ISCHEMIC STROKE

Poststroke depression (PSD)

• depression is the most common mood disorder in patients with cerebrovascular disease (30-60% of patients with CVD)
  • depression occurs after both ischemic and hemorrhagic stroke
  • PSD can develop at any time after a stroke
    • the risk of PSD is highest during the first 3 months
    • the risk remains elevated for up to two years post-stroke or longer
  • the variability in the reported incidence of PSD (20-70%) is due to several factors
    • patient selection
    • timing of assessment
    • diagnostic criteria used
      
    • diagnosis of depression may be complicated by fatigue, aphasia, etc.
• PSD negatively impacts stroke recovery
  • it can lead to poorer functional outcomes, decreased quality of life, and increased mortality
  • patients with PSD may have slower recovery, poorer rehabilitation outcomes, a higher level of dependency, and an increased risk of recurrent CVD [Sibolt, 2013]
• PSD is also associated with more severe cognitive impairment  [Kauhanen, 1999]
• PSD is often unrecognized and untreated
  • depression is often perceived as a natural reaction to stroke and not as a disease
  • diagnosis of PSD is also complicated by overlapping physical symptoms of stroke and depression, cognitive impairment, and communication difficulties
  • routine screening using standardized questionnaires is recommended (AHA/ASA 2019 I/B-NR)
• other mood disorders may be observed (alongside depression or in isolation):
  • apathy (25-50%)
  • anxiety (25-50%)

Understanding PSD is crucial for healthcare providers to recognize the risk factors, implement appropriate screening measures, and provide timely and effective treatment to improve outcomes in stroke survivors. Regular monitoring and supportive care, along with interdisciplinary approaches involving neurology, psychiatry, psychology, and rehabilitation services, are key components in managing PSD.

• depression often leads to cognitive decline and can be mistaken for dementia, condition known as pseudodementia
• specific characteristics in the clinical presentation and course of the disease can serve as a guide to distinguish between the two disorders (see the table)
• improvement in cognitive function following successful treatment of depression confirms the correct diagnosis

The pathogenesis of post-stroke depression is multifactorial and not fully understood, involving a complex interplay of biological, psychological, and social factors

• psychological concept
  • assumes that depression occurs as a reaction to one’s illness, often associated with disability
  • this concept is supported by the occurrence of similar depression in cardiovascular diseases or cancer.
    
• organic concept
  • a consequence of damage to brain areas involved in mood regulation and the influence of stroke on various neurotransmitters (especially serotonin and catecholamines)
    • some authors suggest that lesions in the left hemisphere, especially in the prefrontal area, play a more important role, while other authors deny the existence of a clinical-topographic correlation
  • stroke also induces an inflammatory response in the brain, which has been associated with the development of depression
  • the organic concept is supported by the fact that no clear relationship has been found between the severity of neurological deficit and the presence of depression, and that depression occurs even in patients with clinically silent ischemic lesions (detected by CT or MRI)
• other contributing factors
  • certain medications used in stroke recovery may have depressive side effects
  • stresses related to personal life, work, financial concerns, limited social support, and increased social isolation after a stroke may also contribute depression

This complexity necessitates a multidisciplinary approach to effectively manage PSD, including medical, psychological, and social support interventions. Regular screening and early identification of depression in stroke survivors are critical for timely and appropriate intervention.

• the main symptoms of depression according to the ICD 10 classification are summarized in the table below
• symptoms should not result from direct exposure to a substance (medication, drugs) or a medical condition (e.g., hypothyroidism) and should not be attributed to grief (e.g., loss of a loved one, etc.)
• diagnosis is based on a structured interview and scales that allow quantitative assessment of depression and tracking of its course over time
• if the diagnosis is unclear, a trial of antidepressants is recommended

• only a minority of PSD patients achieve spontaneous remission even without treatment
• early and effective treatment of PSD can have a significant positive impact on the course of recovery, with SSRIs reducing depression and anxiety and improving neurological deficit   [Mead, 2012]
• it is not yet known whether stroke patients could benefit from routine temporary use of SSRIs

• the mainstay of treatment includes SSRIs + psychotherapy and early intensive rehabilitation  [Andersen,1994]   [Wiart, 200]   [Rasmussen,2003]
  • SSRIs inhibit the reuptake of serotonin into nerve endings, thereby increasing the amount of serotonin in the synaptic cleft, which acts on postsynaptic receptors
  • SSRI have little or no affinity for cholinergic, histaminergic, and various adrenergic and dopaminergic receptors
  • antidepressant effects can be expected after 10-20 days of treatment; if the patient does not respond after 3 weeks, consider increasing the dose
  • treatment should be continued for at least 6 months
  • concomitant use of MAOIs is contraindicated