http://journal.frontiersin.org/article/10.3389/fnhum.2015.00318/full?
- Department of Neurology, Faculty of Medicine, Shimane University, Izumo, Japan
Introduction
Apathy is defined as a lack of motivation that is not
caused by a disturbance in consciousness, cognitive impairment, or
emotional distress (Marin et al., 1991), and this symptom can cause dysfunctions in elaboration, execution and management of goal-directed behaviors (Brown and Pluck, 2000).
Nowadays, apathy is recognized as a frequent neuropsychiatric symptom
not only in neurodegenerative diseases, such as Parkinson’s disease (Dujardin et al., 2007), Huntington’s disease (Di Maio et al., 1993), and progressive supranuclear palsy (Litvan et al., 1996), but also in stroke (Starkstein et al., 1993), dementia (Kuzis et al., 1999), and brain injury (Diaz et al., 2012). Studies have shown that apathy does influence patients’ quality of life (Yeager and Hyer, 2008) and recovery from illness (Politis et al., 2004).
Although the exact mechanism is still not clear, the
prefrontal-basal-ganglia system is thought to play a key role in apathy (Levy and Dubois, 2006).
Most lesion studies have identified the prefrontal cortex and basal
ganglia as target regions responsible for apathy symptoms. Apathy
symptoms are observed after direct lesions of prefrontal cortex (Eslinger and Damasio, 1985; Stuss et al., 2000), and they can also appear indirectly in many diseases that are accompanied by lesions in the basal-ganglia (Laplane et al., 1989; Engelborghs et al., 2000).
For instance, auto-activation deficit was observed in PSP, in which the
basal-ganglia dysfunction caused the prefrontal hypometabolism (D’Antona et al., 1985; Baron, 1994).
These findings suggest that apathy is associated with disruption of the
network involving the frontal lobe and basal ganglia (Middleton and Strick, 2000; Kimura et al., 2003).
Apathy can occur not only in patient populations but
also in healthy individuals free of obvious pathology. However, only one
study has assessed the structural changes associated with apathy in
healthy participants free of any related brain diseases (Grool et al., 2014).
In that study, gray matter volume reductions in the frontal and
temporal lobes as well as the thalamus were related to apathy symptoms,
but no significant changes in the basal ganglia were noted. One reason
for this might be that they assessed apathy symptoms using only three
items from a geriatric depression scale. Apathy symptoms should be
assessed by more elaborate instruments that have been specifically
developed for apathy assessment. In this study, we assessed apathy using
the apathy scale originally developed by Starkstein et al. (1992) and subsequently modified for use with the Japanese population (Okada et al., 1997).
Here, we studied whether apathetic healthy subjects showed any
structural changes in the brain including within the
prefrontal-basal-ganglia system.
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