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Hypothalamic-pituitary-adrenocortical axis dysfunction in epilepsy.

Aynara C Wulsin1, Matia B Solomon2, Michael D Privitera3

  • 1Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, College of Medicine, Cincinnati, OH, United States; Neuroscience Program, University of Cincinnati, College of Medicine, Cincinnati, OH, United States; Department of Anesthesia, Cincinnati Childrens Hospital Medical Center, Cincinnati, OH, United States; Department of Pediatrics, Cincinnati Childrens Hospital Medical Center, Cincinnati, OH, United States.

Physiology & Behavior
|May 20, 2016
PubMed
Summary
This summary is machine-generated.

Temporal lobe epilepsy (TLE) is linked to a hyperactive stress response system (hypothalamic-pituitary-adrenal axis). This dysfunction may trigger seizures and worsen psychiatric conditions like depression and anxiety in TLE patients.

Keywords:
CRHGlucocorticoidsPsychopathologiesStressTemporal lobe epilepsy

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Psychiatry

Background:

  • Epilepsy is a prevalent neurological disorder, with temporal lobe epilepsy (TLE) being common in adults.
  • TLE patients often exhibit a hyperactive hypothalamic-pituitary-adrenal (HPA) axis and elevated glucocorticoids.
  • Stress is a frequent seizure trigger in TLE, and comorbid depression and anxiety are highly prevalent.

Purpose of the Study:

  • To examine evidence of HPA axis disruption in TLE.
  • To explore potential mechanisms underlying HPA axis dysfunction in TLE.
  • To discuss the implications of HPA dysfunction for seizure activity and psychiatric comorbidities.

Main Methods:

  • Review of existing studies on HPA axis function in TLE patients.
  • Analysis of the role of glucocorticoids in neuronal excitability and seizure susceptibility.
  • Examination of the link between HPA axis dysfunction and stress-related psychopathologies.

Main Results:

  • Evidence suggests a disrupted HPA axis in TLE patients.
  • Elevated glucocorticoids may increase seizure susceptibility and contribute to psychopathologies.
  • Abnormal stress responses in TLE could facilitate seizures and psychiatric comorbidities.

Conclusions:

  • HPA axis dysfunction is implicated in TLE pathophysiology.
  • Glucocorticoid excess may link TLE, seizure triggers, and psychiatric issues.
  • Targeting HPA axis dysregulation may offer therapeutic potential for TLE and its comorbidities.