Poststroke emotional disturbances and a tryptophan hydroxylase 2 gene polymorphism

OBJECTIVES: Emotional dysfunction is a common finding in stroke patients. Despite reports on serotonergic involvement in the etiology of poststroke emotional dysfunction (PSED), the role of serotonin synthesizing tryptophan hydroxylase 2 (TPH2) genes in the development of PSED remains unclear. METHODS: Genotyping of TPH2 rs4641528 and rs10879355 was performed from genomic DNA of 383 stroke patients collected previously and stored at −70°C. Potential associations between TPH2 genes and poststroke depression (PSD), poststroke emotional incontinence (PSEI), and poststroke anger proneness (PSAP) were investigated 3 months poststroke. RESULTS: Among the 383 patients, 69 (18%) had PSD, 41 (11%) had PSEI, and 93 (24%) had PSAP. The TPH2 rs4641528 genotype frequencies differed significantly between patients with and without either PSD or PSEI, although no significant differences were found between the patients with and without PSAP. In multiple logistic regression analysis, PSD was related to the National Institutes of Health Stroke Scale (NIHSS) score at admission (95% confidence interval [CI]: 1.047–1.230, p < .01), modified Rankin scale score at 3 months (95% CI: 0.135–0.848, p < .05), and TPH2 rs4641528 C allele (95% CI: 1.039–5.631, p < .05), whereas PSEI was associated only with the NIHSS score at admission (95% CI: 1.053–1.259, p < .01) and the TPH2 rs4641528 C allele (95% CI: 1.029–11.678, p < .05). CONCLUSIONS: Our findings suggest that the TPH2 rs4641528 C allele may play a role in the pathogenesis of PSD and PSEI but not PSAP in Korean stroke patients.