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Comorbid masticatory impairment delays recovery from acute cerebral ischemia and locomotor hypoactivity after subarachnoid hemorrhage in mice

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Clinical and Experimental Pharmacology and Physiology

Published online on


Tooth loss and related changes in the functionality may lead to worse outcome of stroke patients, but the link involved in this pathway remains unclear. This study aimed to determine the effect of comorbid masticatory impairment on acute cerebral ischemia and neurobehavioral outcome after experimental subarachnoid hemorrhage (SAH). Thirty C57BL/6 mice with (molar‐less) or without (control) prior treatment of cutting off the upper molars (separated by at least one week), were subjected to SAH by endovascular perforation. Grading of SAH and acute cerebral infarction were assessed by T2*‐ and diffusion‐weighted MR images, respectively. Cerebral blood flow (CBF) by continuous arterial spin labeling and parameters related to locomotor activity and exploration ability by open‐field test were analyzed serially until 2 weeks after SAH. In all mice, global CBF depression was notable immediately after SAH induction (P<0.001), which recovered close to the baseline levels until day 7. However, molar‐less mice demonstrated a prolonged hypoperfusion (<50% of the baseline CBF) as compared to the control (3 ± 2 vs. 1 ± 1 days; P=0.037). The average distance traveled and the ratio of central‐area distance/total traveled distance by open‐field test between 1 and 2 weeks was significantly lower in molar‐less mice than in the control mice (P<0.05), although the occurrence of post‐SAH new infarction were not statistically different (P>0.05). These data suggest a possible link between comorbid masticatory impairment and early brain injury/ischemia to deteriorate neurobehavioral functional outcome in patients after SAH. This article is protected by copyright. All rights reserved.