Work Type



Fall 2016

Faculty Advisor

Dr. Roger Allen




Purpose/Hypothesis: Stress has been studied as a credible trigger of spasticity, but evidence is limited concerning temporal relationships. Case studies of complex regional pain syndrome (CRPS) and fibromyalgia (FM) have established a ten-day delay between psychogenic stress and episodic pain flares. This is explained by a stress induced release of thyroxine (T4) from the thyroid gland via the hypothalamus-pituitary-thyroid (HPT) axis, which reaches its peak effect by day 10. Models suggest that T4 may increase peripheral nerve excitability, which could increase sensitivity in 1A fibers from muscle spindles, leading to hyper-excitability in motor neuron pools. The purpose of our study is to explore the temporal relationship between stress & spasticity, to see if subjects experience latent increases in spasticity due to stress.

Subjects: Subjects ranged from 48-84 years old, including one male with CVA history & one female with CVA history s/p thyroidectomy.

Materials/Methods: Every day for 12 weeks, participants completed stress and spasticity inventories. Stress was measured with a visual analog stress scale (VASS) and spasticity with a visual analog functional scale (VAFS) assessing the degree of difficulty to execute a standard daily task due to spasticity severity. Quantitative criteria were established defining days of peak stress and days of peak spasticity. Final temporal relationship results between stress and spasticity were analyzed with serial lag correlations for 0-12 day lags.

Results: After 12 weeks of data collection, the male manifested a significant correlation to spasticity related function ten days after criterion peak stress days. Serial lag analysis on peak stress days for this person revealed a 70% correlation supporting a 10-day impact on peak spasticity. The female subject revealed one event in spasticity-related function 10 days after peak stress event, which yields an insignificant 10-day lag correlation of 9.1%. This subject, with history of thyroidectomy, reports taking daily administration of levothyroxine. Consequently, her results are not surprising, since her HTP pathway cannot be influenced by stress.

Conclusions: Based on results, evidence supports an increase in CVA-related spasticity ten days after high stress episodes. This relationship was not observed in our female subject s/p thyroidectomy, lending inverse support to the hypothesis that latent ten-day effects may be due to the HPT axis.

Clinical Relevance: Patients and therapists frequently are at a loss to explain episodic elevations in spasticity severity. If a consistent temporal relationship between stress and spasticity is confirmed, it would give caregivers, patients, and therapists insight into understanding and predicting episodes of decreased function following high stress days.


University of Puget Sound