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The role of interleukin-6 (IL-6) as a risk factor for developing depressive symptoms, neuropsychological impairment, and related functional and neurological symptom severity during the acute phase of ischemic stroke is still underexplored. Here, the authors assessed this issue, in 48 patients without significant clinical history for major medical illnesses or other factors that promote inflammation, 72 hours after a first-ever acute ischemic stroke. In the acute phase of ischemic stroke, increased IL-6 plays a key role in the onset of depressive disorders, apathy/amotivation, somatic symptoms of depression, and neurological/functional symptoms, resulting in higher disability and poor outcome of stroke patients.

Stroke has been shown to lead to depressive disorders, anxiety disorders and other emotional consequences. Although the cause of these disorders is a subject of debate, stroke has clearly been shown to lead to the production of pro-inflammatory cytokines, which we hypothesized to play a role in the production of post-stroke emotional disorders. Thus we investigated here whether acute stroke might be associated with changes in the normal serum levels of IL-18 and if these changes were related to stroke severity, as well as to the presence and severity of alexithymia and depression. Thirty patients with a first-ever symptomatic ischemic stroke were included. Alexithymia (Toronto Alexithymia Scale; TAS-20), depression (Hamilton Depression Rating Scale; HDRS-17) and serum IL-18 were assessed. Stroke patients showed serum levels of IL-18 significantly related to stroke severity. Furthermore, a strong positive correlation was observed between IL-18 levels and severity of alexithymia, particularly among patients with right-hemisphere lesions. Specifically, circulating concentrations of IL-18 were significantly increased in patients with categorical alexithymia (TAS-20 score 61), as compared with both non alexithymic patients and control subjects. In addition, stroke was more severe in alexithymic patients, as compared to non alexithymic patients. Following multivariate regression, serum IL-18 levels appeared to be specifically associated with alexithymia rather than with stroke severity in patients with right-hemisphere lesions only. These results suggest that IL-18 might be specifically implicated in the pathogenesis of post-stroke alexithymia, ultimately contributing to impaired recovery from stroke.