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G Goldenberg

Publications and source records attributed to G Goldenberg.

At least 19 recordsLinked to original sources

Cerebellar volume in humans related to magnitude of classical conditioning.

Neural circuits in the cerebellum are essential for eyeblink classical conditioning, and hippocampal activation is also present during acquisition. Anatomical (volumetric) brain MRI, delay eyeblink conditioning and neuropsychological tests were administered to eight healthy older subjects. The correlation between cerebellar volume (corrected for total cerebral volume) and conditioned response percentage was 0.81 (p < 0.02), but neither hippocampal nor total cerebral volume correlated with conditioning or any neuropsychological test scores. There was no relationship between age and cerebellar volume, but the correlation between hippocampal volume and age was -0.80 (p < 0.02). These volumetric results add to the increasing evidence in humans demonstrating a relationship between the integrity of the cerebellum and eyeblink classical conditioning.

Aged↗

Effects of unilateral brain damage on grip selection, coordination, and kinematics of ipsilesional prehension.

To determine whether the left and right hemispheres play specific roles in goal-directed movements, prehension with the ipsilesional hand was tested in patients with unilateral brain damage. The task required that subjects rotate the hand while reaching for a bar that was presented in different orientations in the frontal plane, thus making high demands on visuospatial processing. The grasped bar had to be put into a hole: under one task condition the placement of the bar was specified, while under another it was not. The constrained task required that the subject anticipate the placing action when planning the initial prehensile movement. Grip selection, reaction times, kinematics of the transport movement, and coordination of hand rotation during transport were assessed in ipsilesional movements of 22 patients with either left or right brain damage (LBD and RBD) and in control subjects. Patients in both groups exhibited performance deficits; however, impairment characteristics differed profoundly between the groups. RBD patients showed prolonged reaction time and degraded kinematics in the unconstrained task, whereas LBD patients performed relatively well when only the orientation of the bar varied, but slowly and frequently incoordinated when the subsequent action was specified. Our findings emphasize the dominant role of the right hemisphere in processing visuospatial aspects of goal-directed movements, whereas the left hemisphere subserves non-spatial aspects of preplanning under increased task demands. Correlations of the patient's performance with results from clinical tests showed that neither deficits in visuospatial perception of RBD patients nor apraxia of LBD patients could account for the observed abnormalities in the use of the ipsilesional hand.

Adult↗

Prehension with the ipsilesional hand after unilateral brain damage.

Sensorimotor deficits in the hand ipsilateral to a brain lesion have been reported in different motor tasks. We evaluated performance of the ipsilesional hand in 12 patients with either left (LBD) or right brain damage (RBD) by kinematic analysis in order to precisely characterize possible deficits in the two components of prehension (transport and grasp). Both patient groups exhibited performance deficits in the main kinematic parameters, e.g., reduced velocity of the transport component and prolonged movement time. However, while LBD patients showed a more general slowing, RBD patients prolonged in particular the last phase of the movement toward the object. We suggest that relevant visuospatial representations and the adequate mapping of motor processes may be impaired after RBD. In contrast, LBD caused a more unspecific disturbance pattern, supporting the view that the precise parameterization of motor programs is impaired. Maximum grip aperture was normal in both patient groups. However, since aperture could be biased by slowed movement, the notion that the grasp component was preserved remains speculative. The patient's ability to scale the maximum velocity of the transport component to adapt to changes in movement amplitude and to scale the maximum hand aperture of the grasp component to adapt to object size was preserved in both groups. Thus both hemispheres can have competence for this scaling mechanism.

Adult↗

Matching and imitation of hand and finger postures in patients with damage in the left or right hemispheres.

To disentangle perceptual, conceptual and motor aspects of imitation of gestures, reproduction of meaningless postures of either the hand or the fingers was examined in two conditions. In the matching test a target gesture had to be identified among an array of four gestures performed by different persons and seen under different angles of views. For imitation, the same gestures had to be imitated. Thirty-five patients with LBD, 21 patients with RBD, and 17 healthy controls were examined. LBD patients had more difficulties with imitation than with matching while RBD patients had more difficulties with matching than with imitation. Regardless of whether imitation or matching was tested, LBD patients made more errors with hand than with finger postures whereas RBD patients made more errors with finger than with hand postures. This constellation of results is compatible with the assumption that errors are caused by faulty visuoperceptual processing in RBD, and by defective conceptual mediation in LBD. Defective motor execution does not appear to be a significant source of imitation errors in either group.

Adult↗

Basal forebrain amnesia: does the nucleus accumbens contribute to human memory?

OBJECTIVE: To analyse amnesia caused by basal forebrain lesions. METHODS: A single case study of a patient with amnesia after bleeding into the anterior portion of the left basal ganglia. Neuropsychological examination included tests of attention, executive function, working memory, recall, and recognition of verbal and non-verbal material, and recall from remote semantic and autobiographical memory. The patient's MRI and those of other published cases of basal forebrain amnesia were reviewed to specify which structures within the basal forebrain are crucial for amnesia. RESULTS: Attention and executive function were largely intact. There was anterograde amnesia for verbal material which affected free recall and recognition. With both modes of testing the patient produced many false positive responses and intrusions when lists of unrelated words had been memorised. However, he confabulated neither on story recall nor in day to day memory, nor in recall from remote memory. The lesion affected mainly the nucleus accumbens, but encroached on the inferior limb of the capsula interna and the most ventral portion of the nucleus caudatus and globus pallidus, and there was evidence of some atrophy of the head of the caudate nucleus. The lesion spared the nucleus basalis Meynert, the diagnonal band, and the septum, which are the sites of cholinergic cell concentrations. CONCLUSIONS: It seems unlikely that false positive responses were caused by insufficient strategic control of memory retrieval. This speaks against a major role of the capsular lesion which might disconnect the prefrontal cortex from the thalamus. It is proposed that the lesion of the nucleus accumbens caused amnesia.

Amnesia↗

The more you know the less you can tell: inhibitory effects of visuo-semantic activation on modality specific visual misnaming.

WH, a 77-years old right-handed psychoanalyst, displayed modality specific visual misnaming as a sequel of an embolic stroke in the left posterior cerebral artery. WH's errors in visual object naming consisted mainly of semantic paraphasias and perseverations. His verbalizations during testing sometimes manifested a conflict between correct responses and perseverations. Analysis of the stream of information from visual perception via semantics to phonology suggested incomplete access from vision to semantics as the source of errors. The disconnection did not affect verbo-visual matching, though he was unable to reject names that did not correspond to visual stimuli. Action naming was relatively spared, but naming of pictures of actions with objects was worse than naming of pictures of intransitive actions. Tactile naming worsened with simultaneous vision of objects. In visual object naming the error rate increased with increasing familiarity of objects. We propose that an interaction of excitation and inhibition within a single semantic system can explain the clinical phenomena of modality specific visual misnaming.

Aged↗

Tool use and mechanical problem solving in apraxia.

Moorlaas (1928) proposed that apraxic patients can identify objects and can remember the purpose they have been made for but do not know the way in which they must be used to achieve that purpose. Knowledge about the use of objects and tools can have two sources: It can be based on retrieval of instructions of use from semantic memory or on a direct inference of function from structure. The ability to infer function from structure enables subjects to use unfamiliar tools and to detect alternative uses of familiar tools. It is the basis of mechanical problem solving. The purpose of the present study was to analyze retrieval of instruction of use, mechanical problem solving, and actual tool use in patients with apraxia due to circumscribed lesions of the left hemisphere. For assessing mechanical problem solving we developed a test of selection and application of novel tools. Access to instruction of use was tested by pantomime of tool use. Actual tool use was examined for the same familiar tools. Forty two patients with left brain damage (LBD) and aphasia, 22 patients with right brain damage (RBD) and 22 controls were examined. Only LBD patients differed from controls on all tests. RBD patients had difficulties with the use but not with the selection of novel tools. In LBD patients there was a significant correlation between pantomime of tool use and novel tool selection but there were single cases who scored in the defective range on one of these tests and normally on the other. Analysis of LBD patients' lesions suggested that frontal lobe damage does not disturb novel tool selection. Only LBD patients who failed on pantomime of object use and on novel tool selection committed errors in actual use of familiar tools. The finding that mechanical problem solving is invariably defective in apraxic patients who commit errors with familiar tools is in good accord with clinical observations, as the gravity of their errors goes beyond what one would expect as a mere sequel of loss of access to instruction of use.

Adult↗

The meaning of meaningless gestures: a study of visuo-imitative apraxia.

In two patients with damage to the inferior portion of the left angular gyrus severely defective imitation of meaningless gestures contrasted with preserved performance of meaningful gestures to verbal command and with preserved imitation of meaningful gestures. In one patient the imitation deficit was restricted to the imitation of hand positions while imitation of finger configurations was normal. In both patients replication of the hand positions on a mannikin was as defective as imitation on themselves. This pattern of preserved and impaired performances is incompatible with two-stage models of apraxia which posit that defective imitation stems from damage to an executional stage of gesture production. Interruption of a direct route from perception to execution of action could account for the dissociation between defective imitation of meaningless and preserved performance of meaningful gestures. We propose that functioning of this route requires the integrity of general knowledge about the structure of the human body.

Aged↗

Brain/behaviour dissociation on old/new distinction in a patient with amnesic syndrome.

Event-related potentials (ERP) were recorded in a recognition memory task in 5 healthy subjects and an amnesic patient. A list of high-imagery words with low probability in everyday language was presented visually for 200 ms each. A second list, consisting of 50% previously presented ('old') words and 50% 'new' words was presented immediately after the first list. Old/new distinction was determined by the subject's motor response. For each subject single trial analysis of ERPs was performed. In each healthy subjects, correct old/new distinction was associated with significant ERP differences from 500 to 900 ms after stimulus onset. It was, therefore, assumed that task and recording procedures were appropriate for the study of ERPs with recognition memory. The main finding is a dissociation between brain activity and behaviour with old/new distinction in the patient with amnesic syndrome. Frequently, the patient incorrectly classified previously shown words ('old' words) to be presented for the first time ('new'). But ERP showed that brain processing of 'old' words which had incorrectly been classified to be 'new' is different from correctly classified new words. ERP differences were significant between 900 and 1200 ms after stimulus presentation. These data indicate preserved memory functions which are not assessed at the behavioural level in the memory recognition task.

Adult↗

Speed of motor execution and apraxia.

We used a reaction time paradigm to explore the relationship between motor execution and apraxia. The task required reaching for one to three keys. The instruction was varied by introducing a model of a hand indicating which fingers to use. Whereas patients with right-brain damage were slower than controls regardless of condition, the performance of patients with left-brain damage was only impaired when movements had to be carried out according to the model. Although this indicates a deficit in movement planning, there was no correlation between the impairment of patients with left-brain damage and clinical manifestations of apraxia. It thus remains an open question whether the impairment reflects an aspect of motor dominance of the left hemisphere that is too subtle to be detected by clinical apraxia testing, or whether it is related to task demands outside the domain of motor control. In any case, the results of this study demonstrate the need to control cognitive task demands when exploring motor capabilities of patients with left-brain damage.

Adult↗

Ideomotor apraxia and cerebral dominance for motor control.

Ideomotor apraxia is a symptom of left hemisphere damage. Patients with ideomotor apraxia commit errors when imitating movements with their left, non-paralyzed hand. This has been taken as evidence for a motor dominance of the left hemisphere. It has been hypothesized that the left hemisphere is dominant for internal preprogramming of skilled movements of either hand. We investigated the kinematics of movement trajectories of imitation of meaningless gestures. Group analysis confirmed that hesitant, feedback-controlled movement prevail in patients with apraxia, but analysis of single cases revealed the existence of kinematically normal movements leading to apractic errors. Enhanced reliance on feedback-control appears to be a compensatory strategy rather than the source of apractic errors. In a second study we explored the alternative hypothesis that patients with apraxia lack a general concept of the human body which is necessary to mediate the translation of a target position seen on the model into a target position on the patient's body. Imitation of movements was examined on oneself and on a mannikin. Patients with apraxia who made errors when imitating on themselves committed errors also when imitating on the mannikin. Taken together, both studies support the view that the source of errors in the imitation of gestures is to be sought at a conceptual level. This casts doubts on the alleged dominance of the left hemisphere for motor control.

Apraxias↗

Kinematic analysis of movement imitation in apraxia.

Accuracy of the final position and kinematics of movement were analysed during the imitation of meaningless gestures in patients with unilateral brain lesions who performed with the hand ipsilateral to the lesion and in control subjects. Controls imitated the gestures virtually without spatial errors. The kinematics of their movements was characterized by single-peaked and approximately bell-shaped velocity profiles of the transport phase combined with no or only minor corrective movements in the final phase. Patients with right brain damage (RBD) performed as well as control subjects with respect to both spatial accuracy of final hand-positions and kinematic parameters of the movement trajectories. Patients with left brain damage (LBD) committed spatial parapraxias and had a much higher frequency of kinematic abnormalities. However, there was no correlation between kinematic abnormalities and apraxic errors. There were kinematically abnormal movements which reached a correct final position as well as kinematically normal movements leading to apraxic errors. One possible explanation for the combined occurrence of kinematic abnormalities and parapraxias in LBD patients would be that they are independent sequels of left hemisphere lesions. An alternative account is that the associations and dissociations result from an interaction between one common basic deficit and strategies to cope with this deficit. The basic deficit may concern the mental representation of the target position. The LBD patients may react to the absence of an appropriate representation of the target by one of two alternative strategies; they may switch to a strategy of slowed, on-line controlled movements to find the required final position, or they may move their hand smoothly at normal speed to a roughly specified location without taking note of their deficiency. Depending on whether these strategies are successful or not they would lead to the observed associations and dissociations between kinematic abnormalities and spatial parapraxias.

Adult↗

Defective imitation of gestures in patients with damage in the left or right hemispheres.

OBJECTIVES: Defective imitation of meaningless gestures has repeatedly been demonstrated in patients with apraxia and has been interpreted as being due to a deficit of motor execution. There is, however, controversy as to whether some impairment of imitation also occurs in patients with right brain damage. The aim was to compare defective imitation in patients with left and right brain damage and to explore whether there are qualitative differences between them. METHODS: Imitation was examined in 80 patients with left brain damage (LBD) and aphasia, 40 patients with right brain damage (RBD), and 60 controls for three types of gestures:hand positions, finger configurations, and combined gestures which required a defined hand position as well as a defined configuration of the fingers. RESULTS: Regardless of whether imitation of hand positions and finger configurations were tested each on their own or together, they showed differential susceptibility to RBD and LBD. Whereas imitation of finger configurations was about equally impaired in RBD and LBD, defective imitation of hand positions occurred almost exclusively in patients with LBD, and whereas controls as well as patients with RBD committed less errors with hand positions than with finger configurations, the reverse was the case in patients with LBD. CONCLUSIONS: The pattern of results goes against a deficit of motor execution as being the cause of defective imitation in patients with LBD, as it is difficult to see why such a deficit should affect proximal movements necessary for reaching hand positions more than differential finger movements. An alternative explanation would be that in patients with LBD errors are due to defective mediation by knowledge about the human body whereas in patients with RBD they stem from faulty visuospatial analysis of the demonstrated gesture.

Adult↗

Unimanual motor learning impaired by frontomedial and insular lesions in man.

We correlated impaired unimanual motor learning with the lesion site in 53 patients with chronic lesions predominantly of the frontal lobe. The lesions were assessed using computed tomography (CT), then transferred to standard templates of nine slices parallel to the canthomeatal plane and digitized with a raster matrix of 3 mm by 3 mm width. The learning task was to track a moving target on a computer screen with a dot guided by the preferred hand, while the horizontal coupling between hand movement and screen was inverted. The mean tracking error was recorded over eight successive trials of 80s duration. If the mean error of the last three trials was not lower than that of the first three trials, impaired motor learning was assumed. We correlated performance and lesion with a contingency table analysis for each raster element. Impaired motor learning was associated with a lesion within the supplementary motor area and adjacent anterior cingulate, and within the anterior insular region. Our results indicate that these regions are critical for motor learning and functional plasticity in man. Our data support activation patterns obtained with positron emission tomography.

Adolescent↗

Imitating gestures and manipulating a mannikin--the representation of the human body in ideomotor apraxia.

Imitation of meaningless gestures was examined in patients with left brain damage (LBD), right brain damage (RBD) and controls. In addition to imitation on the own body, patients were asked to replicate the gestures on a life-sized mannikin. Manual dexterity was assessed by manipulation of beads, and general visuospatial abilities by block-design. LBD patients who displayed apraxia when imitating gestures on their own bodies scored dramatically worse than any other group when imitation was assessed on the mannikin. By contrast, on block-design and manipulation of beads patients with RBD were inferior not only to LBD patients without apraxia but also to apractic patients. Analysis of CT scans revealed that apraxia occurred with frontal, parietal and deep lesions, and that the impairment on the manipulation of the mannikin was present regardless of lesion site. The results support the contention that the basic deficit underlying impaired imitation of meaningless gestures in apraxia is to be sought at a conceptual level. Possibly, patients with apraxia are not able to evoke and represent conceptual knowledge about the human body which is necessary for performing the apparently simple task of imitating gestures.

Aged↗