Serum-cortisol reflects severity and mortality in acute stroke

Christensen, Hanne; Boysen, Gudrun; Johannesen, Helle Hjorth

doi:10.1016/j.jns.2003.09.013

Cited by 113 publications

(74 citation statements)

References 27 publications

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“…Thereby, autonomic dysfunction is underlying the impaired physiologic regulation of heart rate and blood pressure as well as the increased secretion of catecholamines and cortisol 6, 37, 38, 39. The insular cortex has been identified as a crucial area within the central nervous system relevant for autonomic regulation 11, 30, 40, 41, 42.…”

Section: Discussionmentioning

confidence: 99%

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Bieber

Werner

Tanai

et al. 2017

Annals of Neurology

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ObjectiveCardiac diseases are established risk factors for ischemic stroke incidence and severity. Conversely, there is increasing evidence that brain ischemia can cause cardiac dysfunction. The mechanisms underlying this neurogenic heart disease are incompletely understood. Although it is established that ischemic stroke is associated with cardiac arrhythmias, myocardial damage, elevated cardiac enzymes, and plasma catecholamines in the acute phase, nothing is known about the delayed consequences of ischemic stroke on cardiovascular function.MethodsTo determine the long‐term cardiac consequences of a focal cerebral ischemia, we subjected young and aged mice to a 30‐minute transient middle cerebral artery occlusion and analyzed cardiac function by serial transthoracic echocardiography and hemodynamic measurements up to week 8 after surgery. Finally, animals were treated with metoprolol to evaluate a pharmacologic treatment option to prevent the development of heart failure.ResultsFocal cerebral ischemia induced a long‐term cardiac dysfunction with a reduction in left ventricular ejection fraction and an increase in left ventricular volumes; this development was associated with higher peripheral sympathetic activity. Metoprolol treatment prevented the development of chronic cardiac dysfunction by decelerating extracellular cardiac remodeling and inhibiting sympathetic signaling relevant to chronic autonomic dysfunction.InterpretationFocal cerebral ischemia in mice leads to the development of chronic systolic dysfunction driven by increased sympathetic activity. If these results can be confirmed in a clinical setting, treating physicians should be attentive to clinical signs of heart failure in every patient after ischemic stroke. Therapeutically, the successful β‐blockade with metoprolol in mice could also have future clinical implications. Ann Neurol 2017;82:729–743

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Section: Discussionmentioning

confidence: 99%

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Bieber

Werner

Tanai

et al. 2017

Annals of Neurology

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“…shame, see also Eisenberger et al, 2003;Najib et al, 2004;Panksepp, 2005). Physiologically, error detection is accompanied by skin conductance responses and changes in heart rate (Hajcak et al, 2003(Hajcak et al, , 2004, and both ACC and (especially) the insula are implicated in such responses (Kuniecki et al, 2003), as well as in cortisol and energy (glucose) regulation (Allport et al, 2004;Christensen et al, 2004;Ottowitz et al, 2004) and errorrelated processes (Menon et al, 2001). Additionally, both ACC and insula have a necessary role in the normal occurrence of the ERN (Ullsperger et al, 2002;Ullsperger and Cramon, in press) and are implicated by neuroimaging studies in depersonalization (Lanius et al, 2005;Phillips et al, 2001) and in risk-avoidance and punishment in relation to neuroticism (Paulus et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Task engagement and the relationships between the error-related negativity, agreeableness, behavioral shame proneness and cortisol

Tops

Boksem

Wester

et al. 2006

Psychoneuroendocrinology

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SummaryPrevious results suggest that both cortisol mobilization and the errorrelated negativity (ERN/Ne) reflect goal engagement, i.e. the mobilization and allocation of attentional and physiological resources. Personality measures of negative affectivity have been associated both to high cortisol levels and large ERN/Ne amplitudes. However, measures of positive social adaptation and agreeableness have also been related to high cortisol levels and large ERN/Ne amplitudes. We hypothesized that, as long as they relate to concerns over social evaluation and mistakes, both personality measures reflecting positive affectivity (e.g. agreeableness) and those reflecting negative affectivity (e.g. behavioral shame proneness) would be associated with an increased likelihood of high task engagement, and hence to increased cortisol mobilization and ERN/Ne amplitudes. We had female subjects perform a flanker task while EEG was recorded. Additionally, the subjects filled out questionnaires measuring mood and personality, and salivary cortisol immediately before and after task performance was measured. The overall pattern of relationships between our measures supports the hypothesis that cortisol mobilization and ERN/Ne amplitude reflect task engagement, and both relate positively to each other and to the personality traits agreeableness and behavioral shame proneness. We discuss the potential importance of engagement-disengagement and of concerns over social evaluation for research on psychopathology, stress and the ERN/Ne.

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“…One major influence of the degree of recovery after a stroke might be stress. Clinical studies have shown that high levels of the stress hormone cortisol shortly after a stroke are predictive of poor functional outcome and high morbidity (Murros et al, 1993;Christensen et al, 2004). Additionally, May et al (2002) found that psychological distress is a predictor of fatal stroke in humans.…”

Section: Introductionmentioning

confidence: 99%

Delayed recovery and exaggerated infarct size by post-lesion stress in a rat model of focal cerebral stroke

et al. 2008

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Stress might be one of the most salient intrinsic factors influencing the risk of stroke and its outcome. Previous studies have linked stress to increased infarct size and exaggerated cognitive deficits in rodent models of stroke. This study compares the effects of chronic restraint stress, representing a psychological stressor, prior to or after motor cortex devascularization lesion on motor recovery in rats. Daily testing in a skilled reaching task revealed initially exaggerated deficits in limb use caused by pre-lesion stress in the absence of increased infarct size. Both preand post-lesion stresses affected movement by delaying recovery and limiting compensation of lesion-induced deficits. Nevertheless, only rats that experienced post-lesion stress showed enlarged infarct size. This was accompanied by enlarged edema formation in the lesion hemisphere of poststress animals on day 2 post-lesion. There were no significant differences in infarct size between post-lesion day 2 and day 15. The data demonstrate that both pre-and post-lesion chronic restraint stresses affect motor recovery after ischemic lesion. Lesion volume, however, is influenced by the timing of a stressful experience relative to the lesion. These findings suggest that stress represents a critical variable determining the outcome after stroke.

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Serum-cortisol reflects severity and mortality in acute stroke

Cited by 113 publications

References 27 publications

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

Task engagement and the relationships between the error-related negativity, agreeableness, behavioral shame proneness and cortisol

Delayed recovery and exaggerated infarct size by post-lesion stress in a rat model of focal cerebral stroke

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