Ideational Apraxia

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Asuka Nakajima - One of the best experts on this subject based on the ideXlab platform.

  • Progressive transcortical sensory aphasia and progressive Ideational Apraxia owing to temporoparietal cortical atrophy
    BMC Neurology, 2015
    Co-Authors: Michitaka Funayama, Asuka Nakajima
    Abstract:

    Background In contrast to frontotemporal lobar degeneration, atrophy of the focal posterior lateral cortex has not been thoroughly studied. Three clinical types of focal cortical atrophy have been described: 1) logopenic variant of primary progressive aphasia, which presents with impaired repetition despite normal articulation; 2) posterior cortical atrophy, which presents with prominent visuospatial deficits; and 3) primary progressive Apraxia. All three clinical types are characterized by specific patterns of hypometabolism/hypoperfusion: the left posterior perisylvian area in the logopenic variant of primary progressive aphasia, bilateral parietooccipital areas in posterior cortical atrophy, and the parietal cortex in primary progressive Apraxia. However, not every patient clearly fits into one of these categories. Case presentation Here we describe two patients with atypical focal cortical presentations. They presented with a history of a few years of progressive transcortical sensory aphasia characterized by fluent output with normal grammar and syntax, normal repetition, sentence comprehension deficits, and anomia without loss of word meaning. They also presented with progressive Apraxia that began at the initial stages. Some forms of posterior symptoms including acalculia, agraphia, and visuospatial deficits were also observed. Hypoperfusion was noted mainly in the left temporoparietal region, which is slightly posterior to the perisylvian area. Conclusions Although our cases lack in CSF findings and PIB scan, these two cases and previous reports might suggest the existence of a subgroup of patients presenting with transcortical sensory aphasia, Apraxia, and posterior symptoms (acalculia, agraphia, and visuospatial deficits) in the setting of Alzheimer’s disease. This subgroup may reflect the spectrum of clinical manifestations between logopenic variant of primary progressive aphasia and posterior cortical atrophy.

  • progressive transcortical sensory aphasia and progressive Ideational Apraxia owing to temporoparietal cortical atrophy
    BMC Neurology, 2015
    Co-Authors: Michitaka Funayama, Asuka Nakajima
    Abstract:

    In contrast to frontotemporal lobar degeneration, atrophy of the focal posterior lateral cortex has not been thoroughly studied. Three clinical types of focal cortical atrophy have been described: 1) logopenic variant of primary progressive aphasia, which presents with impaired repetition despite normal articulation; 2) posterior cortical atrophy, which presents with prominent visuospatial deficits; and 3) primary progressive Apraxia. All three clinical types are characterized by specific patterns of hypometabolism/hypoperfusion: the left posterior perisylvian area in the logopenic variant of primary progressive aphasia, bilateral parietooccipital areas in posterior cortical atrophy, and the parietal cortex in primary progressive Apraxia. However, not every patient clearly fits into one of these categories. Here we describe two patients with atypical focal cortical presentations. They presented with a history of a few years of progressive transcortical sensory aphasia characterized by fluent output with normal grammar and syntax, normal repetition, sentence comprehension deficits, and anomia without loss of word meaning. They also presented with progressive Apraxia that began at the initial stages. Some forms of posterior symptoms including acalculia, agraphia, and visuospatial deficits were also observed. Hypoperfusion was noted mainly in the left temporoparietal region, which is slightly posterior to the perisylvian area. Although our cases lack in CSF findings and PIB scan, these two cases and previous reports might suggest the existence of a subgroup of patients presenting with transcortical sensory aphasia, Apraxia, and posterior symptoms (acalculia, agraphia, and visuospatial deficits) in the setting of Alzheimer’s disease. This subgroup may reflect the spectrum of clinical manifestations between logopenic variant of primary progressive aphasia and posterior cortical atrophy.

Tim Shallice - One of the best experts on this subject based on the ideXlab platform.

  • The simulation of action disorganisation in complex activities of daily living
    Cognitive Neuropsychology, 2005
    Co-Authors: Richard P Cooper, Mvrna F. Schwartz, Peter Yule, Tim Shallice
    Abstract:

    Action selection in everyday goal-directed tasks of moderate complexity is known to be subject to breakdown following extensive frontal brain injury. A model of action selection in such tasks is presented and used to explore three hypotheses concerning the origins of action disorganisation: that it is a consequence of reduced top-down excitation within a hierarchical action schema network coupled with increased bottom-up triggering of schemas from environmental sources, that it is a more general disturbance of schema activation modelled by excessive noise in the schema network, and that it results from a general disturbance of the triggering of schemas by object representations. Results suggest that the action disorganisation syndrome is best accounted for by a general disturbance to schema activation, while altering the balance between top-down and bottom-up activation provides an account of a related disorder—utilisation behaviour. It is further suggested that Ideational Apraxia (which may result from l...

  • The simulation of action disorganisation in complex activities of daily living
    COGN NEUROPSYCHOL, 2005
    Co-Authors: Tim Shallice
    Abstract:

    Action selection in everyday goal-directed tasks of moderate complexity is known to be Subject to breakdown following extensive frontal brain injury. A model of action selection in such tasks is presented and used to explore three hypotheses concerning the origins of action disorganisation: that it is a consequence of reduced top-down excitation within a hierarchical action schema network coupled with increased bottom-up triggering of schemas from environmental sources, that it is a more general disturbance of schema activation modelled by excessive noise in the schema network, and that it results from a general disturbance of the triggering of schemas by object representations. Results suggest that the action disorganisation syndrome is best accounted for by a general disturbance to schema activation, while altering the balance between top-down and bottom-up activation provides an account of a related disorder-utilisation behaviour. It is further suggested that Ideational Apraxia (which may result from lesions to left temporoparletal areas and which has similar behavioural consequences to action disorganisation syndrome on tasks of moderate complexity) is a consequence of a generalised disturbance of the triggering of schemas by object representations. Several predictions regarding differences between action disorganisation syndrome and Ideational Apraxia that follow from this interpretation are detailed.

  • The simulation of action in complex activities of daily living
    Cognitive Neuropsychology, 2005
    Co-Authors: Tim Shallice
    Abstract:

    Action selection in everyday goal-directed tasks of moderate complexity is known to be subject to breakdown following extensive frontal brain injury. A model of action selection in such tasks is presented and used to explore three hypotheses concerning the origins of action disorganisation: that it is a consequence of reduced top-down excitation within a hierarchical action schema network coupled with increased bottom-up triggering of schemas from environmental sources, that it is a more general disturbance of schema activation modelled by excessive noise in the schema network, and that it results from a general disturbance of the triggering of schemas by object representations. Results suggest that the action disorganisation syndrome is best accounted for by a general disturbance to schema activation, while altering the balance between top-down and bottom-up activation provides an account of a related disorder—utilisation behaviour. It is further suggested that Ideational Apraxia (which may result from lesions to left temporoparietal areas and which has similar behavioural consequences to action disorganisation syndrome on tasks of moderate complexity) is a consequence of a generalised disturbance of the triggering of schemas by object representations. Several predictions regarding differences between action disorganisation syndrome and Ideational Apraxia that follow from this interpretation are detailed.

  • Neural basis of pantomiming the use of visually presented objects
    NeuroImage, 2004
    Co-Authors: Raffaella I Rumiati, Tim Shallice, Peter H. Weiss, Giovanni Ottoboni, Johannes Noth, Karl Zilles, Gereon R. Fink
    Abstract:

    Neuropsychological studies of patients suffering from Apraxia strongly imply a left hemisphere basis for skilful object use, the neural mechanisms of which, however, remain to be elucidated. We therefore carried out a PET study in 14 healthy human volunteers with the aim to isolate the neural mechanisms underlying the sensorimotor transformation of object-triggers into skilled actions. We employed a factorial design with two factors (RESPONSE: naming, pantomiming; and TRIGGER: actions, objects) and four conditions (IA: imitating the observed pantomime; IO: pantomiming the use of the object shown; NA: naming the observed pantomime; NO: naming the object shown). The design thus mainly aims at investigating the interaction [i.e. (IO–IA)–(NO–NA)] which allows the assessment of increased neural activity specific to the sensorimotor transformation of object-triggers into skilled actions. The results (P < 0.05, corrected) showed that producing a wide range of skilled actions triggered by objects (controlled for perceptual, motor, semantic, and lexical effects) activated left inferior parietal cortex. The data provide an explanation for why patients with lesions including left parietal cortex suffer from Ideational Apraxia as assessed by impaired object use and pontomining to visually presented objects (Brain 111 (1988) 1173; Cogn. Neuropsychol. 18 (2001) 671).

  • a form of Ideational Apraxia as a selective deficit of contention scheduling
    Cognitive Neuropsychology, 2001
    Co-Authors: Raffaella I Rumiati, Sergio Zanini, L Vorano, Tim Shallice
    Abstract:

    In this paper we studied three brain-damaged patients: the first two, DR and FG, had limb Apraxia whilst the third was a control patient (WH2) with an executive function disorder but without limb Apraxia. DR and FG were impaired in carrying out everyday actions, whilst they maintained the ability to sequence photographs representing those same activities. The failure in the action production task was not caused by visual agnosia for objects, as the patients could recognise them from sight. Nor was it produced by a loss of knowledge about their functions (De Renzi & Lucchelli, 1988), as DR and FG could identify objects from descriptions of their use. WH2's pattern of performance doubly dissociated from that of the apraxic patients, namely spared action production on the multiple object test, but faulty sequencing of photographs. WH2's difficulties in sequencing photographs were not due to a failure to understand the task, as she could sequence stimuli other than actions (e.g., shapes and numbers). Nor were...

Michitaka Funayama - One of the best experts on this subject based on the ideXlab platform.

  • Progressive transcortical sensory aphasia and progressive Ideational Apraxia owing to temporoparietal cortical atrophy
    BMC Neurology, 2015
    Co-Authors: Michitaka Funayama, Asuka Nakajima
    Abstract:

    Background In contrast to frontotemporal lobar degeneration, atrophy of the focal posterior lateral cortex has not been thoroughly studied. Three clinical types of focal cortical atrophy have been described: 1) logopenic variant of primary progressive aphasia, which presents with impaired repetition despite normal articulation; 2) posterior cortical atrophy, which presents with prominent visuospatial deficits; and 3) primary progressive Apraxia. All three clinical types are characterized by specific patterns of hypometabolism/hypoperfusion: the left posterior perisylvian area in the logopenic variant of primary progressive aphasia, bilateral parietooccipital areas in posterior cortical atrophy, and the parietal cortex in primary progressive Apraxia. However, not every patient clearly fits into one of these categories. Case presentation Here we describe two patients with atypical focal cortical presentations. They presented with a history of a few years of progressive transcortical sensory aphasia characterized by fluent output with normal grammar and syntax, normal repetition, sentence comprehension deficits, and anomia without loss of word meaning. They also presented with progressive Apraxia that began at the initial stages. Some forms of posterior symptoms including acalculia, agraphia, and visuospatial deficits were also observed. Hypoperfusion was noted mainly in the left temporoparietal region, which is slightly posterior to the perisylvian area. Conclusions Although our cases lack in CSF findings and PIB scan, these two cases and previous reports might suggest the existence of a subgroup of patients presenting with transcortical sensory aphasia, Apraxia, and posterior symptoms (acalculia, agraphia, and visuospatial deficits) in the setting of Alzheimer’s disease. This subgroup may reflect the spectrum of clinical manifestations between logopenic variant of primary progressive aphasia and posterior cortical atrophy.

  • progressive transcortical sensory aphasia and progressive Ideational Apraxia owing to temporoparietal cortical atrophy
    BMC Neurology, 2015
    Co-Authors: Michitaka Funayama, Asuka Nakajima
    Abstract:

    In contrast to frontotemporal lobar degeneration, atrophy of the focal posterior lateral cortex has not been thoroughly studied. Three clinical types of focal cortical atrophy have been described: 1) logopenic variant of primary progressive aphasia, which presents with impaired repetition despite normal articulation; 2) posterior cortical atrophy, which presents with prominent visuospatial deficits; and 3) primary progressive Apraxia. All three clinical types are characterized by specific patterns of hypometabolism/hypoperfusion: the left posterior perisylvian area in the logopenic variant of primary progressive aphasia, bilateral parietooccipital areas in posterior cortical atrophy, and the parietal cortex in primary progressive Apraxia. However, not every patient clearly fits into one of these categories. Here we describe two patients with atypical focal cortical presentations. They presented with a history of a few years of progressive transcortical sensory aphasia characterized by fluent output with normal grammar and syntax, normal repetition, sentence comprehension deficits, and anomia without loss of word meaning. They also presented with progressive Apraxia that began at the initial stages. Some forms of posterior symptoms including acalculia, agraphia, and visuospatial deficits were also observed. Hypoperfusion was noted mainly in the left temporoparietal region, which is slightly posterior to the perisylvian area. Although our cases lack in CSF findings and PIB scan, these two cases and previous reports might suggest the existence of a subgroup of patients presenting with transcortical sensory aphasia, Apraxia, and posterior symptoms (acalculia, agraphia, and visuospatial deficits) in the setting of Alzheimer’s disease. This subgroup may reflect the spectrum of clinical manifestations between logopenic variant of primary progressive aphasia and posterior cortical atrophy.

Laurel J Buxbaum - One of the best experts on this subject based on the ideXlab platform.

  • Ideomotor Apraxia: a Call to Action
    Neurocase, 2001
    Co-Authors: Laurel J Buxbaum
    Abstract:

    Although ideomotor Apraxia (IM) has been a topic of investigation since the early 20th century, progress in studying the models of various investigative groups. As a result, it is difficult to draw conclusions about the expected performance of IM patients on various tests of praxis (e.g. pantomime, single object use, gesture imitation, and naturalistic action); the relationship of IM to Ideational Apraxia (IA); the degree to which specific error types are diagnostic of one or the other disorder; the relationship of semantic knowledge to gesture representations; and the role of spatiomotor systems external to the stored gesture representation system. Here an updated model of IM is presented, informed by recent physiological and functional neuroimaging literature, as a step towards resolving some of these concerns. The model is intended to lay the groundwork for future investigations of specific performance patterns in different subtypes of IM.

  • Ideational Apraxia and naturalistic action
    Cognitive Neuropsychology, 1998
    Co-Authors: Laurel J Buxbaum
    Abstract:

    It is frequently claimed that Ideational Apraxia, an impairm ent of the performance of complex actions with objects, is a left-hemisphere syndrome. We assessed the consequences of lefthemisphere damage for naturalistic action performance in two studies. In Study 1, we compared the action errors of left-hemisphere stroke patients (LCVA) to previously reported patients with right-hemisphere stroke (RCVA) and closed head injury (CHI), and found that LCVA were no more vulnerable to errors of action than the other patient groups once differences in severity were controlled. In Study 2, we compared the naturalistic action performance of a patient with severe Ideational Apraxia and left-hemisphere damage to that of two RCVA patients of equal clinical severity. There was considerable quantitative and qualitative similarity in the errors of the three patients. From these and other findings, we argue that deficits in left-hem isphere systems do not compromise com plex action in a unique or transparent manner. We of...

  • Naturalistic action and praxis in callosal Apraxia
    Neurocase, 1995
    Co-Authors: Laurel J Buxbaum, Myrna F. Schwartz, H. Branch Coslett, Tania G. Carew
    Abstract:

    Abstract We report a subject who, subsequent to closed head injury, demonstrated a severe left hand Ideational Apraxia and apraxic agraphia, consistent with callosal disconnection syndrome. In contrast to the left hand, performance of the right hand was unimpaired on traditional tests of gesture to command, sight of object, and with actual object use, but proved deficient on tests of spatial and constructional ability. We examined the consequences of these hand-specific deficits for the performance of naturalistic action tasks. The patient made errors with each hand; however, the right hand performed more poorly than the left hand. In addition, the types of errors made by each hand differed in a manner consistent with the results of neuropsychological testing and indicative of disconnection phenomena. We suggest that unlike gesture, naturalistic action requires the contribution of the specialized abilities of each hemisphere, integrated across callosal structures. Traditional testing of gesture may undere...

Richard P Cooper - One of the best experts on this subject based on the ideXlab platform.

  • tool use and related errors in Ideational Apraxia the quantitative simulation of patient error profiles
    Cortex, 2007
    Co-Authors: Richard P Cooper
    Abstract:

    The behaviour of Ideational apraxic patients on simple tasks involving multiple objects is typically marked by a variety of errors. While some of these errors concern the sequential organisation of action through time, many relate to the misuse of, or failure to use, necessary or appropriate tools. In this paper we apply the computational model of Cooper & Shallice (2000) to five standard multiple object tasks used in clinical assessment and demonstrate how, when lesioned, the model can account for the error profiles of two Ideational apraxic patients discussed by Rumiati et al. (2001). Application of the model to the multiple object tasks demonstrates the generality of the model, while the account of the error profiles extends previous work (Cooper et al., 2005) in which Ideational Apraxia was argued to arise from a generalised disturbance of object representations that are held to trigger action schemas.

  • The simulation of action disorganisation in complex activities of daily living
    Cognitive Neuropsychology, 2005
    Co-Authors: Richard P Cooper, Mvrna F. Schwartz, Peter Yule, Tim Shallice
    Abstract:

    Action selection in everyday goal-directed tasks of moderate complexity is known to be subject to breakdown following extensive frontal brain injury. A model of action selection in such tasks is presented and used to explore three hypotheses concerning the origins of action disorganisation: that it is a consequence of reduced top-down excitation within a hierarchical action schema network coupled with increased bottom-up triggering of schemas from environmental sources, that it is a more general disturbance of schema activation modelled by excessive noise in the schema network, and that it results from a general disturbance of the triggering of schemas by object representations. Results suggest that the action disorganisation syndrome is best accounted for by a general disturbance to schema activation, while altering the balance between top-down and bottom-up activation provides an account of a related disorder—utilisation behaviour. It is further suggested that Ideational Apraxia (which may result from l...