Regions Of Sensorimotor Cortex Research Articles

Serial processing and the “phonetic route:” Lessons learned in the functional reorganization of deep dyslexia

A patient with chronic agrammatic Broca's aphasia presented with symptoms of deep dyslexia, in which it is presumed that phonologic processing of the written message is disrupted. Functional reorganization of the “nonlexical” or phonetic route of reading was undertaken according to principles of A. R. Luria, whereby the patient must learn consciously to control behaviors that had formerly been unconcious and automatic. This patient's responses in treatment made it clear that the phonetic route encompasses at least two dissociable functions, grapheme-phoneme conversion and sequential analysis. This is discussed in light of Luria's ideas regarding the functions of the precentral and postcentral regions of sensorimotor cortex.

Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating short-latency activity

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.(ABSTRACT TRUNCATED AT 400 WORDS)

Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating long-latency activity.

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.

A selective decrease in the number of GABAergic somata occurs in pre-seizing monkeys with alumina gel granuloma

Previous studies have shown that a loss of GAB Aergic neuronal somata is associated with a loss of GABAergic terminals at chronic cortical epileptic foci in monkeys. The present study was undertaken to determine whether GABAergic neuronal loss occurs prior to the onset of clinical seizures in monkeys that were treated with alumina gel but did not display seizures. Seven adolescent ( Macaca mulatta) monkeys received alumina gel implants into the left pre- and post-central gyri, specifically centered in hand-face regions of sensorimotor cortex. Three other monkeys were used as controls. Two of these were surgical controls and the third was a normal animal. Three monkeys (pre-seizing) were sacrificed 2–4 weeks after the alumina gel implant but prior to clinically active seizures. Three other monkeys with chronic seizure activity (chronically seizing) were sacrificed 3–6 months after the implant. Tissue sections were taken from an area adjacent to the alumina gel granuloma (focus), from a site distal to it (parafocus) and from the non-epileptic contralateral side. Sections from all monkeys were processed for glutamate decarboxylase (GAD) immunocytochemistry and then examined with a light microscope. In addition, adjacent sections were stained with a Nissl stain and the total number of neurons was counted in these sections. Statistical analysis showed a significant decrease in the number of GAD-positive cells in the pre-seizing and chronic animals. The pre-seizing monkeys showed a significant loss of 23–44% at the focus in contrast to the total number of neurons which did not change significantly. The loss of GAD-positive cells was greater in the chronic animals that showed significant losses at both the focus and parafocus, 42–61% and 15–26%, respectively. It is important to note that the chronic monkeys displayed an 11–61% significant loss of total neurons at the epileptic focus. The surgical control animals showed no seizure activity and no significant loss of total neurons or GAD-positive cells. The main finding of this study indicates that a selective loss of GAD-positive neuronal somata occurs in pre-seizing monkeys with alumina gel implants. This finding is consistent with the previously reported loss of GABAergic terminals in pre-seizing monkeys. Since virtually all monkeys treated with alumina gel develop seizures, the results of this study add further support to the hypothesis that GABA neuronal loss plays a causal role in focal epilepsy.

A review of recent observations concerning the synaptic organization of the basilar pontine nuclei.

Ultrastructural studies are described that have identified in the basilar pontine nuclei (BPN), the synaptic boutons formed by the corticopontine, cerebellopontine, tectopontine, and dorsal column nuclei-pontine afferent projection systems. In addition, immunocytochemical studies visualized neuronal somata, dendrites, and synaptic boutons that contain immunoreactivity for GABA or the synthesizing enzyme glutamic acid decarboxylase (GAD). Based upon differences in the mode of degeneration and postsynaptic locus of degenerative synaptic boutons in the BPN, it is suggested that two types of cortical neurons and three classes of deep cerebellar nuclear cells project to the BPN. For similar reasons, it appears that two types of neurons in the dorsal column nuclei project to the BPN while only one type of afferent synaptic bouton takes origin from the superior colliculus. Furthermore it appears that the population of BPN neurons projecting to the paramedian lobule receives convergent inputs from the cutaneous periphery and the corresponding region of sensorimotor cortex. Studies employing GAD immunohistochemistry indicate that GABA-ergic neurons and axon terminals are present in the BPN and thus support the suggestion that a local inhibitory interneuron is present within the BPN. Taken together these observations suggest that basilar pontine neurons might play a more active role in the integration of various types of information destined for the cerebellar cortex than has previously been recognized.

Neonatal vs. adult sensorimotor cortex damage: The ability to use spared cortical fragments of target tissue to guide tactile learning

In an earlier study, it was found that rats with little or no sparing of sensorimotor cortex areas SmI and SmII performed extremely poorly on a battery of five tactile discriminations, whether the lesions were made on the 2nd day of life or at maturity. In contrast, infant-operated rats with 13%–28% of the anterolateral part of SmI spared performed better than adult- or infant-operated animals with larger, more complete lesions, although their learning scores were still worse than those of sham-operated animals. In order to determine whether adult-operated rats could use spared fragments of target tissue as well as the infant-operated animals could, lesions sparing 15%–31% of the same regions of sensorimotor cortex were made in mature rats that were subsequently tested for their ability to learn the discrimination problems. The results provide some support for the hypothesis that infant-operated animals can make more efficient use of spared fragments of target tissue than can their adult-operated counterparts even though, in both age groups, animals with subtotal lesions perform better than do animals with almost all or all of the sensorimotor cortex destroyed.