Lesion symptom mapping of manipulable object naming in nonfluent aphasia: Can a brain be both embodied and disembodied?

Abstract

Embodied cognition offers an approach to word meaning firmly grounded in action and perception. A strong prediction of embodied cognition is that sensorimotor simulation is a necessary component of lexical–semantic representation. One semantic distinction where motor imagery is likely to play a key role involves the representation of manufactured artefacts. Many questions remain with respect to the scope of embodied cognition. One dominant unresolved issue is the extent to which motor enactment is necessary for representing and generating words with high motor salience. We investigated lesion correlates of manipulable relative to nonmanipulable name generation (e.g., name a school supply; name a mountain range) in patients with nonfluent aphasia (N = 14). Lesion volumes within motor (BA4, where BA = Brodmann area) and premotor (BA6) cortices were not predictive of category discrepancies. Lesion symptom mapping linked impairment for manipulable objects to polymodal convergence zones and to projections of the left, primary visual cortex specialized for motion perception (MT/V5+). Lesions to motor and premotor cortex were not predictive of manipulability impairment. This lesion correlation is incompatible with an embodied perspective premised on necessity of motor cortex for the enactment and subsequent production of motor-related words. These findings instead support a graded or “soft” approach to embodied cognition premised on an ancillary role of modality-specific cortical regions in enriching modality-neutral representations. We discuss a dynamic, hybrid approach to the neurobiology of semantic memory integrating both embodied and disembodied components.

Keywords:

• Semantic memory
• Aphasia
• Lesion correlation
• Category specificity
• Embodied cognition.

Notes

¹ This hypothesis applies to an intact semantic system. In the context of damage to convergence zones (e.g., Alzheimer's disease), fragmentary support from afferent modal cortices may become a necessary compensatory mechanism (Rorden, 2007).

² Wallerian degeneration in the central nervous system can occur slowly, producing structural changes that are often only visible on structural MRI months after the primary injury (but see Druks et al., 2006). We observed Wallerian degeneration in the motor tracts of several patients, extending through the brainstem. This degeneration was visible as a circumscribed “hole” on the T1 structural image that ran continuous with the original lesion in the descending axial plane. We know of no VLSM studies to date that have explicitly addressed the anatomical quandary posed by this phenomenon. Our rationale for marking this damage is that it there is no principled way of discerning the margins of the primary infarct relative to the chronic changes inflicted by secondary metabolic and inflammatory processes. Note, this phenomenon contrasts sharply with that of diffuse cerebral atrophy where causal relations between the primary injury and nonspecific atrophy are unclear.

³ The VLSM results lack specificity to determine whether behavioural deficits are associated with damage to cortical nodes themselves or their afferent/efferent pathways. This is a serious inferential limitation imposed by VLSM. A better approach would involve integrating VLSM with diffusion tensor imaging to understand the role of disconnection. In the VLSM analyses using the automated anatomical labelling anatomical atlas, for example, descriptive statistics include white matter as one undifferentiated structure. Although numerous atlas resources exist for specifying white matter pathways, the sensitivity of non-diffusion-weighted imaging (e.g., T1-3d MRI) is limited.