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Indirect Motor Pathways

Indirect Motor Pathways

The indirect motor or extrapyramidal pathways originate in the brainstem, the lower portion of the brain that connects it to the spinal cord. They consist of several distinct tracts, each with specialized functions. The four main tracts of the indirect motor pathways are the vestibulospinal tract, the reticulospinal tract, the tectospinal tract, and the rubrospinal tract.
The vestibulospinal tract originates in the vestibular nuclei of the brainstem. The vestibular system detects changes in...

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Related Experiment Video

Updated: Apr 2, 2026

Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI

Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI

Published on: April 18, 2011

Enhanced Reticulospinal Output in Subacute Spinal Cord Injury Patients with Spasticity.

Dalia De Santis¹, Monica A Perez^2,3,4

¹Shirley Ryan AbilityLab, Chicago, Illinois 60611.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|March 31, 2026

Summary

This summary is machine-generated.

Spinal cord injury (SCI) spasticity is linked to increased reticulospinal tract activity in the subacute phase, persisting long-term. This heightened reticulospinal drive, not corticospinal changes, appears crucial for spasticity development after SCI.

Keywords:

corticospinal electrophysiology quadriceps reticulospinal spasticity spinal cord injury subacute

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Activity-based Training on a Treadmill with Spinal Cord Injured Wistar Rats

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Published on: January 16, 2019

Area of Science:

Neuroscience
Neurology
Rehabilitation Medicine

Background:

Spasticity is a common and debilitating complication following spinal cord injury (SCI).
The precise mechanisms underlying spasticity development, particularly in the early phases post-injury, remain incompletely understood.
Damage to descending motor tracts, including the corticospinal and reticulospinal tracts, is implicated in SCI-related spasticity.

Purpose of the Study:

To investigate the role of motor pathway reorganization in the subacute phase of SCI.
To determine the association between spasticity and reticulospinal tract function using the StartReact response.
To examine changes in corticospinal excitability and voluntary motor output in relation to spasticity.

Main Methods:

Assessed the StartReact response (reaction time to startling stimuli) in individuals with subacute incomplete SCI (with and without spasticity) and controls.
Measured motor evoked potentials (MEPs) via transcranial magnetic stimulation and maximal voluntary contractions (MVCs) of the quadriceps femoris.
Utilized clinical and kinematic assessments to evaluate spasticity.
Conducted follow-up measurements one year post-injury in a subset of participants.

Main Results:

Individuals with spasticity exhibited significantly shorter reaction times to startling cues, indicating heightened reticulospinal influences.
MEP size and MVCs were similarly reduced in both SCI groups compared to controls, suggesting widespread corticospinal impairment.
Follow-up data confirmed persistent exaggerated StartReact responses and reduced MEP amplitudes in individuals with spasticity.

Conclusions:

Spasticity in subacute SCI is associated with an early upregulation of reticulospinal pathways.
This enhanced reticulospinal drive appears to be a critical factor in the pathogenesis of spasticity.
Corticospinal tract function is reduced post-SCI irrespective of spasticity, while reticulospinal alterations are specific to spasticity development.