Anosognosia, a term first coined in 1914 by M.J. Babinksi, is the lack of insight or awareness of impairment. For example, a patient with anosognosia who fractured both legs in a motor-vehicle accident might be seen frequently trying to get out of their wheelchair to walk. Though anosognosia has long fascinated clinicians and researchers, the underlying causal mechanisms remain unclear. Because anosognosia is associated with a wide variety of psychiatric or neurologic disorders, research findings are typically more applicable to the particular associated disorder (e.g., schizophrenia, stroke, hemiplegia) rather than being representative of all patients with anosognosia. Anosognosia for hemiplegia (AH) typically occurs following lesions in right-sided or bilateral frontal, temporal, and/or parietal areas (Moro et al., 2011; Pia et al., 2004). Specifically, AH appears to be related to lesions in the right inferior frontal cortex, temporal cortex, thalamus, basal ganglia, hippocampal formation, insula, and white matter (Craig, 2009; Orefi et al., 2008; Vallar & Ronchi, 2006; Vocat et al., 2010). When subcortical areas are not involved, damage to parietal and frontal structures appear to cause anosognosia more frequently than damage to temporal areas (Pia et al., 2004).
Unawareness of hemiplegia was first called anosognosia by Babinski one century ago. This paper reviews some of the major theories that may account for this disorder. Weinstein and Kahn posited that anosognosia was a psychological defense mechanism; however, clinical as well as studies using transient hemispheric anesthesia reveal anosognosia for hemiplegia is more commonly associated with right than left hemisphere dysfunction, which is not entirely compatible with this denial hypothesis. Discovery is dependent on sensory feedback. Some patients with anosognosia will recognize their hemiparesis when their paretic hand is placed into ipsilesional hemispace suggesting that de-afferentation and inattention-neglect may be important mechanisms. Some patients with anosognosia have asomatognosia and hence being unaware that their paretic arm belongs to them they do not recognize that they have a deficit. Some patients have phantom movements and some may confabulate because they have a hemispheric disconnection. The feed-forward hypothesis posits that without an attempt to move, there is no expectation of movement and in the absence of arm movement there will be no discord that leads to discovery. Thus, motor neglect may be another cause of anosognosia. A defect in a theoretical comparator where expectations are compared to feedback may also be a cause of anosognosia, but further evidence is needed to support this postulate. Based on the studies of anosognosia for hemiplegia we have reviewed it appears that normal self-awareness depends on several modular systems. Further research of these possible mechanisms is needed to discern their relative importance and treatment. If these mechanisms do not fully account for anosognosia, investigators will need to develop and test new hypotheses.
Citation: Heilman, K. M. (2014). Possible mechanisms of anosognosia of hemiplegia. Cortex, 61, 30-42. doi:10.1016/j.cortex.2014.06.007
- Anosognosia Workshop at NAMI Conference from 07.03.10 - https://vimeo.com/13277920
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