Lesions Of Cortex Research Articles

P29-T Mapping primary motor cortex with navigated TMS in unusual corticospinal lateralization for epilepsy surgery

Background The corticospinal tract has a sequential development in which the ipsilateral projections are gradually withdrawn, whereas the contralateral projections persist. A unilateral lesion in the motor cortex during early life may cause a reorganization in this process with preservation of uncrossed corticospinal connections in the spared hemisphere. As a result, all the motor function is lateralized in one hemisphere. Individuals with this kind of lesions also have an increased risk of drug-resistant epilepsy and may be candidates for epilepsy surgery. In these cases, it is important to evaluate the motor function for surgical treatment. Material and methods We present a series of 4 patients with pharmacoresistant epilepsy and early-life primary motor cortex lesion that were studied for epilepsy surgery. We used nTMS to investigate if there was still functional motor activity in one or both frontal cortices. Results In three cases there was no activity in the pathological cortex obtaining a bilateral response in the normal cortex. Two of them underwent fMRI using a motor task showing bilateral motor cortical function in one patient, and unilateral activation of ipsilateral motor cortex in the other patient. The last patient showed a crossed response. Two patients were operated without new postoperative deficits. Conclusions nTMS helps to define unusual lateralization of motor cortex and to guide a secure resection with the least motor deficits.

Structural and functional connectivity correlates with motor impairment in chronic supratentorial stroke: a multimodal magnetic resonance imaging study.

The aim of this study was to identify differences in structural and functional brain connectivity between poststroke mild and severe motor impairment. Twenty-four chronic stroke patients who underwent resting-state functional MRI and diffusion tensor image were retrospectively included. All patients were classified into two groups (mild motor impairment: 11 patients and severe motor impairment: 13 patients) according to their Fugl-Meyer motor assessment score. Tract-based spatial statistics and group independent component analyses were applied to investigate between-group differences in structural and functional connectivity, respectively. The fractional anisotropy values of motor-related brain regions in the affected hemisphere were significantly higher in mild motor impairment than in severe motor impairment (corrected P<0.05). The internetwork functional connectivity between (i) the supplementary motor area and primary motor cortex in the affected hemisphere, (ii) the supplementary motor area and dorsolateral prefrontal cortex in the unaffected hemisphere, and (iii) the ischemic lesion and primary motor cortex in the unaffected hemisphere was significantly higher in mild motor impairment than in severe motor impairment (PFWE<0.05). Better motor recovery after stroke could be facilitated by means of treatments aimed at enhancing structural and functional connectivity among motor-related brain regions such as noninvasive brain stimulation and neurodevelopmental therapy.

Neuronal mechanisms of motion detection underlying blindsight assessed by functional magnetic resonance imaging (fMRI)

Brain imaging offers a valuable tool to observe functional brain plasticity by showing how sensory inputs reshape cortical activations after a visual impairment. Following a unilateral post-chiasmatic lesion affecting the visual cortex, patients may suffer a contralateral visual loss referred to homonymous hemianopia. Nevertheless, these patients preserve the ability to unconsciously detect, localize and discriminate visual stimuli presented in their impaired visual field. To investigate this paradox, known as blindsight, we conducted a study using functional magnetic resonance imaging (fMRI) to evaluate the structural and functional impact of such lesion in a 33-year old patient (ML), who suffers a complete right hemianopia without macular sparing and showing strong evidences of blindsight. We thus performed whole brain and sliced thalamic fMRI scan sequences during an event-related motion detection task. We provided evidence of the neuronal fingerprint of blindsight by acquiring and associating neural correlates, specific structures and functional networks of the midbrain during blindsight performances which may help to better understand this condition. Accurate performance demonstrated the presence of residual vision and the ability to unconsciously perceive motion presented in the blind hemifield, although her reaction time was significantly higher in her blind-field. When the normal hemifield was stimulated, we observed significant contralateral activations in primary and secondary visual areas as well as motion specific areas, such as the supramarginal gyrus and middle temporal area. We also demonstrated sub-thalamic activations within the superior colliculi (SC) and the pulvinar. These results suggest a role of secondary subcortical structures in normal spontaneous motion detection. In a similar way, when the lesioned hemifield was stimulated, we observed contralateral activity in extrastriate areas with no activation of the primary lesioned visual cortex. Moreover, we observed activations within the SC when the blind hemifield was stimulated. However, we observed unexpected ipsilateral activations within the same motion specific areas, as well as bilateral frontal activations. These results highlight the importance of abnormal secondary pathways bypassing the primary visual area (V1) in residual vision. This reorganization in the structure and function of the visual pathways correlates with behavioral changes, thus offering a plausible explanation for the blindsight phenomenon. Our results may potentially impact the development of rehabilitation strategies to target subcortical pathways.

The next-generation sphingosine-1 receptor modulator BAF312 (siponimod) improves cortical network functionality in focal autoimmune encephalomyelitis.

Autoimmune diseases of the central nervous system (CNS) like multiple sclerosis (MS) are characterized by inflammation and demyelinated lesions in white and grey matter regions. While inflammation is present at all stages of MS, it is more pronounced in the relapsing forms of the disease, whereas progressive MS (PMS) shows significant neuroaxonal damage and grey and white matter atrophy. Hence, disease-modifying treatments beneficial in patients with relapsing MS have limited success in PMS. BAF312 (siponimod) is a novel sphingosine-1-phosphate receptor modulator shown to delay progression in PMS. Besides reducing inflammation by sequestering lymphocytes in lymphoid tissues, BAF312 crosses the blood-brain barrier and binds its receptors on neurons, astrocytes and oligodendrocytes. To evaluate potential direct neuroprotective effects, BAF312 was systemically or locally administered in the CNS of experimental autoimmune encephalomyelitis mice with distinct grey- and white-matter lesions (focal experimental autoimmune encephalomyelitis using an osmotic mini-pump). Ex-vivo flow cytometry revealed that systemic but not local BAF312 administration lowered immune cell infiltration in animals with both grey and white matter lesions. Ex-vivo voltage-sensitive dye imaging of acute brain slices revealed an altered spatio-temporal pattern of activation in the lesioned cortex compared to controls in response to electrical stimulation of incoming white-matter fiber tracts. Here, BAF312 administration showed partial restore of cortical neuronal circuit function. The data suggest that BAF312 exerts a neuroprotective effect after crossing the blood-brain barrier independently of peripheral effects on immune cells. Experiments were carried out in accordance with German and EU animal protection law and approved by local authorities (Landesamt für Natur, Umwelt und Verbraucherschutz Nordrhein-Westfalen; 87-51.04.2010.A331) on December 28, 2010.

Advanced methodology for multiple sclerosis lesion exploring: Towards a computer aided diagnosis system

Abstract The exploration and diagnosis of severe neuropathologies is one of the essential tasks that could be reinforced and aided by advanced techniques in medical imagery. Cortex lesions and tumors are examples of pathologies where Magnetic Resonance Imagery modalities are the essential tools for exploration and tracking. Our main added value in this research field was focused on Multiple Sclerosis lesions exploration aiming to offer a clinical computer aided tool capable of helping clinicians during their daily explorations. An automatic method for brain segmentation and Multiple Sclerosis lesion exploration was in fact attentively conceived and tested. Firstly, the brain segmentation was performed using an atlas based Gaussian mixture model, followed by the calculation of a probabilistic lesion map on which an empirical threshold, characterized by a set of constraints, was applied together with a lesion refinement algorithm in order to create a binary lesion mask. The approach was applied to four clinical databases. Compared to various existing methods, the approach showed its efficiency in differentiating normal brain tissues with averages of 0.78 ± 0.04 , 0.85 ± 0.04 and 0.89 ± 0.04 for Dice, sensitivity and specificity, respectively. Besides, it proved the possibility of accurately identifying lesions even in noisy images, and low lesion load, giving averages of 0.75 ± 0.04 , 0.90 ± 0.08 and 0.75 ± 0 . 12 for the previous metrics, respectively. Furthermore, it is able to distinguish between the lesion center and the contiguous dirty white matter, which was carefully validated by clinicians. As a perspective, our approach could be extended to explore other neuropathologies such as Alzheimer’s or Parkinson’s diseases.

Deficits in Behavioral Functions of Intact Barrel Cortex Following Lesions of Homotopic Contralateral Cortex.

Focal unilateral injuries to the somatosensory whisker barrel cortex have been shown cause long-lasting deficits in the activity and experience-dependent plasticity of neurons in the intact contralateral barrel cortex. However, the long-term effect of these deficits on behavioral functions of the intact contralesional cortex is not clear. In this study, we used the “Gap-crossing task” a barrel cortex-dependent, whisker-sensitive, tactile behavior to test the hypothesis that unilateral lesions of the somatosensory cortex would affect behavioral functions of the intact somatosensory cortex and degrade the execution of a bilaterally learnt behavior. Adult rats were trained to perform the Gap-crossing task using whiskers on both sides of the face. The barrel cortex was then lesioned unilaterally by subpial aspiration. As observed in other studies, when rats used whiskers that directly projected to the lesioned hemisphere the performance of Gap-crossing was drastically compromised, perhaps due to direct effect of lesion. Significant and persistent deficits were present when the lesioned rats performed Gap-crossing task using whiskers that projected to the intact cortex. The deficits were specific to performance of the task at the highest levels of sensitivity. Comparable deficits were seen when normal, bilaterally trained, rats performed the Gap-crossing task with only the whiskers on one side of the face or when they used only two rows of whiskers (D row and E row) intact on both side of the face. These findings indicate that the prolonged impairment in execution of the learnt task by rats with unilateral lesions of somatosensory cortex could be because sensory inputs from one set of whiskers to the intact cortex is insufficient to provide adequate sensory information at higher thresholds of detection. Our data suggest that optimal performance of somatosensory behavior requires dynamic activity-driven interhemispheric interactions from the entire somatosensory inputs between homotopic areas of the cerebral cortex. These results imply that focal unilateral cortical injuries, including those in humans, are likely to have widespread bilateral effects on information processing including in intact areas of the cortex.

Perioperative Multimodal Evaluation and Surgical Tactics of Tumor-Related Epilepsy: 2-Dimensional Operative Video

Treatment of tumor-related epilepsy (TRE), especially for tumors near critical areas, requires surgeons to strike a balance between the epileptic benefit and functional outcome after surgery. Here, we present a case in which multimodal evaluation facilitated the achievement of such surgical balance. Informed patient consent was obtained. A 17-yr-old female presented with seizure attacks for 2 yr. Magnetic resonance imaging (MRI) revealed a right parietal mass lesion with hypointense signal on T1W imaging, hyperintense signal on T2W imaging, and homogeneous enhancement. Carbamazepine and valproate administration were unable to control the intermittent seizures. From the patient's history and imaging, the initial diagnosis was refractory TRE. Whether lesionectomy would achieve seizure freedom in this case was not certain. Therefore, dESI (dense array EEG source imaging) was used to localize the epileptic zone preoperatively; results showed that the epileptic zone was very close to the lesion in the primary motor cortex. Surgery was carried out under awake-anesthesia, with the aid of multimodal neuronavigation, intraoperative neurophysiological monitoring, and intraoperative MRI evaluation. A gross total lesion resection was achieved while preserving critical motor areas. Histopathology revealed ganglioglioma grade I diagnosis. No motor deficits following surgery were detected except slight increase of muscle tension in the right lower limb. At 6-mo follow-up, the patient was without any motor impairment or any other neurological deficits and completely seizure-free with the antiepileptic drug Carbamazepine 1200 mg/day.

Dysplastic cerebellar gangliocytoma (Lhermitte–Duclos disease) in the immediate postpartum period

Lhermitte–Duclos disease, also known as dysplastic cerebellar gangliocytoma, is a rare lesion of the cerebellar cortex with both neoplastic and hamartomatous features. A “tiger-striped” cerebellar lesion with unilateral hemispheric expansion and preservation of the gyral pattern is a characteristic finding on magnetic resonance imaging brain. It usually occurs in the setting of Cowden's syndrome, an autosomal dominant condition characterized by multiple hamartomas and neoplastic lesions in skin and internal organs. Evolution of dysplastic cerebellar gangliocytoma during pregnancy is not well known, given its rarity. We describe a young female who presented in the immediate postpartum period with acute hydrocephalus secondary to the left cerebellar gangliocytoma and was treated successfully with surgery. The background setting of Cowden's syndrome was not present in our case.

P90. Super selective amytal injection (Wada-Test) in a 14 year old with left sided parieto-insular epilepsy due to Focal cortical dysplasia

Introduction The classical Wada-test is performed by injecting a narcotic (usually amobarbital) into the left internal carotid artery (ICA) in order to establish language dominance. In the presurgical workup of epilepsy, it has largely been replaced by less invasive methods such as functional MRI and functional Transcranial Doppler Ultrasound. In exceptional cases, the Wada-test can be performed superselectively: the narcotic is injected into a branch of the middle cerebral artery (MCA). This allows proving or excluding language function in a small brain volume. We document the utility of a superselective Wada test in a 14-year-old girl with a dysplastic lesion in the left supramarginal cortex and dorsal insula. Methods A 14 year old girl presented with pharmacoresistant epilepsy. 3 T MRI revealed a left dorsal insular/supramaginal gyrus FLAIR hyperintensity suspicious of focal cortical dysplasia as the likely epileptogenic lesion. Multimodal presurgical work-up confirmed this. Yet, it was questionable if an extended lesionectomy would harm language function. Left ACI Wada-Test was inconclusive. Therefore, a superselective Wada-Test of an M3 branch of the left MCA/perirolandic artery was performed. Results Following the application of 70 mg Amobarbital, both EEG-slowing in electrodes C3, P3, and T5 and repeat angiography confirmed the correct localization of barbiturate action. During the superselective Wada-test, the patient was able to complete a comprehensive test battery of language functions (counting, naming, reading, calculating, spontaneous speech) without evident dysfunction. Neuronavigation and intraoperative electrophysiological monitoring supported an extended lesionectomy, preserving the white matter adjacent to the pyramidal tract. Early after surgery, the patient suffered from a Gerstmann’s syndrome and slight amnestic aphasia. However, this resolved within the first postoperative weeks. Histopathology confirmed focal cortical dysplasia type IIb. Following surgery, the patient is now seizure free for 18 months under reduced antiepileptic drugs. Her academic performance has improved compared to the preoperative status. Conclusion The Wada-test simulates the effect of resective or disconnective surgery on language functions by temporarily inactivating brain areas. Technical advances in catheter angiography allow injecting the narcotic into single MCA-branches or other arteries of similar diameter, thus simulating the effect of small cortical resections. In selected patients, this method can be a valuable supplement of multimodal presurgical workup, and may obviate the need for intra- or extraoperative cortical mapping.

Benefit of magnetic source localization in challenging refractory epilepsies

About 23 million people worldwide suffer from medically refractory epilepsy. Surgery might be the best treatment option with a reasonable chance of seizure freedom. Surgical success depends on the exact definition of the epileptogenic zone (EZ). Magnetoencephalography (MEG) is one of the newer additions to the noninvasive presurgical work-up. This study gives an overview of the impact of MEG on the management of epilepsy patients, focusing on (1) the influence on presurgical evaluation, (2) the identification of patients with the greatest benefit, and (3) possible surgical outcome predictors. An extensive Medline literature search was conducted for studies published from 1990. MEG is in clinical use in the presurgical evaluation of epilepsies for the identification of the EZ and outcome prediction. In cases of failed surgery, it serves as a means to locate the remaining epileptogenic cortex. The usefulness of MEG has been reported for a wide range of localizations including challenging areas like the insula. In cases of multiple possible culprit lesions, MEG can mark the epileptogenic lesion, whereas in cases of nonlesional magnetic resonance imaging (MRI) findings, MEG can pinpoint a lesional or nonlesional epileptogenic cortex area. The role of MEG in the presurgical evaluation of epilepsy was shown with rates of modified approaches in 20–35% of cases. This holds true especially for cases with extratemporal epilepsy. The value of MEG source localization is highest in extratemporal epilepsy, in MRI-negative or multilesional cases, if other modalities yield contradictory or inconclusive results, or in cases of suspected multifocal epilepsy. There is clear evidence that MEG yields nonredundant information and influences the therapeutic course of patients. Various patient groups likely to benefit from MEG were identified. Considering the poor chances of seizure freedom with continued medical treatment, these patients should not be denied source localization, which could result in surgery with favorable outcomes.

L-Cysteine suppresses hypoxia-ischemia injury in neonatal mice by reducing glial activation, promoting autophagic flux and mediating synaptic modification via H2S formation

We previously reported that l-Cysteine, an H2S donor, significantly alleviated brain injury after hypoxia-ischemic (HI) injury in neonatal mice. However, the mechanisms underlying this neuroprotective effect of l-Cysteine against HI insult remain unknown. In the present study, we tested the hypothesis that the protective effects of l-Cysteine are associated with glial responses and autophagy, and l-Cysteine attenuates synaptic injury as well as behavioral deficits resulting from HI. Consistent with our previous findings, we found that treatment with l-Cysteine after HI reduced early brain injury, improved behavioral deficits and synaptic damage, effects which were associated with an up-regulation of synaptophysin and postsynaptic density protein 95 expression in the lesioned cortex. l-Cysteine attenuated the accumulation of CD11b+/CD45high cells, activation of microglia and astrocytes and diminished HI-induced increases in reactive oxygen species and malondialdehyde within the lesioned cortex. In addition, l-Cysteine increased microtubule associated protein 1 light chain 3-II and Beclin1 expression, decreased p62 expression and phosphor-mammalian target of rapamycin and phosphor-signal transducer and activator of transcription 3. Further support for a critical role of l-Cysteine was revealed from results demonstrating that treatment with an inhibitor of the H2S-producing enzyme, amino-oxyacetic acid, reversed the beneficial effects of l-Cysteine described above. These results demonstrate that l-Cysteine effectively alleviates HI injury and improves behavioral outcomes by inhibiting reactive glial responses and synaptic damage and an accompanying triggering of autophagic flux. Accordingly, l-Cysteine may provide a new a therapeutic approach for the treatment of HI via the formation of H2S.

Human Pluripotent Stem-Cell-Derived Cortical Neurons Integrate Functionally into the Lesioned Adult Murine Visual Cortex in an Area-Specific Way

SummaryThe transplantation of pluripotent stem-cell-derived neurons constitutes a promising avenue for the treatment of several brain diseases. However, their potential for the repair of the cerebral cortex remains unclear, given its complexity and neuronal diversity. Here, we show that human visual cortical cells differentiated from embryonic stem cells can be transplanted and can integrate successfully into the lesioned mouse adult visual cortex. The transplanted human neurons expressed the appropriate repertoire of markers of six cortical layers, projected axons to specific visual cortical targets, and were synaptically active within the adult brain. Moreover, transplant maturation and integration were much less efficient following transplantation into the lesioned motor cortex, as previously observed for transplanted mouse cortical neurons. These data constitute an important milestone for the potential use of human PSC-derived cortical cells for the reassembly of cortical circuits and emphasize the importance of cortical areal identity for successful transplantation.

Sevoflurane post-conditioning attenuates traumatic brain injury-induced neuronal apoptosis by promoting autophagy via the PI3K/AKT signaling pathway.

BackgroundSevoflurane post-conditioning exerts nerve-protective effects through inhibiting caspase-dependent neuronal apoptosis after a traumatic brain injury (TBI). Autophagy that is induced by the endoplasmic reticulum stress plays an important role in the secondary neurological dysfunction after a TBI. However, the relationship between autophagy and caspase-dependent apoptosis as well as the underlying nerve protection mechanism that occurs with sevoflurane post-conditioning following a TBI remains unclear.MethodsThe Feeney TBI model was used to induce brain injury in rats. Evaluation of the modified neurological severity scores, measurement of brain water content, Nissl staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay were used to determine the neuroprotective effects of the sevoflurane post-conditioning. Both immunofluorescence and Western blot analyses were used to detect the expression of autophagy-related proteins microtubule-associated protein 1 light chain 3-II and Beclin-1, pro-apoptotic factors, as well as the activation of the phosphatidylinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway within the lesioned cortex.ResultsAutophagy and neuronal apoptosis were activated in the lesioned cortex following the TBI. Sevoflurane post-conditioning enhanced early autophagy, suppressed neuronal apoptosis, and alleviated brain edema, which improved nerve function after a TBI (all P < 0.05). Sevoflurane post-conditioning induced the activation of PI3K/AKT signaling after the TBI (P < 0.05). The neuroprotective effects of sevoflurane post-conditioning were reversed through the autophagy inhibitor 3-methyladenine treatment.ConclusionNeuronal apoptosis and the activation of autophagy were involved in the secondary neurological injury following a TBI. Sevoflurane post-conditioning weakened the TBI-induced neuronal apoptosis by regulating autophagy via PI3K/AKT signaling.

Post-stroke Intranasal (+)-Naloxone Delivery Reduces Microglial Activation and Improves Behavioral Recovery from Ischemic Injury.

Ischemic stroke is the leading cause of disability, and effective therapeutic strategies are needed to promote complete recovery. Neuroinflammation plays a significant role in stroke pathophysiology, and there is limited understanding of how it affects recovery. The aim of this study was to characterize the spatiotemporal expression profile of microglial activation and whether dampening microglial/macrophage activation post-stroke facilitates the recovery. For dampening microglial/macrophage activation, we chose intranasal administration of naloxone, a drug that is already in clinical use for opioid overdose and is known to decrease microglia/macrophage activation. We characterized the temporal progression of microglia/macrophage activation following cortical ischemic injury in rat and found the peak activation in cortex 7 d post-stroke. Unexpectedly, there was a chronic expression of phagocytic cells in the thalamus associated with neuronal loss. (+)-Naloxone, an enantiomer that reduces microglial activation without antagonizing opioid receptors, was administered intranasally starting 1 d post-stroke and continuing for 7 d. (+)-Naloxone treatment decreased microglia/macrophage activation in the striatum and thalamus, promoted behavioral recovery during the 14-d monitoring period, and reduced neuronal death in the lesioned cortex and ipsilateral thalamus. Our results are the first to show that post-stroke intranasal (+)-naloxone administration promotes short-term functional recovery and reduces microglia/macrophage activation. Therefore, (+)-naloxone is a promising drug for the treatment of ischemic stroke, and further studies should be conducted.

MRI manifestations of immunosuppressive drugs associated encephalopathy after allogeneic hematopoietic stem cell transplantation in children with aplastic anemia

Objective To summarize the MRI manifestations of immunosuppressive drugs associated encephalopathy after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in children with aplastic anemia. Methods Fifteen patients with immunosuppressive drugs associated encephalopathy after allogeneic hematopoietic stem cell transplantation for aplastic anemia during January 2014 to October 2016 were analyzed retrospectively. There were 7 males and 8 females, aged from 3 to15 years old, with the median age of 7 years old. Ten cases presented dizziness and headache while other 4 cases presented blurred vision, blind and gaze. Only one case suffered from seizure and loss of consciousness. MRI patterns including distribution, morphology and signal intensity were analyzed after treatment. Follow up MRI were performed after reducing drug dose and symptom remission. The duration of immunosuppressive drugs associated encephalopathy of the 15 cases were 1-14 months, with 6 months in 9 cases. Results Focal lesions were found in 11 cases, in which the deep nuclei were involved in one case and the white matter was involved in 10. Four patients showed both cerebral cortex and white matter lesions, including cerebellum and brainstem invasion in one patient. No corpus callosum lesions were found. Various degree of brain atrophy was found in all patients. Cortical lesions showed swelling and involved subcortical white matter presented as arc shape or strip-like lesions. Patchy patterns were found in deep white matter. Thin layer shaped lesions were found in the periventricular white matter. Small flake-like lesions were found in the brain stem and the cerebellum. The lesions showed hypointensity on T1WI, equal or high signal on T2WI. T2WI FLAIR showed equal or high signal;DWI in the cortex and subcortical white matter lesions showed iso-or high signal, while other lesions were isointense. Eight cases acquired clinical relief in short term without obvious improvement on MRI image. Both clinical symptoms and imaging findings improved in 6 cases. One case showed clinical relief but progression on MRI. Conclusions MRI is an effective way to find immunosuppressive drugs-related encephalopathy in children with aplastic anemia after allogeneic hematopoietic stem cell transplantation. It can help the diagnosis and provide the information for clinical treatment. Key words: Anemia, aplastic; Hematopoietic stem cell transplantation; Magnetic resonance imaging

Chronic kidney disease: Pathological and functional evaluation with intravoxel incoherent motion diffusion-weighted imaging.

Because chronic kidney disease (CKD) is a worldwide problem, accurate pathological and functional evaluation is required for planning treatment and follow-up. Intravoxel incoherent motion diffusion-weighted imaging (IVIM-DWI) can assess both capillary perfusion and tissue diffusion and may be helpful in evaluating renal function and pathology. To evaluate functional and pathological alterations in CKD by applying IVIM-DWI. Prospective study. In all, 72 CKD patients who required renal biopsy and 20 healthy volunteers. 1.5T. All subjects underwent IVIM-DWI of the kidneys, and image analysis was performed by two radiologists. The mean values of true diffusion coefficient (D), pseudo diffusion coefficient (D*), and perfusion fraction (f) were acquired from renal parenchyma. Correlation between IVIM-DWI parameters and estimated glomerular filtration rate (eGFR), as well as pathological damage, were assessed. One-way analysis of variance (ANOVA), paired sample t-test and Spearman correlation analysis. The paired sample t-test revealed that IVIM-DWI parameters were significantly lower in medulla than cortex for both patients and controls (P < 0.01). Regardless of whether eGFR was reduced, ANOVA revealed that f values of renal parenchyma were significantly lower in patients than controls (P < 0.05). Spearman correlation analysis revealed that there were positive correlations between eGFR and D (cortex, r = 0.466, P < 0.001; medulla, r = 0.491, P < 0.001), and between eGFR and f (cortex, r = 0.713, P < 0.001; medulla, r = 0.512, P < 0.001). Negative correlations were found between f and glomerular injury (cortex, r = -0.773, P < 0.001; medulla, r = -0.629, P < 0.001), and between f and tubulointerstitial lesion (cortex, r = -0.728, P < 0.001; medulla, r = -0.547, P < 0.001). IVIM-DWI might be feasible for noninvasive evaluation of renal function and pathology of CKD, especially in detection of renal insufficiency at an early stage. 1 Technical Efficacy: Stage 3 J. Magn. Reson. Imaging 2018;47:1251-1259.

Atonic seizures in children with surgically remediable epilepsy: a motor system seizure phenotype?

Atonic seizures are common in some epileptic syndromes beginning in infancy or early childhood but they are rarely described in epilepsy with focal seizures of structural aetiology. We aimed to characterize the electroclinical features of atonic seizures in surgically remediable paediatric patients and to study the spatiotemporal organization of the underlying epileptogenic networks. We retrospectively analysed two consecutive, longitudinally evaluated and surgically treated paediatric patients presenting with atonic seizures as a manifestation of pharmacoresistant epilepsy of structural aetiology, evidenced by scalp- and stereotactic intracerebral video-EEG-recordings. A quantitative analysis of the epileptogenic zone organization was performed using the "epileptogenicity index". Long-lasting generalized ictal atonia, occurring in infancy, was a predominant clinical feature in both patients, with some hints of focal origin present in one case. The seizure phenotype evolved at later age into subtle segmental atonia, associated with prominent positive motor signs. The epileptogenic zone was localized within the dorsolateral or mesiolateral premotor region. Its spatial organization was focal, matching the lesional cortex in one and distributed involving several lesional and non-lesional structures in the other case. The emergence of atonic semiology temporally correlated with involvement of both lateral and mesial premotor, as well as primary motor areas. We hypothesize that atonic seizures may be considered as a motor system seizure phenotype in the setting of structural epilepsy. Complete removal of the epileptogenic area provided excellent seizure control.

When the affordances disappear: Dynamical and computational explanations of optic ataxia

Two options fuel the debate on the cognitive processes underlying the perception of affordances. On the one hand, the ecological theory of affordance fits with the methodological assumptions of the dynamical systems theory of cognition. On the other hand, it is nowadays common to conceive the perception of affordances within a computational framework. This article defends the explanatory power of a computational approach and aims to extend the concept of affordance beyond the boundaries of the dynamical systems theory of cognition. For that purpose, I consider the case of patients suffering from optic ataxia, a condition in which some aspects of visual guidance over reaching with the hand are lost following a lesion in the left parietal cortex. Etiological considerations, indeed, reveal that a computational approach to the perception of affordances allows for an explanation of ataxic behavior that is not available to the dynamical systems theory.

The effect of electroacupuncture on proteomic changes in the motor cortex of 6-OHDA Parkinsonian rats

Electroacupuncture (EA) has been reported to alleviate motor deficits in Parkinson’s disease (PD) patients, and PD animal models. However, the mechanisms by which EA improves motor function have not been investigated. We have employed a 6-hydroxydopamine (6-OHDA) unilateral injection induced PD model to investigate whether EA alters protein expression in the motor cortex. We found that 4weeks of EA treatment significantly improved spontaneous floor plane locomotion and rotarod performance. High-throughput proteomic analysis in the motor cortex was employed. The expression of 54 proteins were altered in the unlesioned motor cortex, and 102 protein expressions were altered in the lesioned motor cortex of 6-OHDA rats compared to sham rats. Compared to non-treatment PD control, EA treatment reversed 6 proteins in unlesioned and 19 proteins in lesioned motor cortex. The present study demonstrated that PD induces proteomic changes in the motor cortex, some of which are rescued by EA treatment. These targeted proteins were mainly involved in increasing autophagy, mRNA processing and ATP binding and maintaining the balance of neurotransmitters.

9-cis retinoic acid induces neurorepair in stroke brain

The purpose of this study was to examine the neurorestorative effect of delayed 9 cis retinoic acid (9cRA) treatment for stroke. Adult male rats received a 90-min right distal middle cerebral artery occlusion (dMCAo). Animals were separated into two groups with similar infarction sizes, based on magnetic resonance imaging on day 2 after dMCAo. 9cRA or vehicle was given via an intranasal route daily starting from day 3. Stroke rats receiving 9cRA post-treatment showed an increase in brain 9cRA levels and greater recovery in motor function. 9cRA enhanced the proliferation of bromodeoxyuridine (+) cells in the subventricular zone (SVZ) and lesioned cortex in the stroke brain. Using subventricular neurosphere and matrigel cultures, we demonstrated that proliferation and migration of SVZ neuroprogenitor cells were enhanced by 9cRA. Our data support a delayed and non-invasive drug therapy for stroke. Intranasal 9cRA can facilitate the functional recovery and endogenous repair in the ischemic brain.