# Neuroendocrine Stress Response in Acute Stroke: Physiological and Clinical Perspectives

## TL;DR

This paper reviews how the body's stress response, including hormonal and nervous system changes, affects patients during acute stroke and recovery.

## Contribution

The paper provides a comprehensive narrative review of neuroendocrine and autonomic responses in acute stroke and their clinical relevance.

## Key findings

- Acute ischemic stroke activates the HPA axis and sympathetic nervous system.
- Disruptions in neuroendocrine signaling correlate with systemic stress and autonomic imbalance.
- Biomarkers like cortisol and melatonin may indicate physiological stress and recovery patterns.

## Abstract

Acute ischemic stroke constitutes a significant systemic stress event that initiates a complex cascade of neuroendocrine and autonomic responses. Central to this process is activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system, reflecting the brain’s integrated response to acute cerebral injury. These changes are accompanied by widespread alterations in physiological regulation, including endocrine signaling, autonomic balance, circadian organization, and cardiovascular control. Understanding the nature and coordination of these responses is important for gaining insight into the broader pathophysiological impact of acute ischemic stroke beyond focal neuronal damage. This narrative review provides an overview of the mechanisms underlying HPA axis activation, circadian rhythm dysregulation, and autonomic dysfunction in the setting of acute ischemic stroke. Particular emphasis is placed on the interactions between neuroendocrine signaling and cardiovascular regulation, highlighting how disruptions in these systems may reflect the severity of systemic stress and autonomic imbalance. The review also discusses the relevance of neuroendocrine and autonomic biomarkers, including cortisol, melatonin, and ambulatory blood pressure parameters, as integrative indicators of physiological stress, autonomic regulation, and recovery patterns in acute stroke.