Confusion, Hyperactive Delirium, and Secondary Mania in Right Hemispheric Strokes: A Focused Review of Neuroanatomical CorrelatesDavid L. Perez1,2,3,4*, Eva Catenaccio4 and Jane Epstein3,4
- Corresponding Author:
- Dr. David L. Perez M.D
Brigham and Women's Hospital
Departments of Neurology and Psychiatry
75 Francis Street, Boston, MA 02115
E-mail: [email protected] com
Received date: June 01, 2011; Accepted date: July 15, 2011; Published date: September 20, 2011
Citation: Perez DL, Catenaccio E, Epstein J (2011) Confusion, Hyperactive Delirium, and Secondary Mania in Right Hemispheric Strokes: A Focused Review of Neuroanatomical Correlates. J Neurol Neurophysiol S1. doi:10.4172/2155-9562.S1-003
Copyright: © 2011 Perez DL, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Affective and behavioral neuropsychiatric disturbances are frequently encountered in post-stroke patients. While the neural correlates of conditions such as post-stroke depression and apathy have been well investigated, confusion, hyperactive delirium, and secondary mania are less well detailed. In This article, a case of right hemispheric stroke presenting with acute confusion and agitation is described to introduce the topic, followed by a focused review of the post-stroke right hemispheric lesional correlates of non-agitated confusion, hyperactive delirium, and secondary mania. These three post-stroke syndromes have both overlapping and non-overlapping structural components. Non-agitated confusional states may preferentially involve higher order perceptual/attentional association cortices (parietal, occipital, prefrontal) and related subcortical connections. Right hemispheric post-stroke patients with hyperactive delirium often share similar lesion sites, but also have a greater tendency to involve limbic related medial temporal lobe structures. Lesions particularly associated with secondary mania include orbitofrontal-subcortical circuits and medial temporal lobe structures.