Abstract
This study proposed a pupillary light reflex (PLR) inherent model based on the system identification method to demonstrate the dynamic physiological mechanism of the PLR, in which pupillary constriction and dilation are controlled by the sympathetic and parasympathetic nervous system. This model was constructed and verified by comparing the simulated and predicted PLR response with that of healthy participants. The least root-mean-square error (RMSE) of simulated PLR response was less than 0.7% when stimulus duration was under 3 ms. The RMSE of predicted PLR response increased by approximately 6.76%/s from the stimulus duration of 1 ms to 3 s, when the model directly used the parameters extracted from the PLR at the stimulus duration of 10 ms. When model parameters were derived from the regression by the measured PLR response, the RMSE kept under 8.5%. The model was applied to explore the PLR abnormalities of the people with Diabetic Mellitus (DM) by extracting the model parameters from 42 people with DM and comparing these parameters with those of 42 healthy participants. The parameter in the first-order term of the elastic force of the participants with DM was significantly lower than that of the healthy participants (p < 0.05). The sympathetic force and sympathetic action delay of the participants with DM were significantly larger (p < 0.05) and longer (p < 0.0001) than that of the healthy ones, respectively. The reason might be that the sympathetic nervous system, which controls the dilator muscle, degenerated in diabetic patients.
Highlights
The autonomic nervous system (ANS) is composed of sympathetic nervous systems (SNS) and parasympathetic nervous systems (PSNS) [1]
We proposed a pupillary light reflex (PLR) inherent model modified by Fan’s model [37]
The elastic force, the viscous force, and the ANS forces were assumed to be zero when the pupil was in a dark-adapted resting state, and the SNS force was assumed to join the pupillary constriction before the maximum pupil constriction and still active in pupillary dilation while the force of PSNS stopped
Summary
The autonomic nervous system (ANS) is composed of sympathetic nervous systems (SNS) and parasympathetic nervous systems (PSNS) [1]. The amplitude, duration, and velocity of pupillary constriction and dilation in PLR may be used to explore the severity of diabetic autonomic neuropathy but may not directly offer the relation between ANS and PLR abnormalities. This relation may be explored through a physiologically-based PLR model. The elastic force, the viscous force, and the ANS forces were assumed to be zero when the pupil was in a dark-adapted resting state, and the SNS force was assumed to join the pupillary constriction before the maximum pupil constriction and still active in pupillary dilation while the force of PSNS stopped This model, which used the second-order differential equation, describes the pupillary constriction and dilation innervated by SNS and PSNS. The model parameters were extracted and compared from PLR data of 42 healthy participants and 42 ones with DM
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