Superior Laryngeal Nerve Function in an Alzheimer's Disease Rat Model: A Pilot Study

Alzheimer's Disease (AD) is associated with reduced laryngeal sensation, decreased pharyngeal strength, and silent aspiration. Aspiration pneumonia is a leading cause of death in advanced AD. Superior laryngeal nerve(SLN) dysfunction is hypothesized to be responsible for poor laryngeal sensation and aspiration pneumonia. The purpose of this study was to compare SLN neurophysiology in an AD rat model to control animals.

SLN-evoked studies were performed via stimulation of the main trunk in 4-month-old adult apolipoprotein-E4 (ApoE4-KI) rats (n = 8) versus wild-type rats (n = 10). Recording electrodes were placed on the internal branch of the SLN (iSLN) and cricothyroid muscles. Stimulated swallow force measurements from hyoid elevation were compared between groups. Outcome measures included both sensory and motor evoked responses. Additionally, force and frequency of electrically and tactile stimulated swallow reflexes were analyzed.

Sensory nerve action potential duration was significantly longer in APOE-KI rats than controls with a mean difference (95% CI) of 2.24 ms (1.08-3.41). Both compound motor action potential latency and total duration were significantly longer in the APOE4-KI rats than controls with a mean difference (95% CI) of 0.22 (0.115-0.33) and 2.18 (0.90-3.4) respectively. Tactile-stimulated swallow frequency was significantly lower in the AD cohort vs. controls with a mean difference of -5.4 swallows/10 s (-7.6, -3.2).

SLN evoked responses were significantly longer with a decrease in swallow frequency in an AD rat model compared to age-matched controls. This work suggests differences in SLN signaling between the cohorts. This work may provide a mechanistic understanding of SLN dysfunction and a tractable model to test new treatments for swallow dysfunction.

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