# Parkinson’s disease impairs grip force release during a sinusoidal force tracking task

## TL;DR

Parkinson’s disease affects the ability to release grip force during a task requiring precise hand control, more so than aging alone.

## Contribution

This study reveals that Parkinson’s disease disproportionately impairs grip force release compared to force generation.

## Key findings

- People with Parkinson’s disease showed greater deficits in grip force release than in generation.
- Older adults had impaired force generation and amplitude scaling compared to younger adults.
- Force amplitude progressively decreases in both older adults and those with Parkinson’s disease.

## Abstract

The generation, modulation, and release of grip force underlie skilled manual dexterity and object interaction. Advancing age and neurological disease compromise force generation; the impact of age and pathology on the dynamic control of grip force release is unclear. The aim of this project was to determine the impact of age and Parkinson’s disease (PD) on grip force generation and release. Young adults (YA, n = 10, 18–28 years), older adults (OA, n = 10, 57–77 years), and people with PD (PwPD, n = 10, 56–75 years) completed a sinusoidal force tracking task using a precision grip with their dominant hand. Maximum grip force was not different between groups, however, OA relative to YA exhibited deficits in force generation, release and amplitude scaling. Although PwPD had global declines in force control, force release was disproportionately affected compared to force generation. The ability to scale force during its generation and release was compromised by PD. Two-point discrimination of the thumb and index fingers was impaired in PwPD and was moderately correlated with force tracking accuracy and force amplitude. While aging impacts grip force generation and release similarly during a task requiring continuous grip force modulation, PD disproportionately affects grip force release compared to generation. Force amplitude progressively decreases in older adults and PwPD. Potential sources of PD deficits include neural circuitry changes between the prefrontal cortex and striatum, impaired sensorimotor integration, and altered motor unit structure and function. Additional work is focused on identifying the neural mechanism(s) underlying impaired control and regulation of grip forces in PwPD.