Abstract Details

Title Correlation Between Plasma Glutamate Levels and Post Stroke Depression

Topic Cerebrovascular Disease and Interventional Neurology

Presentation(s) P6 - Poster Session 6 (5:30 PM-6:30 PM)

Poster/Presentation
Number 13-003

Background

Post stroke depression (PSD) often causes a delay to patient recovery following ischemic stroke, leading to disability and enhanced mortality. The pathogenesis of PSD is still relatively unknown. Glutamatergic dysfunction is a key factor in depressive disorders, and excess glutamate release post stroke can be associated with higher plasma glutamate levels in the blood and cerebrospinal fluid. If plasma glutamate levels are disrupted, it serves as a prime candidate for neurologic dysfunction, which could lead to depressive symptoms.

Objective Determine if there is an association between plasma glutamate levels and depressive symptoms post stroke.

Design/Methods Participants that had imaging evidence of an ischemic stroke in the past six months were screened for PSD using the Hamilton Depression Rating Scale (HAMD-17) and were categorized as either depressed (>8) or not depressed (<8). Peripheral blood was drawn and plasma biomarkers were analyzed using the Amino Acid Quantitative Plasma set. An unpaired T-test was used for statistical analysis.

Results Six patients were categorized as depressed, with HAMD scores ranging from 8-13. Five patients were categorized as not depressed, with HAMD scores ranging from 1-4. Normal ranges of plasma glutamic acid range from 13-113 nmol/ml. Non-depressed patients had average glutamic acid levels of 58.6 mmol/ml and depressed patients had average glutamic acid levels of 77.2 mmol/ml. Although depressed patients did have a higher average glutamate level compared to non-depressed patients, this difference was not statistically significant (p=0.338).

Conclusions There was a trend toward higher glutamate levels in depressed patients compared to non-depressed patients following ischemic stroke, suggesting that glutamate is an important molecule to study as a potential biomarker of PSD. However, these results need to be confirmed in larger studies. The impact of PSD on patient recovery could benefit from a clearer understanding of the pathogenesis of PSD and glutamatergic dysfunction remains an important avenue for exploration.

Authors/Disclosures
PRESENTER	No disclosure on file
Jessica Frey, MD (West Virginia University)	The institution of Dr. Frey has received research support from Tourette Association of America.
Nicholas Koenig	Mr. Koenig has nothing to disclose.
Amelia K. Adcock, MD (WVU School of Medicine, Dept. of Neurology)	The institution of an immediate family member of Dr. Adcock has received research support from NIH.