Table 1.
Summary of supportive literature indicating stress and glucocorticoid activity influence stroke outcome.
| Suggestive that stress increases stroke risk and elevated glucocorticoids may be detrimental | ||
|---|---|---|
| Marklund et al. (2004) | Human | Hypercortisolism is associated with cognitive dysfunction after stroke, while bothn unusually high and unusually low circulating cortisol levels are associated with increased mortality after stroke. |
| Gomes et al. (2005) | Human | Review of published clinical studies using glucocorticoid administration to treat neurological disorders; conclude that it is not beneficial in treatment of acute stroke. |
| Anne et al. (2007) | Human | High acute phase cortisol concentrations in first-ever stroke patients predict long-term mortality in a multivariate analysis. |
| Kivimaki et al. (2008) | Human | A prospective cohort study in which individuals who reported job strain had a 1.76 times higher age-adjusted risk of incident ischemic disease than those without job strain. |
| Surtees et al. (2008) | Human | A prospective study in which individuals with lower scores on the Mental Health Inventory (MHI-5; suggesting mental distress) had an 11% increased risk of stroke. |
| Tsutsumi et al. (2009) | Human | A prospective study of Japenese men in which those with job stress (high job demands and low job control) have a 2-fold increase in stroke risk. |
| Suggestive that stress and elevated glucocorticoids exacerbate experimental cerebral ischemia | ||
| DeVries et al. (2001) | Mouse (focal ischemia) | Chronic social stress suppresses post-ischemic bcl-2 gene expression; infarct size is correlated with post-ischemic corticosteroid concentrations. |
| Sugo et al. (2002) | Mouse (focal ischemia) | Exposure to chronic social stress or treatment with exogenous corticosterone before stroke increases resulting infarct size and cognitive deficits. Treatment with a glucocorticoid receptor antagonist prevents the effects of social stress on infarct volume and cognitive performance. |
| Madrigal et al. (2003) | Rat (focal ischemia) | One hour of restraint daily for 7 days increases infarct size while 6 h of restraint daily for 21 days decreases infarct size. |
| Caso et al. (2006) | Rat (focal ischemia) | Restraint stress increases post-stroke TNF-α and TNF receptor 1 expression. Pharmacological blockade of TNF-α decreases stroke-induced infarct size and measures of oxidative stress. |
| Caso et al. (2007) | Rat (focal ischemia) | Exposure to restraint stress prior to stroke increases post-ischemic IL-1β in the cerebral cortex and infarct size. Treatment with an IL-1β antibody reduces ischemia-induced infarct size, neurological deficits and behavioral deficits. |
| McDonald et al. (2008) | Rat (sub-threshold focal ischemia) | Infusion of a low dose of endothelin-1 into the hippocampus had no effect on non-stressed rats. By contrast, the same dose resulted in neuronal death and cognitive deficits among stressed rats. |
| Caso et al. (2008) | Mouse (focal ischemia) | Restraint stress increases post-ischemic neuroinflammation and infarct size in wild-type mice, but not transgenic mice that lack toll-like receptor-4 expression. |
| Neigh et al. (2009) | Mouse (global ischemia) | Exposure to restraint stress prior to cardiac arrest/CPR increases ischemia-induced microglial activation and neuronal damage. |
| Suggestive of the potential for neonatal programming of neuronal responses to injury | ||
| Horvath et al. (2004) | Rat (NMDA infusion) | Brief maternal separation during the first weeks of life significantly increases adult neurodegeneration following infusion with N-methyl-D-aspartate (NMDA). |
| Craft et al. (2006) | Mouse (focal ischemia) | Brief maternal separation during the first 2 weeks of life decreases the corticosteroid response to experimental stroke in adulthood, but increases post-stroke pro-inflammatory cytokine expression, edema, infarct volume, and mortality. |