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Emotional expression and cognition are unlinked in pseudobulbar affective disorder
In the past half-century, the neuroanatomical regulators of emotion have become better understood. The rediscovery of the limbic areas and their intimate links with the basal ganglia, especially the ventral striatum and associated orbitofrontal cortex, and the special role of the right hemisphere in emotional experience has been central to this understanding.1 However, the complexity of the relationship between these circuits and areas of isocortex and the descending pathways to midbrain and brainstem nuclei in volitional and emotional faciobulbar expression remain less well understood. Emotional disorder is a major feature of frontal brain disease, and complex emotional states and gelastic seizures are well-recognised features of some forms of epilepsy. Uncontrolled, disabling and unstable mood change characteristics of pseudobulbar affective disorder may develop after diffuse traumatic brain injury, in frontal or multi-infarct cerebrovascular disease, multiple sclerosis and degenerative brain diseases, which can lead to depressive illness, bipolar disorder and emotional lability.
The relationship between the experience of emotion and its motor expression was first clearly formulated in 1884–1885 in the James-Lange theory of the emotions.2 This theory suggested that emotional feelings and behaviours stemmed from the …
Contributors MS and MRT contributed equally to this commentary.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
Correction notice This paper has been amended since it was published Online First. Owing to a scripting error, some of the publisher names in the references were replaced with ‘BMJ Publishing Group’. This only affected the full text version, not the PDF. We have since corrected these errors and the correct publishers have been inserted into the references.
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