Tooth-brushing epilepsy: an SEEG study and surgical treatment.

We report a patient with reflex tooth-brushing-triggered epilepsy, associated with a post-central lesion within the right somatosensory face area. Contralateral facial sensory and motor phenomena, associated with contralateral upper limb extension, were present at seizure onset after gingival stimulation, but seizures could also be induced by contact with solid food or liquids. Spontaneous seizures also were recorded. Secondary generalization was infrequent. Stereoelectroencephalography implantation was performed, with seizure recording and cortical/subcortical stimulation for mapping, to identify the precise extent of surgical resection. Complete postoperative control of epilepsy was achieved, accompanied by a mild and transient neurological deficit. [Published with video sequence].

Terminal Arbors of Callosal Axons Undergo Plastic Changes in Early-Amputated Rats.

Sensory information is processed in specific brain regions, and shared between the cerebral hemispheres by axons that cross the midline through the corpus callosum. However, sensory deprivation usually causes sensory losses and/or functional changes. This is the case of people who suffered limb amputation and show changes of body map organization within the somatosensory cortex (S1) of the deafferented cerebral hemisphere (contralateral to the amputated limb), as well as in the afferented hemisphere (ipsilateral to the amputated limb). Although several studies have approached these functional changes, the possible finer morphological alterations, such as those occurring in callosal axons, still remain unknown. The present work combined histochemistry, single-axon tracing and 3D microscopy to analyze the fine morphological changes that occur in callosal axons of the forepaw representation in early amputated rats. We showed that the forepaw representation in S1 was reduced in the deafferented hemisphere and expanded in the afferented side. Accordingly, after amputation, callosal axons originating from the deafferented cortex undergo an expansion of their terminal arbors with increased number of terminal boutons within the homotopic representation at the afferented cerebral hemisphere. Similar microscale structural changes may underpin the macroscale morphological and functional phenomena that characterize limb amputation in humans.

Sleep deprivation has a neuroprotective role in a traumatic brain injury of the rat.

During the process of a brain injury, responses to produce damage and cell death are activated, but self-protective responses that attempt to maintain the integrity and functionality of the brain are also activated. We have previously reported that the recovery from a traumatic brain injury (TBI) is better in rats if it occurs during the dark phase of the diurnal cycle when rats are in the waking period. This suggests that wakefulness causes a neuroprotective role in this type of injury. Here we report that 24h of total sleep deprivation after a TBI reduces the morphological damage and enhances the recovery of the rats, as seen on a neurobiological scale.

fMRI of the sensorimotor cortex in patients with traumatic brain injury after intensive rehabilitation.

For evaluating the patterns of brain activation in sensorimotor areas following motor rehabilitation, seven male patients diagnosed with TBI underwent an fMRI study before and after being subjected to motor rehabilitation. Six patients showed a reduction in the BOLD signal of their motor cortical areas during the second fMRI evaluation. A decrease in cerebellum activation was also observed in two patients. Newly activated areas, were observed in four patients after treatment. In addition, an increase in the activation of the supplementary motor area (SMA) following rehabilitation was observed in only one test subject. The findings show that motor rehabilitation in TBI patients produces a decrease in the BOLD signal for the sensorimotor areas that were activated prior to treatment. In addition, we observed the recruitment of different brain areas to compensate for functional loss due to TBI in line with the cortical reorganisation mechanism.

[Changes in the functional magnetic resonance imaging of the sensorimotor cortex in traumatic brain injury after intensive rehabilitation]. / Cambios en resonancia magnética funcional de la corteza sensitivomotora en pacientes con traumatismo craneoencefalico tras un programa intensivo de rehabilitación.

AIM: To evaluate the potential reorganization of the sensorimotor cortex in a patient with traumatic brain injury after an intensive motor rehabilitation. PATIENTS AND METHODS: A 17-year-old male with severe traumatic brain injury was submitted to functional magnetic resonance imaging (fMRI) analyses of motor control before and after motor rehabilitation. The motor tasks performed during fMRI were finger tapping, ankle plantar flexion, and toe flexion. RESULTS: Prior to treatment, the cerebrally activated areas for the right hand during finger tapping were the primary motor (M1), supplementary motor area (SMA), superior parietal and postcentral areas. For the left hand, the areas were the M1 and the cerebellum. After treatment, the activated areas were the pre and postcentral areas for the right hand and the precentral area for the left hand. For the foot motor-task, the activated areas prior to treatment were the paracentral area for the right foot, and the SMA, paracentral and poscentral areas for the left. After treatment, activation for the right foot was seen in the paracentral area, and activation for the left foot was seen in the paracentral area and SMA. CONCLUSIONS: The decrease in the post-treatment activation pattern could be explained as a cortical reorganization, which in the current study was related to motor skill and motor automatism acquired by the patient.

Neurodegeneration and prolonged immediate early gene expression throughout cortical areas of the rat brain following acute administration of dizocilpine.

N-methyl-d-aspartate receptor antagonist drugs (NMDA-A), such as dizocilpine (MK801), induce long-lasting behavioral disturbances reminiscent to psychotic disorders in humans. To identify cortical structures affected by NMDA-A, we used a single dose of MK801 (10 mg/kg) that caused low and high neurodegeneration in intact and orchiectomized male rats, respectively. Degenerating somas (neuronal death) and axonal/synaptic endings (terminal degeneration) were depicted by a silver technique, and functionally affected cortical neuronal subpopulations by Egr-1, c-Fos, and FosB/DeltaFosB-immunolabeling. In intact males, MK801 triggered a c-Fos induction that remained high for more than 24 h in selected layers of the retrosplenial, somatosensory and entorhinal cortices. MK801-induced neurodegeneration reached its peak at 72 h. Degenerating somas were restricted to layer IV of the granular subdivision of the retrosplenial cortex, and were accompanied by suppression of Egr-1 immunolabeling. Terminal degeneration extended to selected layers of the retrosplenial, somatosensory and parahippocampal cortices, which are target areas of retrosplenial cortex. Induction of FosB/DeltaFosB by MK801 also extended to the same cortical layers affected by terminal degeneration, likely reflecting the damage of synaptic connectivity. In orchiectomized males, the neurodegenerative and functional effects of MK801 were exacerbated. Degenerative somas in layer IV of the retrosplenial cortex significantly increased, with a parallel enhancement of terminal degeneration and FosB/DeltaFosB-expression in the mentioned cortical structures, but no additional areas were affected. These observations reveal that synaptic dysfunction/degeneration in the retrosplenial, somatosensory and parahippocampal cortices might underlie the long-lasting impairments induced by NMDA-A.

A case of tactile agnosia with a lesion restricted to the post-central gyrus.

Tactile agnosia has been described after lesions of the primary sensory cortex but the exact location and extension of those lesions is not clear. We report the clinical features and imaging findings in a patient with an acute ischemic stroke restricted to the primary sensory area (S1). A 73-year-old man had a sudden onset of a left alien hand, without left hemiparesis. Neurological examination showed intact primary sensory functions, but impaired recognition of shape, size (macrogeometrical) and texture (microgeometrical) of objects; damage confined to the post-central gyrus, sparing the posterior parietal cortex was demonstrated on MRI. An embolic occlusion of the anterior parietal artery was suspected as mechanism of stroke. Tactile agnosia with impaired microgeometrical and macrogeometrical features' recognition can result from a single lesion in the primary sensory cortex (S1) in the right parietal hemisphere, sparing other regions of the cerebral cortex which presumably participate in tactile object recognition.

Efecto de dosis única intraperitoneal de cipermetrina en la corteza cerebral somatosensorial de ratones CF- 1 / Effect of a single doses intraperitoneal of cypermethrin in brain somatosensory area of mice CF-1

La cipermetrina es un pesticida ampliamente utilizado en agricultura y en salud pública. Sus efectos histopatológicos a nivel de sistema nervioso central han sido poco estudiados, aún cuando se han demostrado casos de intoxicación en humanos, con importante compromiso neurológico. El propósito de este trabajo es conocer los efectos de una dosis única intraperitoneal de cipermetrina sobre la morfología neuronal de corteza somatosensorial (láminas superficiales y profundas) de ratones CF-1. 35 ratones fueron separados en tres grupos: control (n=5), control vehículo (n=15) y experimental (n=15); los dos últimos grupos sacrificados los días 1, 8, 18, 26 y 35, en grupos de a tres. Los encéfalos fueron removidos, fijados, y procesados con técnica de rutina, para un análisis morfométrico. Análisis estadístico con Kruskal Walli's test. Fueron evidenciadas alteraciones morfológicas correspondientes a muerte neuronal en todas las láminas estudiadas, a los distintos intervalos de tiempo.

The cypermethrin is a pesticide widely used in agriculture and public health. Their histopathological effects at central nervous system level, little have been studied, even though has demonstrated cases of poisoning in humans with important neurological commitment. The aim of this work is to know the effects a intraperitoneal single dose of cypermethrin on neuronal morphology of somatosensory cortex (superficial and deep laminae) of mice CF-1. 35 mice were separated in three groups: control (n=5), control vehicle (n=15) and experimental (n=15); the two last sacrificed groups 1, 8, 18, 26 and 35 days, three animals per group. The brain were removed, fixed, and process with routine technique, for a morphometric analysis. Statistical analysis with Kruskal Wallís test. We demonstrated corresponding morphologic alterations until death neuronal, in all studied laminae, at the different time intervals.

Glial changes in primate cerebral cortex following long-term sensory deprivation.

Significant morphological modifications in the layout of primate-specific (interlaminar) astroglia were found in somatosensory areas 3a, 3b, 1 and 2 eleven to thirteen months after transection of the posterior spinal cord in adult Macaca monkeys. These observations plus lack of evidence of a persistent reactive astrocytosis suggest that changes in the spatial arrangement of interlaminar glia may be an integral part of the long-term process of structural reorganization of the cerebral cortex following cortical deafferentation.

Gangliosides minimize motor disabilities and histopathological changes in cortical lesioned and transplanted rats.

The effect of bovine brain gangliosides was studied in rats lesioned by partial suction of the right somatosensory cortex and also in rats implanted with a piece of fetal brain tissue in this area. In both experiments a group of animals received 30 mg/kg i.p. of gangliosides daily for a period of 7 days after surgery. In lesioned rats, the untreated group showed a lower maintenance on a tight rope test at 7 as well as at 14 days, as compared with a sham-operated group (p < 0.05). In transplanted rats ganglioside treatment prevented the increase of the probability of falls from a horizontal bar at days 7 and 14 post-operations and the probability of slips on a vertical bar at day 7 (p < 0.05). Rats were killed at day 15 and brain coronal sections were obtained. Nuclear area and circularity were measured in a sample of cortical and grafted cells in a computer aid-image analyzer. Ganglioside protection on the normal size and shape of the nuclei in the ipsilateral cortex in lesioned as well as in transplanted rats (p < 0.01) was found. A higher nuclear area in ganglioside than in saline treated grafts was noted. Results suggest a protective action of the gangliosides against the lesion-induced motor dysfunction and secondary cortical cell degeneration.

Asymbolia for pain: a sensory-limbic disconnection syndrome.

We describe the behavioral and neuroanatomical features of asymbolia for pain occurring in 6 patients following unilateral hemispheric damage secondary to ischemic lesions in 5 and traumatic hematoma in 1. In the absence of primary sensory deficits, these 6 patients showed a lack of withdrawal and absent or inadequate emotional responses to painful stimuli applied over the entire body, as well as to threatening gestures. Five patients also failed to react to verbal menaces. Patients appeared unconcerned about the defect and seemed unable to learn appropriate escape or protective responses. Common associated abnormalities were rapidly resolving hemiparesis, cortical-type sensory loss, unilateral neglect, and body-schema disorders. Neuroradiological examination disclosed left hemispheric lesions in 4 patients and right hemispheric involvement in 2. Although lesion extension differed, the insular cortex was invariably damaged in all 6 patients. These findings suggest that insular damage may play a critical role in the development of the syndrome by interrupting connections between sensory cortices and the limbic system.