If our stroke medical 'professionals' would actually rub their two functioning neurons together the spark generated just might lead to the realization that depression treatment is totally unnecessary once 100% recovery protocols are available. Solve the primary problem of 100% recovery and you don't have to work on the secondary problem of depression. Do you blithering idiots ever think at all?
Does fluoxetine reduce apathetic and depressive symptoms after stroke? An analysis of the Efficacy oF Fluoxetine—a randomized Controlled Trial in Stroke trial data set
Abstract
Objective:
Apathy
is a common and disabling symptom after stroke with no proven
treatments. Selective serotonin reuptake inhibitors are widely used to
treat depressive symptoms post-stroke but whether they reduce apathetic
symptoms is unknown. We determined the effect of fluoxetine on
post-stroke apathy in a post hoc analysis of the EFFECTS (Efficacy oF
Fluoxetine—a randomized Controlled Trial in Stroke) trial.
Methods:
EFFECTS
enrolled patients ⩾18 years between 2 and 15 days after stroke onset.
Participants were randomly assigned to receive oral fluoxetine 20 mg
once daily or matching placebo for 6 months. The Montgomery–Åsberg
Depression Rating Scale (MADRS) was administered at baseline and
6 months. Individual items on this scale were divided into those
reflecting symptoms of apathy and depression. Symptoms were compared
between fluoxetine and placebo groups.
Results:
Of
1500 participants enrolled, complete MADRS data were available for
1369. The modified intention-to-treat population included 681 patients
in the fluoxetine group and 688 in the placebo group. Confirmatory
factor analysis revealed that apathetic, depressive, and anhedonic
symptoms were dissociable. Apathy scores increased in both fluoxetine
and placebo groups (both p ⩽ 0.00001). In contrast, fluoxetine was
associated with a reduction in depressive scores (p = 0.002)
Conclusion:
Post-stroke
apathetic and depressive symptoms respond differently to fluoxetine
treatment. Our analysis suggests fluoxetine is ineffective in preventing
post-stroke apathy.
Introduction
Apathy occurs in one out of three patients after stroke.1
It describes a reduction in goal-directed activity in the cognitive,
behavioral, emotional, or social domains of a patient’s life. Despite
its frequency, apathy is clinically under-recognized, and there are no
proven drug treatment approaches.
Antidepressants,
such as selective serotonin reuptake inhibitors (SSRIs), are often used
to treat post-stroke depression. Whether SSRIs are also effective in
apathy remains uncertain.1
Despite shared symptoms, post-stroke apathy and depression are
dissociable syndromes. Negative emotionality is a key characteristic of
depression that distinguishes it from apathy. Depressed patients may
present with pessimism and hopelessness, while those with apathy show
lack of emotional distress. Recent studies suggest apathy and depression
have different neuroanatomical correlates with white matter track
damage and subsequent complex network disruption underlying apathy, but
not depression.1,2 This suggests they might respond differently to therapeutic interventions.
We
determined whether fluoxetine reduced apathy in a post hoc analysis of
data from the Efficacy oF Fluoxetine, a randomized Controlled Trial in
Stroke (EFFECTS) trial.
More at link.
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