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. 1999 Sep;1(2):68-80.
doi: 10.31887/DCNS.1999.1.2/galexopoulos.

Vascular depression: a new view of late-onset depression

G S Alexopoulos  1 , M L Bruce, D Silbersweig, B Kalayam, E Stern
Affiliations

Vascular depression: a new view of late-onset depression

G S Alexopoulos et al. Dialogues Clin Neurosci. 1999 Sep.

Abstract
in English, Spanish, French

We have suggested that cerebrovascular disease may predispose, precipitate, or perpetuate some late-life depressive syndromes. The mechanisms of "vascular depression" include disruption of cortico-striato-pallido-thalamo-cortical (CSPTC) pathways or their modulating systems. This view is supported by the presentation of vascular depression, which consists of depressive symptoms, cognitive abnormalities, as well as neuroimaging findings that may result from CSPTC impairment. Moreover, clinical and electrophysiological evidence of CSPTC impairment, an abnormality frequently found in patients with vascular depression, appears to be associated with poor response to antidepressant treatment and early relapse and recurrence. The vascular depression hypothesis provides the conceptual background for studies that may have clinical and theoretical impact. Agents influencing dopamine, acetylcholine, and opioid neurotransmitters may be studied in vascular depression, since these are essential neurotransmitters of the frontostriatal circuitry. Drugs used for prevention and treatment of cerebrovascular disease may be shown to reduce the risk for vascular depression or improve its outcomes. The choice of antidepressants in vascular depression may depend on their effect on neurological recovery from ischemic lesions. Finally, identification of specific relationships between specific symptoms, cognitive deficits, and disability may lead to interventions that target the patients' deficits as well as their interactions with psychosocial factors known to contribute to depression. Research can clarify the pathways to vascular depression by focusing on the site of lesion, the resultant brain dysfunction, the presentation of depression and time of onset, and the contribution of nonbiological factors.

Llemos sugerido que la enfermedad cerebrovascular puede predisponer, precipitar o perpetuar algunos síndromes depresivos que aparecen en la edad avanzada. Los mecanismos de la “depresión vascular” de las vías córtico-estriato-pálido-tálamo-corticales (CEPTC) o de sus sistemas de modulación. Esta persepctiva se ve apoyada por el modo en que se manifiesta la deresión vascular, la cual consiste en síntomas depresivos, anoalías cognoscitivas, y constataciones especificas en neuroimágenes, que parecen resultar del deterioro de las vías CEPTC. Además, se asocia a las pruebas clínicas y electrofisiológicas del deterioro de estas vias, lo cual es una anomalía frecuentement observada en pacientes con depresión vascular, una respuesta insuficiente al tratamiento antidepresivo y una pronta recaida y recidiva. La hipótesis de la depresión vascular aporta un sustrato conceptual para estudios que podrían tener un importante impacto clínico y teórico. Deberían estudiarse los fármacos que influyen en los neurotransmisores dopaminérgicos, acetilcolinérgicos y opiáceos en la depresión vascular, ya que se trata de neurotransmisores esenciales del circuito frontoestriatal. Los fármacos utilizados en la prevención y tratamiento de la enfermedad cerebrovascular parencen ser eficaces para reducir el riesgo de depresión vascular o para mejorar sus consecuencias. La elección delos antidepresivos para tratar la depresión vascular depende de sus efectos sobre la recuperución neurológica de las lesiones isquémicas. Finalmente, la identificación de las relaciones especificas entre los síntomas específicos, los déficits cognoscitivos y la consiguiente incapacidad puede conducir a intervenciones dirigidas a los déficits de los pacientes y sus interacciones con factores psicosciales que, como es sabido, contribuyen a la depresión. La investigación puede esclarecer las causus de la depresión vascular, concentrádose en el sitio de la lesión, en la disfunción cerebral resultante, en la manifestación de la depresión en su momento de aparición y en la contribución de los factores no biológicos.

Nous avons suggéré que les maladies cérébrovasculaires favorisent, accélèrent ou perpétuent certains syndromes dépressifs du sujet âgé. Les mécanismes de la «dépression vasculaire» incluent une interruption des voies cortico-striato-pallido-ihalumo-corticales (CSPTC) ou de leurs systèmes régulateurs. Ce point de vue est étayé par le tableau de cette forme de dépression qui combine des symptômes dépressifs, des troubles cognitifs et des données obtenues en imagerie cérébrale, lesquelles résulteraient des altérations des voies CSPTC. En outre, les altérations cliniques et électrophysiologiques reflétant un dysfonctionnement des voies CSPTC sont fréquemment retrouvées chez les patients souffrant de dépression vasculaire et sont associées à une réponse pauvre aux traitements antidépresseurs, à des rechutes précoces et à des récidives. L'hypothèse de la dépression vasculaire constitue une base conceptuelle pour des études qui peuvent avoir un impact clinique et théorique. Les agents qui influent sur certains neurotransmetteurs comme la dopamine, l'acétylcholine et les opioïdes peuvent être étudiés dans celle dépression, car ceux-ci jouent un rôle essentiel dans le circuit frontostriatal. Les médicaments utilisés dans la prévention et le traitement des maladies cérébrovasculaires pourraient avoir un effet démontré sur le risque de dépression vasculaire ou améliorer son pronostic. Le choix d'antidépresseurs adaptés à ce syndrome peut dépendre de leur effet sur la récupération neurologique qui succède aux lésions de nature ischémique. Au bout du compte, la mise en évidence de relations spécifiques entre les symptômes caractéristiques, les troubles cognitifs et le handicap pourrait déboucher sur des interventions visant à la fois les déficits et leurs interactions avec les facteurs psychosociaux qui contribuent a la dépression. La recherche peut clarifier les voies impliquées dans la dépression vasculaire en se focalisant sur le site des lésions, le dysfonctionnement cérébral qui en résulte et la présentation de la dépression au moment où elle s'installe, sans oublier la contribution des facteurs non biologiques.

Keywords: disability; recovery from ischemia; treatment resistance; vascular depression.

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Figures

Figure 1.
Figure 1.. Blood flow velocity In the middle cerebral artery in an 82 -year-old patient with major depression (left) and a 79-year-old psychiatrically normal subject (right). Blood flow velocity was measured with transcranial sonography.
Figure 2.
Figure 2.. Decreased activity in bilateral hippocampi (a) and bilateral anterior cingulate gyri (b), in geriatric patients with major depression vs control subjects using a word generation paradigm, as detected with highsensitivity H2 15O positron emission tomography (PET) activation. Highlighted areas reflect group differences (P<0.01 ) of functional PET results superimposed on a structural T1 weighted template.
Figure 3.
Figure 3.. Increased frontal activation in a 73-year-old patient with major depression (top) compared with a 70-year-old psychiatrically normal subject (bottom). Evoked responses were recorded following the Stroop Color interference task. À total of 162 color-congruent words and 162 color-incongruent words presented for 500 milliseconds every 2 seconds in random order. Topographical maps of evoked potential activity were constructed after sorting the correct responses to the incongruent task and estimating the voltage distributions across the scalp.
Figure 4.
Figure 4.. Cox proportional hazard analysis of 57 elderly patients who had recovered from major depression and received continuation treatment with nortriptyline at plasma levels of 60 to150 ng/mL Seven patients had a relapse during continuation phase. Fitted survival curves with low (first quartile) and high (3rd quartile) scores of the initiation/perseveration (IP) domain of the Mattis Dementia Rating Scale are shown.
Figure 5.
Figure 5.. Cox proportional hazard analysis of 43 elderly patients who had recovered from major depression, completed a 16-week continuation treatment with nortriptyline at plasma levels of 60-150 ng/mL and were randomly assigned to nortriptyline (NT) or placebo (PL) maintenance treatment. Fifteen patients had a recurrence during maintenance treatment phase; 4 were on nortriptyline and 11 were on placebo. Fitted survival curves with low (first quartile) and high (3rd quartile) scores of the initiation/perseveration (IP) domain of the Mattis Dementia Rating Scale are shown.
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