Showing papers by "Kenneth M. Heilman published in 1994"

Posterior neocortical systems subserving awareness and neglect. Neglect associated with superior temporal sulcus but not area 7 lesions.

Abstract: Objective: In humans and monkeys, the intraparietal sulcus separates the superior parietal lobule from the inferior parietal lobule (IPL). Whereas in humans Brodmann's area 7 is above this sulcus, in monkeys it is below and therefore part of the IPL. In humans, the IPL consists of Brodmann's areas 39 and 40. Some investigators contend that the monkey homologue of the human IPL (areas 39 and 40) is the monkey's IPL (area 7). Others contend that it is, at least in part, in the monkey's superior temporal sulcus (STS). In humans, IPL lesions induce neglect. Although IPL lesions in monkeys also have been reported to induce neglect, the STS was involved in these lesions. We sought to learn which of these two areas, when ablated, produces neglect. Design: Study of five adult stump-tailed macaque monkeys by making five isolated STS and six IPL lesions. Results: Inferior parietal lobule lesions were associated with misreaching but not with unilateral neglect. Neglect was observed in association with five of the six STS lesions. Conclusions: With regard to neglect, STS may be the monkey homologue of the human IPL. Animals with STS lesions and humans with IPL lesions may manifest unilateral neglect because these areas are necessary for normal awareness of external stimuli. This awareness may result from the integration of the areas important in stimulus localization (the "where is it?" system) and stimulus identification (the "what is it?" system), as well as the areas important in defining the biologic importance of stimuli, such as the frontal lobes and limbic areas.

Spatial planning deficits in limb apraxia.

Abstract: Geschwind (1975) proposed a disconnection model in which an apraxic subject is unable to carry out movements to command because the left hemisphere that comprehended the verbal command is disconnected from the right premotor and motor areas which controls the left hand. An alternate model, however, proposes that apraxia results from destruction of spatiotemporal representations of learned movement stored in the left hemisphere (Heilman, 1979). The disconnection hypothesis would predict that apraxic subjects should be able to correctly imitate gestures and correctly use actual tools since these tasks do not require language. The movement representation model predicts that imitation and actual tool use would also be impaired. Motion analyses were performed on the trajectories of repetitive ‘slicing’ gestures made in a series of conditions in which contextual cues were introduced in a graded fashion. Four cue conditions were presented: no cues (verbal command), object present, tool present and both object and tool present. Positions of the hand, wrist, elbow, and shoulder were digitized from neighbouring views, reconstructed in three dimensions and analysed with respect to specific spatiotemporal features of the trajectories. Three subjects with limb apraxia, who had lesions that included left parietal cortex, and four neurologically intact subjects participated. The apraxic subjects showed disturbances in planning the movement of the hand in space across the cue conditions. For example, they showed deficits in the plane of motion, the shape of the trajectory and in the coupling of hand speed and trajectory shape even when given full contextual cues. These data support the hypothesis that apraxia can result from the destruction of spatiotemporal representations of learned movement, rather than from a disconnection between the receptive language areas in the left hemisphere and the contralateral motor cortices.

Anosognosia for hemiplegia : an electrophysiologic investigation of the feed-forward hypothesis

Abstract: The cause of anosognosia for hemiplegia (AHP) remains unclear. Weakness is detected when there is a mismatch between the expectancy of movement and the sensory perception of movement. The feed-forward hypothesis of AHP posits that there is a failure of detection because there is a loss of motor intention and expectancy of movement. We tested motor intention by measuring the activation of proximal muscles (pectoralis majoris) while subjects squeezed a dynamometer with each hand. We tested a group of normal controls, a group of patients with hemi-paresis, a patient with neglect, a patient with resolved AHP, and a patient with persistent AHP. The patient with AHP did not contract either of his pectoralis muscles when asked to squeeze with his contralesional, paretic hand, yet he contracted both of them when squeezing the dynamometer with his ipsilesional hand. Normal controls, hemiparetic controls, and the patient with hemispatial neglect contracted both pectorales when asked to squeeze with each hand. The pattern of activation seen in the patients with persistent AHP and resolved AHP demonstrates a loss of motor intention and lends support to the feed-forward hypothesis of AHP.

Motor neglect associated with a discrete parietal lesion

Abstract: The syndrome of motor neglect may follow brain lesions affecting frontal, subcortical, and parietal structures. However, pure motor neglect has not been previously associated with a lesion confined to the parietal lobe. We observed a 79-year-old right-handed man with right-sided limb akinesia and motor neglect without concomitant sensory or visuospatial neglect. MRI showed a left posterior parietal infarct sparing the primary sensorimotor cortex. Transcranial magnetic stimulation showed comparable thresholds for electromyographic activation of the muscles of the right and left arm and normal central motor conduction times, indicating functional integrity of the motor cortex. This case demonstrates that a discrete parietal lesion can produce a pure intentional disorder, independent of sensory or visuospatial neglect.

A comparison of the influences of body and environment centred reference frames on neglect

Abstract: Extrapersonal space can be defined by coordinate systems, or frames of reference, that are centred on the body (viewer) or on the environment. Although these frames are identical in the upright position, when the body is placed in positions orthogonal to gravity, the frames may be dissociable. We compared the influences of environmental and body-centred frames on line bisection in two patients with neglect who, when upright, neglected opposite dimensions of space. Through certain combinations of line placement and body orientation, the body and environmental frames were brought into opposition, and each frame predicted line bisection errors in an opposite direction. When the patients were positioned so that predictions of the two frames contrasted, both bisected lines as predicted by the environmental rather than the body-centred frame.

The what and how of neglect

Abstract: We have defined neglect as a failure to report, respond, or orient to novel or meaningful stimuli presented on the side opposite a brain lesion that cannot be attributed to either elemental sensory or motor deficits (Heilman, Watson, & Valenstein, 1993). Many subtypes of neglect have been described, distinguished by the distribution of abnormal behaviour (e.g. spatial versus personal neglect) and the means by which the abnormal behaviour is elicited (e.g. inattention versus extinction). Although at one time we thought that the variety of neglect subtypes could be explained by variations in severity and in means of elicitation, we currently believe that neglect is not a unitary disorder. There is increasing evidence that neglect can be subdivided by the presumed underlying mechanisms: inattention (sensory neglect), disorders of action and intention (motor neglect), and representational disorders.

Emotion and the Brain: A Distributed Modular Network Mediating Emotional Experience

Abstract: Publisher Summary This chapter explores the neural basis of emotional experience. Although emotional experience may be induced by conditioned stimuli, most emotional behavior and experiences are induced by complex stimuli that may be verbal or nonverbal, visual, auditory, or even tactile. The cerebral cortex of humans has complex modular systems that analyze these stimuli, develop precepts, and interpret meaning. The portions of the brain that process emotional stimuli depend upon the modality and mode of the stimulus. The determination of valence is based upon whether or not the stimulus is beneficial—positive—or detrimental—negative—to the well-being of the person or the person's family or society. The right frontal lobe appears to be important in the mediation of emotions with negative valence and the left frontal lobe in the mediation of emotions with positive valence. Depending upon the nature of the stimulus, some positive and some negative emotions are associated with high arousal and others with low arousal. The right parietal lobe appears to be important in mediating arousal response and the left appears to inhibit the arousal response. Similarly, some positive and negative emotions are associated with motor activation and others are not.

Proximal intentional neglect: a case study.

Abstract: Although neglect has been demonstrated in the horizontal, vertical, and radial planes of space and has been attributed to sensory-attentional, motor-intentional, and representational deficits, motor intentional neglect in the radial plane has not been previously described. A patient who had a right parietal infarct was tested with a modified cancellation task that uses a fixed window, thereby controlling attentional demands and allowing one to dissociate between intentional and representational neglect. This patient showed proximal (radial) intentional neglect (a failure to move towards or in proximal space). Unlike controls whose search times decreased with increasing window size, our patient showed no change in search time as a function of window size. This pattern of behaviour suggests that the patient's search strategy does not incorporate factors such as the relation between a fixed target space and a variably sized aperture, but rather was based on the allocation of a certain amount of resources for a fixed period of time after which, regardless of performance, the patient would stop searching.

Role of the pulvinar in ideomotor praxis.

Abstract: tory rhythm was regular and he could not vary it voluntarily, cough, or take a deep breath to command. Tracheal suction generated vigorous coughing. Spontaneous and volitional blinking remained preserved but he could not voluntarily contract the muscles of the upper or lower face; In response to emotional stimuli, however, there were brisk and pronounced contractions of the upper and lower facial muscles that were generally of similar pattem whether he was upset or amused. When this occurred there were concomitant respiratory gasps involving both thoracic muscles and diaphragm on inspiration and abdominal muscles and latissimus dorsi on expiration. At about five months and just before discharge he had regained some limited volitional control of facial muscles particularly on the right but emotionally induced movements remained much more pronounced. Some voluntary jaw opening and tongue movements had returned, his tracheostomy had been closed, and he was able to take limited nutrition by mouth. Before discharge records of his respiration showed that during quiet breathing his respiratory rate was 21/min with a tidal volume of 0 37 litres: a maximum inspiration from functional residual volume was 0-63 litres, and a maximum expiration from end tidal inspiration was 0-66 litres: involuntary sighs of up to 2-5 litres were recorded. He could hold his breath voluntarily for 10-5 seconds. Carbon dioxide rebreathing yielded a normal ventilatory response and ventilation was maintained in sleep with a normal Paco2. He remained tetraparetic. This patient shows similar respiratory findings to those recently reported,12 with loss of voluntary control of respiration but preservation of metabolic control and evidence of activation in response to emotional stimuli. Voluntary control of facial muscles other than blinking was also lost although pronounced activation with emotional stimuli was preserved. Separate nonvolitional pathways to the motor nuclei of the facial nerve are known to exist in uncontrolled crying or laughter as seen after stroke,' whether due to a lesion in the brainstem or due to cortical damage. Such displays of sentiment are activated by the limbic system and are usually under inhibitory cortical control. In this patient the loss of corticobulbar fibres descending through the ventral pons may affect volitional facial and respiratory movement, but emotionally stimulated activity must be mediated independently by fibres descending in the dorsal or lateral pons to terminate on the facial motor nucleus in the caudal third of the ventrolateral tegmentum, and on pontomedullary respiratory motor neurons.