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Magnetic Resonance Imaging Correlates of Depression After Ischemic Stroke
Risto Vataja, MD;
Tarja Pohjasvaara, MD, PhD;
Antero Leppävuori, MD, PhD;
Riitta Mäntylä, MD;
Hannu Juhani Aronen, MD, PhD;
Oili Salonen, MD, PhD;
Markku Kaste, MD, PhD;
Timo Erkinjuntti, MD, PhD
Arch Gen Psychiatry. 2001;58:925-931.
Background Depression affects up to 40% of patients with ischemic stroke. The relationship
between site and size of brain infarcts and poststroke depression is still
not well characterized. Further possible contribution and interaction of white
matter lesions and brain atrophy has not been studied previously. We conducted
a magnetic resonance image–based study of the radiologic correlates
of depression in a large, well-defined series of patients with ischemic stroke.
Methods Modified DSM-III-R and DSM-IV criteria were used to diagnose depressive disorders during a comprehensive
psychiatric evaluation in 275 of 486 consecutive patients aged 55 to 85 years
3 to 4 months after ischemic stroke. A standardized magnetic resonance imaging
protocol detailed side, site, type, and extent of brain infarcts and extent
of white matter lesions and brain atrophy.
Results Depressive disorders were diagnosed in 109 patients (40%). Patients
with depression had a higher number and larger volume of infarcts affecting
the prefrontosubcortical circuits, especially the caudate, pallidum, and genu
of internal capsule, with left-sided predominance. Extent of white matter
lesions and atrophy did not differ in patients with and without depression.
Independent correlates of poststroke depression in a logistic regression model
were mean frequency of infarcts in the genu of internal capsule on the left
side (odds ratio [OR], 3.2; 95% confidence interval [CI], 1.0-10.1), mean
frequency of infarcts in the pallidum of any side (OR, 1.6; 95% CI, 1.1-2.3),
and mean volume of infarcts in the right occipital lobe (OR, 0.98; 95% CI,
0.96-0.99).
Conclusion Lesions affecting the prefrontosubcortical circuits, especially on the
left side, are correlates of depression after ischemic stroke.
From the Department of Clinical Neurosciences, Memory Research Unit
(Drs Vataja, Pohjasvaara, and Erkinjuntti), the Department of Psychiatry,
Psychiatric Consultation Unit (Dr Leppävuori), the Department of Radiology
(Drs Mäntylä, Aronen, and Salonen), and the Stroke Unit (Dr Kaste),
Helsinki University Central Hospital, Helsinki, Finland; and the Department
of Clinical Radiology, University of Kuopio, Kuopio, Finland (Dr Aronen).
Corresponding author and reprints: Timo Erkinjuntti, MD, PhD, Department
of Clinical Neurosciences, Memory Research Unit, Helsinki University Central
Hospital, PO Box 300, FIN-00029 HUS, Finland (e-mail: timo.erkinjuntti{at}hus.fi).
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