Pineal gland calcification confirmed by CT scan is associated with ischemic stroke

Yaser Moadabi, Metanat Rezaei, Enayatollah Homaei-Rad, Sima Fllah Arzpeyma, Sama Noroozi Guilandehi, Sasan Andalib*

*Kontaktforfatter for dette arbejde

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review


Background. Stroke is the second leading cause of death and the most common debilitating neurological disorder worldwide. The ischemic injury causes inflammation and oxidative stress, and leads to apoptosis, necrosis and activation of autophagal pathways determining final infarct size. Melatonin, a hormone secreted by the pineal gland, is a small molecule that acts as a free radical scavenger, and performs antioxidant activities in several neurodegenerative diseases. Melatonin secretion reduces in aging due to pineal gland calcification and thus the calcification is a representative of reduced melatonin production. In this study, our aim was to evaluate the association of pineal gland calcification and stroke. Material and methods. An analytical cross sectional single center study was conducted. Pineal gland calcification was assessed by CT scan in 179 patients with ischemic stroke and 177 hospital controls. Results. The mean age in the control and stroke groups were 58.18 and 61.2 years, respectively. Pineal gland calcification was found in 77.4% of subjects in the control group and 88.8% of the subjects in the stroke group. Pineal gland calcification, alone, was shown to significantly increase the risk of ischemic stroke (P=0.005; OR=2.3; 95% CI=1.2-4.1). Furthermore, after adjustment for diabetes mellitus, hypertension, hyper lipedema, gender, and age, there was still a significant association of pineal gland calcification with ischemic stroke (P=0.04; OR=2.0; 95% CI=1.0-3.9). Conclusion. The evidence from the present study suggests that pineal gland calcification is associated with ischemic stroke.

TidsskriftRomanian Journal of Neurology: Serie de Neurologie et Psychiatrie
Udgave nummer3
Sider (fra-til)117-120
StatusUdgivet - 2019
Udgivet eksterntJa


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