiety, and locomotion. We used two wild-type (neurotypical) mouse strains, C57BL/6J (C57) inbred and CD-1 outbred mice, and two ASD mouse models, BTBR (a model of idiopathic ASD) and
Cntnap2
−/−
mice (a model of syndromic ASD). We found that both ASD models produced more nose pokes into the rough condition than the smooth condition, suggesting an increased preference for complex tactile stimulation when compared with the neurotypical groups, wherein no differences were observed. Furthermore, we found increased stereotypy and time spent in the center, suggestive of decreased anxiety, only for BTBR mice compared with the other mouse strains. Overall, SNAP is an easy to implement task to assess the degree of preference for complex tactile stimulation in ASD mouse models that can be further modified to exclude possible confounding effects of novelty or anxiety on the sensory preferences.
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.
Cerebral ischemia constitutes the most frequent type of cerebrovascular disease. The reduction of blood supply to the brain initiates the ischemic cascade starting from ionic imbalance to subsequent ...glutamate excitotoxicity, neuroinflammation and oxidative stress, eventually causing neuronal death. Previously, the authors have demonstrated the in vitro cytoprotective and antioxidant effects of a new arylidene malonate derivative, KM-34, against oxidizing agents like hydrogen peroxide, glutamate or Fe3+/ascorbate. Here, we examined for the first time the neuroprotective effect of KM-34 on ischemia/reperfusion models. In vitro, treatment with 10 and 50 μM KM-34 reduced the cellular death (propidium iodide incorporation) induced by oxygen glucose deprivation (OGD) in rat organotypic hippocampal slices cultures. In vivo, stroke was induced in male Wistar rats through middle cerebral artery occlusion (MCAO), followed by 23 h of reperfusion. KM-34 was orally administered 105 min after MCAO onset. We noticed that 1 mg/kg KM-34 reduced infarct volume and neurological score, and increased the latency to fall in the Hanging Wire test compared to vehicle-treated ischemic animals. While ischemic and sham-operated groups showed similar horizontal locomotor activity, vertical counts decreased after MCAO, suggesting that vertical movements are more sensitive to the ischemic injury. Treatment with KM-34 also alleviated the mitochondrial impairment (ROS generation, swelling and membrane potential dissipation) induced by transient MCAO but not significant alterations were found in oxidative stress parameters. Overall, the study provides preclinical evidences confirming the neuroprotective effects of a novel synthetic molecule and paved the way for future investigations regarding its therapeutic potential against brain ischemia/reperfusion injury.
Patients with chronic pain frequently show nondermatomal somatosensory deficits (NDSDs) that are considered to be functional. We hypothesize a multifactorial etiology of NDSDs, including stress.
...Patients with chronic pain disorders frequently show nondermatomal somatosensory deficits (NDSDs) that are considered to be functional. Typically, NDSDs show quadratomal or hemibody distribution ipsilateral to the areas of chronic pain. According to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition and the International Classification of Diseases, 10th revision, such functional somatosensory deficits are classified in the chapter “conversion disorder.” Many publications also used the term “hysterical sensory loss.” However, doubts are increasing about this one-sided psychiatric view. We aimed to better characterize the biopsychosocial factors associated with NDSDs. Therefore, we compared 2 groups of inpatients with chronic pain disorder, of whom 90 suffered from NDSDs and 90 did not. The patients with NDSDs all showed widespread somatosensory deficits with hemibody distribution. On logistic regression analysis, history of a prior physical trauma was positively predictive for patients with NDSDs. Personality disorder and adverse childhood experiences were positively predictive for the control group with chronic pain disorders without NDSDs. The frequencies of comorbid depression and anxiety disorder did not differ statistically between groups. In conclusion, pain patients with NDSDs are, psychopathologically, by no means more noticeable personalities than patients with chronic pain disorder without NDSDs. Similar to complex regional pain syndromes, we assume a multifactorial etiology of NDSDs, including stress. Based on our observations, terms like “hysteric” should not be applied any longer to patients with NDSDs who suffer from chronic pain.
Background. Motor imagery (MI) is increasingly recognized as a treatment option after stroke, but not all stroke patients are able to perform MI. Objective. To examine if severe somatosensory ...deficits would affect MI ability. Methods. The Box and Block Test (BBT) was used to evaluate mental chronometry as 1 component of MI. Two groups of stroke patients and an age-matched healthy control group (CG) were studied. Patient group 1 (n = 10, PG1) had a severe somatosensory impairment on the affected side and PG2 (n = 10) had pure motor strokes. All subjects first performed the BBT in a mental and in a real version. The time needed to move 15 blocks from 1 side of the box to the other was measured. To compare the groups independently of their performance level, a (real performance − MI)/(real performance) ratio was calculated. Corticospinal excitability was measured by transcranial magnetic stimulation at rest and while the subjects performed an imagined pinch grip. Results. The CG performed the BBT faster than both patient groups, and PG1 was slower than PG2. MI ability was impaired in PG1 but only for the affected hand. Transcranial magnetic stimulation data showed an abnormally low MI-induced corticospinal excitability increase for the affected hand in PG1, but not in PG2. Conclusions. Severe somatosensory deficits impaired mental chronometry. A controlled study is necessary to clarify if these patients benefit at all from MI as an additional treatment.
Damage and/or disconnection of the primary somatosensory cortex (SI) after stroke leads to deficits in touch perception. We used magnetoencephalography to test whether specific patterns of ...functionality of the somatosensory cortex are associated with different degrees of postacute somatosensory deficit. Nineteen postacute unilateral stroke patients suffering different degrees of somatosensory deficit (six nonexistent, six moderate, and seven severe) and eight aged-matched controls underwent high-resolution MRI and whole-head magnetoencephalography recordings of somatosensory-evoked fields and of spontaneous slow oscillatory activity. Amplitude of SI activation after tactile stimulation in the affected and nonaffected hemispheres and delta dipole density (DDD) in the postcentral areas were estimated and compared across the four groups. Severe postacute somatosensory deficit was accompanied, in all cases, with absence of SI responses to stimulation in the affected hand and a significant asymmetry in postcentral DDD toward the affected hemisphere. Patients with moderate sensory loss showed asymmetry in their postcentral DDD (four cases toward the affected hemisphere and two toward the unaffected) but no atypical amplitudes in SI activation. Recordings in stroke patients without somatosensory deficit did not differ from those obtained in controls for SI amplitude or postcentral DDD. In stroke patients, amplitude of SI responses and postcentral DDD show a negative correlation. Lack of activation of SI cortex after stimulation of the affected hand and spontaneous slow oscillatory activity in postcentral areas are neurophysiological correlates of somatosensory deficit in the postacute phase of stroke.
Objectives – To study the recovery of somatosensory deficits after acute stroke.
Material and methods – A detailed clinical examination of sensation, median nerve somatosensory evoked potentials ...(SEP), quantitative sensory tests (QST), and subjective evaluation were performed in five acute stroke patients at three control time points up to 12 months after the stroke.
Results – The deficit recovered at least partially in all patients, mostly within 3 months after stroke. The improvement in warm and vibration detection thresholds occurred between 3 and 12 months. The SEP improved both by 3 and 12 months.
Conclusion – The recovery of subjective sensory disturbance occurred in line with the improvement of the clinical sensory tests and QST. The most sensitive measure for somatosensory dysfunction at the early phase was graphesthesia. In our patients, initially normal SEP with a sensory deficit resulted in excellent clinical recovery, whereas initially absent SEP did not necessarily predict poor outcome.
PDF
