Dementia of depression or depression of dementia in stroke?

Andersen, Grethe; Vestergaard, Karsten; Riis, J. Ø.; Ingeman-Nielsen, M

doi:10.1111/j.1600-0447.1996.tb09860.x

Cited by 39 publications

(30 citation statements)

References 23 publications

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“…In addition, for patients with left hemisphere lesions, there was a significant correlation between severity of cognitive impairment and Beck Depression Inventory score, whereas the correlation was nonsignificant in the right hemisphere. 7 Similar findings have also been reported by Morris et al 8 and Andersen et al 9 In spite of this general concurrence of findings, all prior double-blind treatment trials have failed to show an improvement in cognitive function among patients with poststroke depression who were given active antidepressant therapy. 9 -11 This finding led Andersen et al 9 to suggest that the cognitive impairment may be the cause of depression.…”

supporting

confidence: 69%

“…7 Similar findings have also been reported by Morris et al 8 and Andersen et al 9 In spite of this general concurrence of findings, all prior double-blind treatment trials have failed to show an improvement in cognitive function among patients with poststroke depression who were given active antidepressant therapy. 9 -11 This finding led Andersen et al 9 to suggest that the cognitive impairment may be the cause of depression. We subsequently refuted this hypothesis by demonstrating that among patients not treated for depression, there was a correspondence between depression and cognitive function.…”

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confidence: 69%

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Treatment of Cognitive Impairment After Poststroke Depression

Kimura

Robinson

Kosier

2000

Stroke

178

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Background and Purpose-Patients with poststroke major depression have a greater severity of cognitive impairment than nondepressed patients even when matched for size and location of stroke lesion. Prior treatment studies have consistently failed to show an improvement in cognitive function even when poststroke mood disorders responded to antidepressant therapy. We examined the response of cognitive function to treatment with nortriptyline or placebo in a double-blind trial. Methods-Patients with major (nϭ33) or minor (nϭ14) depression participated in a double-blind treatment study with nortriptyline or placebo. They were examined for change in depressive mood, measured by the Hamilton Rating Scale for Depression (HAM-D), and change in cognitive impairment, assessed by the Mini-Mental State Examination (MMSE), after treatment with nortriptyline or placebo. Cognitive treatment response, as measured by the MMSE, was compared between patients whose depression did and did not respond to treatment. Results-Patients whose poststroke depression remitted (predominantly associated with nortriptyline treatment) had significantly greater recovery in cognitive function over the course of the treatment study than patients whose mood disorder did not remit (predominantly associated with placebo treatment). Conclusions-Our findings support the contention that poststroke major depression leads to a "dementia of depression."Prior studies failed to show an effect of treatment because the effect size was too small. Successful treatment of depression may constitute one of the major methods of promoting cognitive recovery in victims of stroke. (Stroke.

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supporting

confidence: 69%

supporting

confidence: 69%

Treatment of Cognitive Impairment After Poststroke Depression

Kimura

Robinson

Kosier

2000

Stroke

178

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“…40 Further analysis shows that the risk is striking for subjects reporting a previous stroke (ORϭ10.77; CI 2.23 to 80.60). Depression may be a premonitory syndrome for VaD in stroke patients 41 or a marker of the importance of cerebral damage.…”

Section: Discussionmentioning

confidence: 99%

Vascular Dementia

Hébert

Lindsay

Verreault

et al. 2000

Stroke

287

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Background and Purpose-Very few population-based studies have systematically examined incident vascular dementia (VaD). From the Canadian Study of Health and Aging cohort, incidence rates of VaD were determined and risk factors analyzed. Methods-This was a cohort incidence study that followed 8623 subjects presumed to be free of dementia over a 5-year period. The risk factors were examined with a nested prospective case-control study. Exposure was determined by means of a risk factor questionnaire administered to the subject or a proxy at the beginning of the study. Results-On the basis of 38 476 person-years at risk, the annual incidence rate was estimated to be 2.52 per thousand undemented Canadians (95% CI 2.02 to 3.02). Including an estimation of the probability of VaD among the decedents, this figure rose to 3.79. For the risk factors study, 105 incident cases of VaD according to the NINCDS-AIREN criteria were compared with 802 control subjects. Significant risk factors were: age (ORϭ1.05), residing in a rural area (2.03), living in an institution (2.33), diabetes (2.15), depression (2.41), apolipoprotein E ⑀4 (2.34), hypertension for women (2.05), heart problems for men (2.52), taking aspirin (2.33), and occupational exposure to pesticides or fertilizers (2.05). Protective factors were eating shellfish (0.46) and regular exercise for women (0.46). There was no relation with sex, education, or alcohol. Conclusions-The study confirmed some previously reported risk factors but also suggested new ones. It raised concerns about the prescription of aspirin and perhaps other factors related to rural life.

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“…Post-stroke cognitive impairment is also very common, where its cause is probably multi-factorial 5 . The role of mood changes in the genesis of post-stroke cognitive impairment remains controversial 6,7 , and there is also controversy regarding the outcome of cognitive impairment following mood impro v e m e n t 6 , 8 . A recent systematic review of p h a rmacological therapies of depression after stro k e concluded that there is no evidence of benefit of ant i d e p ressants in improving cognitive function 3 .…”

mentioning

confidence: 99%

“…A recent systematic review of p h a rmacological therapies of depression after stro k e concluded that there is no evidence of benefit of ant i d e p ressants in improving cognitive function 3 . Most of the studies have analyzed the effects of the tre a tment for depression based on the general intellectual function only, without focusing on specific cognitive domains [6][7][8][9] .…”

mentioning

confidence: 99%

Cognitive improvement after treatment of depressive symptoms in the acute phase of stroke

Simis

Nitrini

2006

Arq. Neuro-Psiquiatr.

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-The outcome of antidepressant treatment for depressive symptoms and cognitive impairm e n t at the acute phase of stroke is controversial. We investigated 93 patients, treating with citalopram 36 with s e v e re depressive symptoms (HAM-D: Hamilton Depression Rating Scale ≥18), whilst 19 patients with mild d e p ressive symptoms, and 38 non-depressed patients, remained untreated. At baseline (two weeks after s t roke), patients with severe depressive symptoms had lower scores in total Dementia Rating Scale (DRS) and in the attention and memory DRS subscales, than the non-depressed patients (p≤0.001). At the end of the three-month follow-up period, these diff e rences had disappeared, but patients initially with mild d e p ressive symptoms had higher HAM-D scores than the non-depressed patients (p=0.015), and lower s c o res in DRS attention and memory subscales (p<0.01), than the patients treated with citalopram. Tre a t m e n t was associated with improved mood, memory and attention, and a placebo-controlled study on the tre a tment of mild depressive symptoms is warranted.KEY WORDS: post-stroke depression, treatment, vascular cognitive impairment, vascular dementia.Melhora cognitiva com tratamento antidepressivo na fase aguda do acidente vascular cere b r a l RESUMO -Os resultados do tratamento com antidepressivo para os sintomas depressivos e compro m e t imento cognitivo da fase aguda do acidente vascular cerebral não estão estabelecidos. Investigamos 93 pacientes, 36 com sintomas depressivos graves (HAM-D: Escala de Depressão de Hamilton ≥18) foram tratados com citalopram, enquanto 19 pacientes com sintomas depressivos leves e 38 não-deprimidos não foram tratados. Ao início do tratamento (duas semanas depois do icto), pacientes com sintomas depressivos graves tinham escores mais baixos na Escala de Avaliação de Demência (DRS) total e nas subescalas de atenção e de memória da DRS do que os pacientes não-deprimidos (p≤0,001). Ao fim de três meses de acompanhamento essas diferenças tinham desaparecido, mas pacientes que inicialmente tinham sintomas depre s s i v o s leves passaram a ter escores mais altos no HAM-D do que os não-deprimidos (p=0,015), e escores mais baixos nas subescalas de atenção e memória da DRS (p<0,01) do que os pacientes tratados com citalopram. O tratamento associou-se a melhora de humor, memória e atenção, e demonstra que é necessário um estudo controlado com placebo para o tratamento de sintomas depressivos leves.PA L AV R A S -C H AVE: acidente vascular cerebral, depressão, tratamento, comprometimento cognitivo vascular, demência vascular.

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Dementia of depression or depression of dementia in stroke?

Cited by 39 publications

References 23 publications

Treatment of Cognitive Impairment After Poststroke Depression

Treatment of Cognitive Impairment After Poststroke Depression

Vascular Dementia

Cognitive improvement after treatment of depressive symptoms in the acute phase of stroke

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