Post-Stroke Depressive Symptoms: Varying Responses to Escitalopram by Individual Symptoms and Lesion Location

 You do realize that depression is a secondary problem and wouldn't exist if you had EXACT REHAB PROTOCOLS LEADING TO 100% RECOVERY?  Solve the primary problem, 100% recovery, and you don't have to waste time on all these secondary issues.  In my opinion all secondary problem research is wasted. I don't care how hard is will be to solve for 100% recovery, talk to survivors sometime and ask how well their recovery is going with NO medical help.

Hope you are OK with failure to recover when you are the 1 in 4 per WHO that has a stroke.

Post-Stroke Depressive Symptoms: Varying Responses to Escitalopram by Individual Symptoms and Lesion Location

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Eun-Jae Lee, Jong S. Kim, Dae-Il Chang, ...

First Published September 10, 2020 Research Article Find in PubMed 

https://doi.org/10.1177/0891988720957108

Article information

Abstract

Objective:

The efficacy of antidepressants in post-stroke depressive symptoms (PSD) varies. We aimed to examine whether the effect of escitalopram on PSD differs according to individual depressive symptoms and stroke lesion location.

Methods:

This is a post hoc analysis of EMOTION (ClinicalTrials.gov, NCT01278498), a randomized, placebo-controlled, double-blind trial that examined the efficacy of escitalopram on depression in acute stroke patients (237 with placebo, 241 with escitalopram). Depressive symptoms were evaluated with the 10-item Montgomery-Åsberg Depression Rating Scale (MADRS). Changes in MADRS and individual item scores at 12 weeks were compared between the treatment groups and among the stroke lesion location groups. Stroke lesion locations were grouped according to the anatomical distribution of serotonin fibers that originate from the midbrain/pons and spread to the forebrain via subcortical structures: “Midbrain-Pons,” “Frontal-Subcortical,” and “Others.” Least-squares means were calculated to demonstrate the independent effect of lesion location.

Results:

Total MADRS scores decreased more significantly in the escitalopram than in the placebo group, while a significant effect of escitalopram was observed in only 3 items: apparent sadness, reported sadness, pessimistic thoughts. In the lesion location analyses, escitalopram users in the Frontal-Subcortical group showed significant improvement in total MADRS scores (placebo [n = 130] vs. escitalopram [n = 148], least-square mean [95% CI]: -2.3 [-3.5 to -0.2] vs. -4.5 [-5.5 to -3.4], p = .005), while those in the Midbrain-Pons and Others groups did not.

Conclusions:

The effect of escitalopram on PSD may be more prominent in patients with particular depressive symptoms and stroke lesion locations, suggesting the need for tailored treatment strategies.

Keywords

stroke, depression, escitalopram

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Post-Stroke Depressive Symptoms: Varying Responses to Escitalopram by Individual Symptoms and Lesion Location

I would suggest that a much better way to treat post stroke depression is to have EXACT STROKE PROTOCOLS LEADING TO 100% RECOVERY. Depression is likely occurring because your doctor knows nothing and tells you nothing about your recovery. If your doctor told you doing 2 million reps of this exercise and you get this result, you would start counting and do the reps. You wouldn't have time to be depressed.

Post-Stroke Depressive Symptoms: Varying Responses to Escitalopram by Individual Symptoms and Lesion Location

Show all authors

Eun-Jae Lee, Jong S. Kim, Dae-Il Chang, ...

First Published September 10, 2020 Research Article 

https://doi.org/10.1177/0891988720957108

Article information

Abstract

Objective:

The efficacy of antidepressants in post-stroke depressive symptoms (PSD) varies. We aimed to examine whether the effect of escitalopram on PSD differs according to individual depressive symptoms and stroke lesion location.

Methods:

This is a post hoc analysis of EMOTION (ClinicalTrials.gov, NCT01278498), a randomized, placebo-controlled, double-blind trial that examined the efficacy of escitalopram on depression in acute stroke patients (237 with placebo, 241 with escitalopram). Depressive symptoms were evaluated with the 10-item Montgomery-Åsberg Depression Rating Scale (MADRS). Changes in MADRS and individual item scores at 12 weeks were compared between the treatment groups and among the stroke lesion location groups. Stroke lesion locations were grouped according to the anatomical distribution of serotonin fibers that originate from the midbrain/pons and spread to the forebrain via subcortical structures: “Midbrain-Pons,” “Frontal-Subcortical,” and “Others.” Least-squares means were calculated to demonstrate the independent effect of lesion location.

Results:

Total MADRS scores decreased more significantly in the escitalopram than in the placebo group, while a significant effect of escitalopram was observed in only 3 items: apparent sadness, reported sadness, pessimistic thoughts. In the lesion location analyses, escitalopram users in the Frontal-Subcortical group showed significant improvement in total MADRS scores (placebo [n = 130] vs. escitalopram [n = 148], least-square mean [95% CI]: -2.3 [-3.5 to -0.2] vs. -4.5 [-5.5 to -3.4], p = .005), while those in the Midbrain-Pons and Others groups did not.

Conclusions:

The effect of escitalopram on PSD may be more prominent in patients with particular depressive symptoms and stroke lesion locations, suggesting the need for tailored treatment strategies.

Keywords stroke, depression, escitalopram

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Efficacy of early administration of escitalopram on depressive and emotional symptoms and neurological dysfunction after stroke: a multicentre, double-blind, randomised, placebo-controlled study

But do these other antidepressants work AND provide better rehabilitation outcomes? Ask your fucking doctor this damned simple question. Not knowing the answer is grounds for firing.

Common antidepressant can help stroke patients improve movement and coordination Sept. 2015 

 

Antidepressants may help people recover from stroke even if they are not depressed Jan. 2013

Efficacy of early administration of escitalopram on depressive and emotional symptoms and neurological dysfunction after stroke: a multicentre, double-blind, randomised, placebo-controlled study

Kim J, Lee E, Chang D, Park J, Ahn S, Cha J, Heo J, Sohn S, Lee B, Kim D, Kim H, Kim S, Kwon D, Kim J, Seo W, Lee J, Park S, Koh S, Kim J, Choi-Kwon S, EMOTION investigators ; Lancet Psychiatry 4 (1), 33-41 (Jan 2017)

Tags:

• Depression
• escitalopram
• Stroke

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BACKGROUND Mood and emotional disturbances are common in patients with stroke, and adversely affect the clinical outcome. We aimed to evaluate the efficacy of early administration of escitalopram to reduce moderate or severe depressive symptoms and improve emotional and neurological dysfunction in patients with stroke.
METHODS This was a placebo controlled, double-blind trial done at 17 centres in South Korea. Patients who had had an acute stroke within the past 21 days were randomly assigned in a 1:1 ratio to receive oral escitalopram (10 mg/day) or placebo for 3 months. Randomisation was done with permuted blocks stratified by centre, via a web-based system. The primary endpoint was the frequency of moderate or severe depressive symptoms (Montgomery-Åsberg Depression Rating Scale [MADRS] ≥16). Endpoints were assessed at 3 months after randomisation in the full analysis set (patients who took study medication and underwent assessment of primary endpoint after randomisation), in all patients who were enrolled and randomly assigned (intention to treat), and in all patients who completed the trial (per-protocol analysis). This trial is registered with ClinicalTrials.gov, number NCT01278498.
FINDINGS Between Jan 27, 2011, and June 30, 2014, 478 patients were assigned to placebo (n=237) or escitalopram (n=241); 405 were included in the full analysis set (195 in the placebo group, 210 in the escitalopram group). The primary outcome did not differ by study group in the full analysis set (25 [13%] patients in the placebo group vs 27 [13%]in the escitalopram group; odds ratio [OR] 1·00, 95% CI 0·56-1·80; p>0·99) or in the intention-to-treat analysis (34 [14%] vs 35 [15%]; OR 1·01, 95% CI 0·61-1·69, p=0·96). The study medication was generally well tolerated; the most common adverse events were constipation (14 [6%] patients who received placebo vs 14 [6%]who received escitalopram), muscle pain (16 [7%] vs ten [4%]), and insomnia (12 [5%] vs 12 [5%]). Diarrhoea was more common in the escitalopram group (nine [4%] patients) than in the placebo group (two [1%]patients).
INTERPRETATION Escitalopram did not significantly reduce moderate or severe depressive symptoms in patients with acute stroke.
FUNDING Dong-A Pharmaceutical and Ministry for Health, Welfare, and Family Affairs, South Korea.

Escitalopram Improves Stroke Recovery Beyond 3 Months of Treatment

Is this any different that this earlier research? I bet your doctor has not created a stroke depression protocol, probably doesn't even know this shit. A great stroke leader would make sure relevant research is translated into stroke protocols and pushed out to all stoke doctors and hospitals. But we have NO stroke leadership, your children and grandchildren will still be screwed after their strokes.

Common antidepressant can help stroke patients improve movement and coordination Sept. 2015 

Antidepressants may help people recover from stroke even if they are not depressed Jan. 2013

http://dgnews.docguide.com/escitalopram-improves-stroke-recovery-beyond-3-months-treatment?

By Chris Berrie
COPENHAGEN, Denmark -- May 31, 2016 -- The antidepressant escitalopram significantly improves recovery for patients who have had a stroke, with benefits occurring regardless of stroke subtype or baseline depression, and continuing beyond 3 months of treatment, according to results of an open-label study presented at the 2nd Congress of the European Academy of Neurology (EAN).
“Depression is very frequently the result of a stroke,” stated coauthor Aurel Simion, MD, PhD, Municipal Clinical Hospital, University of Oradea, Oradea, Romania, speaking here on May 30. Several studies have shown benefits for antidepressant treatment after stroke, he added.
Dr. Simion and colleagues randomised patients who had had an ischaemic stroke to receive secondary preventive treatment with placebo (n = 46; mean age, 69.2 years) or with escitalopram 19 mg/day (n = 43; mean age, 66.3 years), for 3 months, with follow-up to 12 months. Analyses included various stroke and depression rating scales examined at end of treatment and at 12 months.
Stroke subtypes were equally balanced in the total patient population: thrombotic (33%), lacunar (31%), and cardioembolic (36%).
The National Institutes of Health stroke Severity scale (NIHSS) scores showed trends and some significance between placebo and escitalopram according to thrombotic, lacunar and cardioembolic stroke at 3 months (4.57 vs 2.80, P = .194; 4.00 vs 2.31, P = .141; 3.65 vs 1.47, P = .048; respectively), with all showing significant benefits for active treatment at 12 months (6.21 vs 1.00, P< .001; 5.53 vs 0.46, P< .0001; 2.71 vs 0.67, P = .029). These results were paralleled in the Barthel Index stroke severity rating.
Results were similar, respectively, for depression indices of Hamilton Depression Scale (HAM-D17) at 3 months between placebo and escitalopram according to thrombotic, lacunar and cardioembolic stroke (13.86 vs 11.53, P = .24; 15.00 vs 9.23, P = .001; 10.88 vs 7.67, P = .021) and at 12 months (16.93 vs 7.00, P< .001; 16.67 vs 6.08, P< .001; 10.76 vs 5.47, P = .003). Results from the Beck Depression Inventory (BDI ) paralleled those results between placebo and escitalopram according to thrombotic, lacunar and cardioembolic stroke at 3 months (15.64 vs 14.07, P = .499; 20.67 vs 12.92, P = .001; 16.24 vs 11.93, P = .025) and 12 months (21.43 vs 7.93, P< .001; 24.60 vs 8.54, P< .001; 16.24 vs 8.40, P = .003).
Similar results were demonstrated for improvements in Activities of Daily Living between placebo and escitalopram according to thrombotic, lacunar and cardioembolic stroke at 3 months (4.00 vs 5.13, P = .021; 3.67 vs 5.00, P = .046; 4.82 vs 5.53, P = .154; respectively) and at 12 months (3.36 vs 5.87, P< .001; 2.73 vs 5.85, P< .001; 4.76 vs 5.87, P = .014).
Finally, the investigators observed reductions in stroke recurrence for active treatment according to thrombotic, lacunar and cardioembolic stroke at 3 months (21.4% vs 6.7%; 26.7% vs 7.7%; 23.5% vs 0.0%) and at 12 months (28.6% vs 0.0%; 53.3% vs 0.0%; 17.6% vs 6.7%).
The researchers acknowledge that the mechanism by which antidepressant therapy achieves these benefits is not yet fully understood, and is, therefore, controversial. Regardless, “it is a good measure to treat these patients with serotonin reuptake inhibitor antidepressants,” Dr Simion concluded.
Baseline clinical characteristics were similar across the placebo and escitalopram arms for overall mean NIHSS scores (8.52 vs 8.56) and for depression indices, including overall mean HAM-D17 scores (12.3 vs 13.5) and BDI scores (15.5 vs 17.9).
[Presentation title: Improved Post-Ischaemic Stroke Recovery Over 1 Year With Escitalopram for 3 Months. Abstract P31030]

Prevention of poststroke apathy using escitalopram or problem-solving therapy

Having not seen an apathy scale, I wonder if they used tiredness as a marker for depression which would bias all survivors towards a depression diagnosis. 

Prevention of poststroke apathy using escitalopram or problem-solving therapy

Mikami K, Jorge RE, Moser DJ, Arndt S, Jang M, Solodkin A, Small SL, Fonzetti P, Hegel MT, Robinson RG.

Source

Department of Psychiatry, Carver College of Medicine, University of Iowa, IA; Department of Psychiatry, Tokai University School of Medicine, Kanagawa, Japan.

Abstract

OBJECTIVE:

Apathy occurs frequently following stroke and prior studies have demonstrated the negative effect of apathy on recovery from stroke. This study was a secondary analysis examining the efficacy of escitalopram, problem-solving therapy (PST), or placebo administered for 1 year to prevent the onset of apathy among patients with recent stroke.

METHODS:

Patients within 3 months of an index stroke who did not meet DSM-IV diagnostic criteria for major or minor depression and who did not have a serious comorbid physical illness were enrolled. Patients were recruited from three sites: University of Iowa, University of Chicago, and Burke Rehabilitation Hospital. One hundred fifty-four patients without evidence of apathy at initial evaluation were included in the randomized controlled trial using escitalopram (10 mg patients ≤65 years; 5 mg patients >65 years) (N = 51) or placebo (N = 47) or non-blinded PST (12 total sessions) (N = 56) over 1 year. At 3, 6, 9, and 12 months, patients were assessed for diagnosis and severity of apathy using the Apathy Scale.

RESULTS:

Using a Cox proportional hazards model of time to onset of apathy, participants given placebo were 3.47 times more likely to develop apathy than patients given escitalopram and 1.84 times more likely to develop apathy than patients given PST after controlling for age, sex, cognitive impairment, and diabetes mellitus status (adjusted hazard ratio: 3.47, 95% CI: 1.79-6.73 [escitalopram group]; adjusted hazard ratio: 1.84, 95% CI: 1.21-2.80 [PST group]).

CONCLUSION:

Escitalopram or PST was significantly more effective in preventing new onset of apathy following stroke compared with placebo.