Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, July 2, 2015

Gray matter volume changes in the apathetic elderly

I'm sure apathy is pretty prevalent in elderly stroke survivors because they are given no hope for recovery. A great Catch-22 since with less grey matter you are less likely to recover leading to more apathy.
http://journal.frontiersin.org/article/10.3389/fnhum.2015.00318/full?
  • Department of Neurology, Faculty of Medicine, Shimane University, Izumo, Japan
This study is to test the hypothesis that apathy in healthy participants is closely related to the prefrontal-basal-ganglia circuit and associated structural changes. We selected 36 healthy aged participants with (n = 18) or without apathy (n = 18) from our database. Participants underwent structural MRI scanning, providing data for voxel-based morphometric analysis to explore gray matter changes associated with apathy. Compared to the non-apathy group, the apathy group showed reduced gray matter volume of the right putamen, whereas volumes of the bilateral inferior frontal gyri and left inferior occipital gyrus showed increase. When depression scores were included in a regression model as a covariate, apathetic participants showed decreased gray matter volume in the right precentral gyrus compared to the non-apathetic participants. These findings suggest that apathy is associated with the gray matter volume in the prefrontal-basal-ganglia network, and may have a neuroanatomical basis distinct from depression in healthy elderly.

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.

More at link.

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