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Inability to deactivate sympathetic nervous system in brainstem infarct patients
Journal of the Neurological Sciences
|February 1, 1983
Summary
Patients with brainstem infarction showed increased noradrenaline excretion during head-down tilting, unlike controls and hemisphere infarction patients. This suggests sympathetic nervous system activation and impaired nighttime deactivation in brainstem injury.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Endocrinology
Background:
- The sympathetic nervous system (SNS) plays a crucial role in regulating cardiovascular function and catecholamine excretion.
- Head-down tilting is a physiological maneuver used to assess autonomic nervous system responses.
- Cerebral circulation autoregulation is vital for maintaining brain perfusion.
Purpose of the Study:
- To investigate catecholamine urinary excretion patterns in response to head-down tilting in individuals with and without neurological conditions.
- To compare the autonomic responses of patients with hemisphere infarction and brainstem infarction to physiological stress.
- To explore potential links between SNS reactivity, impaired deactivation, and cerebral circulation regulation in brainstem infarct patients.
Main Methods:
- Measurement of urinary catecholamine (noradrenaline) excretion under basal conditions.
- Assessment of catecholamine excretion following 4-degree head-down tilting.
- Comparison of excretion patterns between normotensive controls, hypertensive controls, patients with hemisphere infarction, and patients with brainstem infarction.
Main Results:
- Normotensive and hypertensive controls, along with hemisphere infarction patients, exhibited a significant decrease (~40%) in noradrenaline excretion after head-down tilting.
- Patients with brainstem infarction demonstrated an increase in noradrenaline excretion post-tilting, indicating SNS activation.
- Brainstem infarct patients showed diminished diurnal variation in noradrenaline excretion, with night excretion levels similar to day levels, suggesting impaired nighttime SNS deactivation.
Conclusions:
- Brainstem infarction is associated with an inability to deactivate the sympathetic nervous system during recumbency.
- The observed SNS reactivity disorder in brainstem infarct patients may contribute to abnormal increases in cerebral circulation during night, particularly if autoregulation is impaired.