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Updated: Jul 10, 2025
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Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
Published on: August 15, 2017
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Electroconvulsive therapy improves hematological inflammatory markers in bipolar disorder.
Eman Ali1, Ahmed Embaby2, Shaymaa M Arafa3
1Psychiatry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Psychopharmacology
|November 24, 2023
Summary
Electroconvulsive therapy (ECT) positively impacts bipolar disorder (BD) by improving inflammatory markers, specifically increasing platelet distribution width (PDW) and decreasing red cell distribution width (RDW). This suggests ECT has an anti-inflammatory role in BD.
Area of Science:
- Neuroscience
- Immunology
- Hematology
Background:
- Bipolar disorder (BD) is associated with immune dysfunction and inflammation.
- Abnormal levels of red cell distribution width (RDW) and platelet distribution width (PDW) are observed in BD patients.
- Electroconvulsive therapy (ECT) has been linked to alterations in inflammatory mediators.
Purpose of the Study:
- To investigate the effect of ECT on RDW and PDW in patients with bipolar disorder.
- To assess whether ECT influences inflammatory markers relevant to BD pathophysiology.
Main Methods:
- A prospective cohort study involving 72 patients (age ≥ 16) diagnosed with BD.
- Complete blood count (CBC) was analyzed before and after four ECT sessions.
- Patients were diagnosed with BD according to DSM-IV criteria and indicated for ECT.
Main Results:
- A significant increase in PDW and a significant decrease in RDW were observed post-ECT.
- No significant changes were found in platelet count, mean platelet volume (MPV), or Plateletcrit (PCT) after ECT.
- ECT modulated specific CBC-derived inflammatory markers in BD patients.
Conclusions:
- ECT appears to improve CBC-derived inflammatory markers (RDW and PDW) in bipolar disorder.
- These improvements suggest an anti-inflammatory effect of ECT in BD.
- ECT favorably impacts inflammatory processes in BD without disrupting platelet homeostasis.
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