The affective modulation of motor awareness in anosognosia for hemiplegia

Sahba Besharati, Stephanie J. Forkel, Michael Kopelman, Mark Solms, Paul M. Jenkinson, Aikaterini Fotopoulou
Cortex. 2014-12-01; 61: 127-140
DOI: 10.1016/j.cortex.2014.08.016

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Erratum in
Cortex. 2015 May;66:176.

The possible role of emotion in anosognosia for hemiplegia (i.e., denial of motor
deficits contralateral to a brain lesion), has long been debated between
psychodynamic and neurocognitive theories. However, there are only a handful of
case studies focussing on this topic, and the precise role of emotion in
anosognosia for hemiplegia requires empirical investigation. In the present
study, we aimed to investigate how negative and positive emotions influence motor
awareness in anosognosia. Positive and negative emotions were induced under
carefully-controlled experimental conditions in right-hemisphere stroke patients
with anosognosia for hemiplegia (n = 11) and controls with clinically normal
awareness (n = 10). Only the negative, emotion induction condition resulted in a
significant improvement of motor awareness in anosognosic patients compared to
controls; the positive emotion induction did not. Using lesion overlay and
voxel-based lesion-symptom mapping approaches, we also investigated the brain
lesions associated with the diagnosis of anosognosia, as well as with performance
on the experimental task. Anatomical areas that are commonly damaged in AHP
included the right-hemisphere motor and sensory cortices, the inferior frontal
cortex, and the insula. Additionally, the insula, putamen and anterior
periventricular white matter were associated with less awareness change following
the negative emotion induction. This study suggests that motor unawareness and
the observed lack of negative emotions about one’s disabilities cannot be
adequately explained by either purely motivational or neurocognitive accounts.
Instead, we propose an integrative account in which insular and striatal lesions
result in weak interoceptive and motivational signals. These deficits lead to
faulty inferences about the self, involving a difficulty to personalise new
sensorimotor information, and an abnormal adherence to premorbid beliefs about
the body.


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