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https://drive.google.com/open?id=1sla_duuRjCaF4QSEcO4aQbsYg0LyfuvB
Learning novel visuomotor tasks requires precise processing and transformation of incoming sensory information to produce accurate motor responses. The present study characterized neural activity associated with sensorimotor processes during novel visuomotor learning. We hypothesized that the acquisition of a visuomotor skill would be accompanied by experience-dependent modulation of sensorimotor cortical activity. Subjects controlled a cursor on a computer screen with a joystick. With the goal to move the cursor to a cued target after a brief delay, the relationship between joystick and cursor movement was manipulated such that joystick movement controlled cursor velocity, not displacement (rate task). Individual trials in this task were further divided into early (rate1) and late (rate2) blocks. Event-related potentials (ERPs) were averaged to target presentation, the cue for movement, and movement onset. Subjects were more accurate after practice in late rate2 compared to early rate1 blocks. ERPs associated with movement onset were larger in amplitude and occurred earlier over centroparietal sites following practice. In contrast, ERPs to the cue to move were enhanced frontocentrally initially and diminished with practice. The results suggest that practice on a novel visuomotor task is associated with changes in frontoparietal networks involved in motor preparation and sensorimotor integration. Specifically, practice-related enhancement of movement-related ERPs supports experience-dependent alterations in the network subserving motor preparation.
Andrew P. Yonelinas
Neal E. A. Kroll
Kathleen Baynes
Ian G. Dobbins
C.M. Frederick
Robert T. Knight
Michael S. Gazzaniga
Date: 2001
PubMed: 11476095
Identification of visually presented objects and words is facilitated by implicit memory for past visual experiences with those items. Several behavioral and neuroimaging studies suggest that this form of memory is dependent on perceptual processes localized in the right occipital lobe. We tested this claim by examining implicit mem- ory in patients with extensive right occipital lobe lesions, using lexi- cal-decision, mirror-reading, picture-fragment, and word-fragment- completion tests, and found that these patients exhibited normal levels of priming. We also examined implicit memory in patients with com- plete callosotomies, using standard and divided-visual-field word- fragment-completion procedures, and found that the isolated left hemisphere exhibited normal priming effects. The results indicate that the right occipital lobe does not play a necessary role in visual im- plicit memory, and that the isolated left hemisphere can support nor- mal levels of visual priming in a variety of tasks.
We examined the effects of bilateral orbitofrontal damage on emotional processing and hemispheric attention capacity. Participants (four bilateral orbitofrontal patients and age- matched controls) discriminated between upright and inverted triangles (target). Targets were randomly presented in the left (LVF) or right visual hemifield (RVF, 150 ms). Emotional (pleasant or unpleasant; 150 ms) or neutral stimuli were presented centrally 350 ms prior to the target. Pleasant stimuli decreased whereas unpleasant stimuli increased RTs to LVF targets, with exaggerated effects in patients. Orbitofrontal damage differentially altered processing of emotional stimuli. In addition, orbitofrontal patients showed altered target ERPs, with evidence of increased activity over frontal sites for only LVF targets. The results suggest an interplay between orbitofrontal cortex and the right hemisphere.
Electrophysiological and hemodynamical responses of the brain allow investigation of the neural origins of human attention. We review attention-related brain responses from auditory and visual tasks employing oddball and novelty paradigms. Dipole localization and intra- cranial recordings as well as functional magnetic resonance imaging reveal multiple areas involved in generating and modulating attentional brain responses. In addition, the in ̄uence of brain lesions of circumscribed areas of the human cortex onto attentional mechanisms are reviewed. While it is obvious that damaged brain tissue no longer functions properly, it has also been shown that functions of non-lesioned brain areas are impaired due to loss of modulatory in ̄uence of the lesioned area. Both early (P1 and N1) and late (P3) event-related potentials are modulated by excitatatory and inhibitory mechanisms.. Oscillatory EEG-correlates of attention in the alpha and gamma frequency range also show attentional modulation.
The frontal and parietal cortex are intimately involved in the representation of goal-directed movements, but the crucial neuroanatomical sites are not well established in humans. In order to identify these sites more precisely, we studied stroke patients who had the classic syndrome of ideomotor limb apraxia, which disrupts goal-directed movements, such as writing or brushing teeth. Patients with and without limb apraxia were identified by assessing errors imitating gestures and specifying a cut-off for apraxia relative to a normal control group. We then used MRI or CT for lesion localization and compared areas of overlap in those patients with and without limb apraxia. Patients with ideomotor limb apraxia had damage lateralized to a left hemispheric network involving the middle frontal gyrus and intraparietal sulcus region. Thus, the results revealed that discrete areas in the left hemisphere of humans are critical for control of complex goal-directed movements.
We examined the effects of emotional stimuli on right and left hemisphere detection performance in a hemifield visual discrimination task. A group of 18 healthy subjects were asked to discriminate between upright and inverted triangles (target). Targets were randomly presented in the left or right visual hemifield (150 ms target duration). A brief emotional picture (pleasant or unpleasant; 150 ms stimulus duration) or neutral picture selected from the International Affective Picture System was randomly presented either in the same (47%) or the opposite (47%) spatial location to the subsequent target. Emotional or neutral stimuli offset 150 ms prior to the subsequent target. Subjects were instructed to ignore the pictures and respond to the targets as quickly and accurately as possible. Independent of field of presentation, emotional stimuli prolonged reaction times (PB 0.01) to LVF targets, with unpleasant stimuli showing a greater effect than pleasant stimuli. The current study shows that brief emotional stimuli selectively impair right hemispheric visual discrimination capacity. The findings suggest automatic processing of emotional stimuli captures right hemispheric processing resources and transiently interferes with other right hemispheric functions.
We found that medial frontal cortex activity associated with action monitoring (detecting errors and behavioral conflict) depended on activity in the lateral prefrontal cortex. We recorded the error- related negativity (ERN), an event-related brain potential proposed to reflect anterior cingulate action monitoring, from individuals with lateral prefrontal damage or age-matched or young control participants. In controls, error trials generated greater ERN activity than correct trials. In individuals with lateral prefrontal damage, however, correct-trial ERN activity was equal to error-trial ERN activ- ity. Lateral prefrontal damage also affected corrective behavior. Thus the lateral prefrontal cortex seemed to interact with the anterior cingulate cortex in monitoring behavior and in guiding compensatory systems.
Single neuron, evoked potential and metabolic techniques show that attention influences visual pro- cessing in extrastriate cortex. We provide anatomical, electrophysiological and behavioral evidence that prefrontal cortex regulates neuronal activity in extrastriate cortex during visual discrimination. Event-related potentials (ERPs) were recorded during a visual detection task in patients with damage in dorsolateral prefrontal cortex. Prefrontal damage reduced neuronal activity in extrastriate cortex of the lesioned hemisphere. These electrophysiological abnormalities, beginning 125 ms after stimulation and lasting for another 500 ms, were accompanied by behavioral deficits in detection ability in the contralesional hemifield. The results provide evidence for intrahemispheric prefrontal modulation of visual processing.
Wayne Khoe
Neal E. A. Kroll
Andrew P. Yonelinas
Ian G. Dobbins
Robert T. Knight
Date: 2000
PubMed: 10869576
Recent reports suggest that some amnesic patients perform relatively normally on forced-choice recognition memory tests. Their preserved performance may re ̄ect the fact that the test relies more heavily on assessments of familiarity, a process that is relatively preserved in these patients, than do other recognition tests such as yes±no tests, which may rely more on recollection. The current study examined recognition memory using yes±no and forced-choice procedures in control and amnesic patients in order to determine whether the two tasks dierentially relied on recollection and familiarity, and whether the extent of the recognition memory de®cit observed in amnesia was dependent upon the type of recognition test used to measure performance. Results using the remember±know procedure with healthy subjects showed that there were no substantial dierences in recognition accuracy or in the contribution of recollection to these two tasks. Moreover, amnesic patients were not found to perform better on a forced-choice test than on a yes±no test, suggesting that familiarity contributed equally to these two types of recognition test.
Lesions of the hippocampal formation or transec- tions of the fornix are followed by shrinkage of the medial mammillary nucleus (MMN). We determined whether the shrinkage of this nucleus was due to loss and/or shrinkage of neurons in addition to the loss of neuropil. We examined the MMN in a patient (KB) with an infarct that led to marked atrophy of the left hippocampus and subiculum, leaving the right MMN intact. Unbiased, stereological measure- ment techniques were used to compare the total cell number and individual neuronal cross-sectional ar- eas in both left and right MMN in this patient and in two control human brains. We also analyzed the MMN in four macaque monkeys that underwent ex- perimental unilateral transections of the fornix. The volume of the MMN on the lesioned side in KB was 55% of the unlesioned side (2.8 mm 3 vs 5.1 mm 3 ); the MMN in the monkey cases were reduced to 47–58% of the volume of the nonlesioned side. Neurons in the deafferented MMN of KB and of the monkey subjects were decreased in cross-sectional area (16 –20%, P < 0.0001). There was a trend toward decreased cell numbers (11–15%) on the lesioned side in all cases. We have estimated that the loss in cell number and shrinkage of remaining cells contribute negligibly to the 45% reduction in MMN volume. Therefore, the loss of neuropil (dendrites and afferent and efferent axons) appears to be the major contributor to the change in MMN volume.
Robert T. Knight
Marcia Grabowecky
Date: 2000
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A central feature of consciousness is the ability to control the fourth dimension, time. Humans can effortlessly move their internal mental set from the present moment to a past remembrance and just as easily project themselves into a future event. It is proposed that this capacity to extract oneself from the present and fluidly move forward or backward in time is dependent on the evolution of the human prefrontal cortex. Prefrontal cortex modulates activity in multi-modal association and limbic cortices through widely distributed inhibitory and excitatory pathways. Prefrontal cortex also has a selective bias to novelty, crucial for detecting change and hence for the correct temporal coding of events. These extensive modulatory pathways coupled with an intrinsic link to temporal coding provide a mechanism for rapid engagement of distributed neural networks critical for seamless transitions through the time continuum. Support for this hypothesis is found in the fact that prefrontal damage results in a failure in the ability to extract oneself from the present. Indeed, the hallmark of the severe prefrontal syndrome is persevatory and stimulus-bound behavior--a classic example of a failure in temporal control.
Robert T. Knight
Date: 2000
A review of the literature investigating the neural origins of detection behavior in humans reveals two event-related potential components, P3a and P3b, each with a distinct neural organization and cognitive func- tion. The P3a is involved in automatic novelty detection and characterized by a more anterior cortical distribution, whereas the P3b is concerned with volitional target detection and has a more posterior cortical distribution. Intra- cranial investigation, studies with patients with focal brain lesions, and functional neuroimaging (fMRI) studies converge with the scalp-recorded ERP data in suggesting that a widespread cortical network gives rise to both automatic and controlled detection behavior. The main regions consistently attributed to generating detection related brain activation include the temporal-parietal junction, medial temporal complex, and the lateral prefrontal cortex. The extant human and animal literature addressing the neural networks, neuropharmacological underpinnings, and behavioral signicance of “the P300” potential will be reviewed.
Studies of human amnesia provide evidence for a short-term memory store with information transfer to long term memory occurring within 60 s of sensory encoding. Human and nonhuman primate research has shown that maintenance of this short-term or working memory store is dependent upon frontal cortical activation, although the critical temporal parameters of frontal involvement throughout this 60-s window are undetermined. We examined prefrontal contributions to rapid Žunder 2 s. and sustained Žover 4 s. visual working memory by recording behavioral performance and event-related potentials ŽERPs. in patients with lesions in dorsolateral frontal cortex and age-matched control subjects. Prefrontal lesioned patients generated a reduced sustained frontal positivity at all delays. At short delays, patients generated reduced performance to stimuli presented in the contralesional field. Patients generated a negative potential ŽN400., greatest to contralesionally presented stimuli, that was observed in the control subjects only at long delays. The results indicate that prefrontal lesions impair the frontal component of an anterior–posterior working memory network activated during rapid and sustained visual memory processing. Frontal patients may require activation of limbic cortex, indexed by N400, for maintenance of both rapid and sustained working memory.
Ideomotor limb apraxia is a classic neurological disorder manifesting as a breakdown in co-ordinated limb control with spatiotemporal deficits. We employed kinematic analyses of simple aiming movements in left hemisphere- damaged patients with and without limb apraxia and a normal control group to examine preprogramming and response implementation deficits in apraxia. Damage to the frontal and parietal lobes was more common in apraxics, but neither frontal nor parietal damage was associated with different arm movement deficits. Limb apraxia was associated with intact preprogramming but impaired response implementation. The response implementation deficits were characterized by spatial but not temporal deficits, consistent with decoupling of spatial and temporal features of movement in limb apraxia. While the apraxics’ accuracy was normal when visual feedback was available, it was impaired when visual feedback of either target location or hand position was unavailable. This finding suggests that ideomotor limb apraxia is associated with disruption of the neural representations for the extrapersonal (spatial location) and intrapersonal (hand position) features of movement. The non-apraxic group’s normal kinematic performance demonstrates that the deficits demonstrated in the apraxic group are not simply a reflection of left hemisphere damage per se.
Prefrontal cortex provides both inhibitory and excitatory input to distributed neural cir- cuits required to support performance in diverse tasks. Neurological patients with prefrontal damage are impaired in their ability to inhibit task-irrelevant information during behavioral tasks requiring performance over a delay. The observed enhancements of primary auditory and somatosensory cortical responses to task-irrelevant distractors suggest that prefrontal damage disrupts inhibitory modulation of inputs to primary sensory cortex, perhaps through abnormalities in a prefrontal-thalamic sensory gating system. Failure to suppress irrelevant sensory information results in increased neural noise, contributing to the de®cits in decision making routinely observed in these patients. In addition to a critical role in inhibitory control of sensory ̄ow to primary cortical regions, and tertiary prefrontal cortex also exerts excitatory input to activity in multiple sub-regions of secondary association cortex. Unilateral prefrontal damage results in multi-modal decreases in neural activity in posterior association cortex in the hemisphere ipsilateral to damage. This excitatory modulation is necessary to sustain neural activity during working memory. Thus, prefrontal cortex is able to sculpt behavior through parallel inhibitory and excitatory regulation of neural activity in distributed neural net- works.
To clarify the involvement of prefrontal cortex in episodic memory, behavioral and event-related potential (ERP) measures of recognition were examined in patients with dorsolateral prefrontal lesions. In controls, recognition accuracy and the ERP old-new effect declined with increasing retention intervals. Although frontal patients showed a higher false-alarm rate to new words, their hit rate to old words and ERP old-new effect were intact, suggesting that recognition processes were not fundamentally altered by prefrontal damage. The opposite behavioral pattern was observed in patients with hippocampal lesions: a normal false-alarm rate and a precipitous decline in hit rate at long lags. The intact ERP effect and the change in response bias during recognition suggest that frontal patients exhibited a deficit in strategic processing or postretrieval monitoring, in contrast to the more purely mnemonic deficit shown by hippocampal patients.