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.

Monday, July 7, 2014

Personality And Heart Attacks - A New Look

You'll have to ask your doctor, hospital and stroke association what the correlation is between personality and stroke. It would seem to be an obvious line of study but our stroke associations will do nothing about this.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=143440&CultureCode=en
A new study published in the current issue of Psychotherapy and Psychosomatics has addressed the relationship between personality and heart attacks. Distressed (type D) personality (TDP), characterized by high negative affectivity (NA) and social inhibition (SI), along with depression, anxiety and other negative affects (such as demoralization, hopelessness, pessimism and rumination) have been implicated as potential risk factors for coronary artery disease. While some evidence suggests that the NA dimension of TDP overlaps at least partially with depression, other studies underline how ‘TDP refers to a chronic, more covert form of distress that is distinct from depression'.
In this study, Authors aimed to clarify whether, among never depressed patients at their first acute coronary syndrome (ACS), there is an overlap between the constructs of TDP and depression, evaluating the stability of NA and SI 6 months after the ACS, and their relationship with depressive symptoms. Patients consecutively admitted to the Coronary Intensive Care Unit of the University Hospital of Parma between January 2009 and March 2012 who had their first ACS and no history of major depression (MD) or other psychiatric disorders, were included.
During the follow-up period 30 patients developed depressive symptoms (MD: n = 12; minor depression (md): n = 18), whereas 220 subjects maintained a nondepressive condition throughout the study period. At baseline the NA and SI levels were higher in subjects who developed depression than in patients who did not. However, at the baseline evaluation 19 patients without previous depressive episodes already satisfied the criteria for md. Interestingly, at baseline these subjects showed higher levels of NA and SI than subjects without md. Among patients who developed depression (n = 30) HADS scores significantly changed during the 6-month follow-up: both anxiety and depression scores increased from baseline to the second month of follow-up and then decreased. The same pattern of change was observed for the NA score, whereas the SI score did not vary during follow-up. In nondepressed patients, both HADS depression and anxiety scores and NA score significantly decreased throughout the follow-period, whereas the SI did not change.
In this study, the overlap between depressive psychopathology and NA features is suggested by the course of these two dimensions over time. Indeed, in both depressed and nondepressed patients, NA levels were not stable during the 6-month follow-up, but they changed along with the variation of HADS scores. This finding suggests that the NA dimension is sensitive to mood-state, because its levels increase and decrease according to the fluctuation of severity of depressive and anxious symptoms. This result supports the view that the disposition to experience and report negative emotions (NA) can be sensitive to mood-state. Therefore, the presence of depressive state is crucial when assessing TDP, since NA and anhedonic depression are partially overlapping and co-varying constructs.

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