Upper Motor Neurons

Hello :) In this post we'll be discussing the physiology behind upper motor neurons (UMNs). We'll take a look at the major descending UMN tracts as well as what happens when these tracts are damaged.

Upper motor neurons (UMNs) have cell bodies that are in the cerebral cortex or brain. Their axons descend in the white matter of the spinal cord to synapse with interneurons or lower motor neurons in the grey matter of the ventral horn. The UMNs that have cell bodies in the cerebral cortex are involved with initiating, maintaining and planning sequences of voluntary movements. On the other hand, UMNs with cell bodies in the cerebellum are involved with the regulation of muscle tone, the control of posture and basic “navigational” movements.  Basically, upper motor neurons are synonymous with the central nervous system.

Descending Upper Motor Neuron Tracts

The UMN tracts can be divided into the pyramidal and extrapyramidal systems and this depends on whether the tracts traverse the pyramids of the medulla or not. However, this distinction is more important in primates than in domestic animals as the pyramidal system is more developed in primates. The separation is related to the capacity to perform finely skilled motor movements.

In addition, two general forms of movement exist:

• Voluntary, conscious, skilled movement (learned): mediated by flexor muscles from discrete contractions of a few groups of muscles, most of which are distant to the spinal cord. The cell bodies of neurons innervating these muscles are located more dorsolaterally on the cross section of a spinal cord. 
• Postural, anti-gravity muscle tone: mediated by extensor muscles from the contractions of large groups of muscles, most of which are located closer to the spinal cord. Cell bodies of neurons innervating these muscles are arranged ventromedially in the spinal cord.

Pyramidal System

These tracts have neurons with cell bodies that are mostly in the motor area of the cerebral cortex. These fibres cross over to the contralateral side at the pyramids of the medulla. In primates, most of the neurons form a monosynaptic pathway from the cerebrum and influence the LMNs directly. Lesions of tracts within this system in humans results in severe contralateral motor deficits. However, similar lesions in domestic animals results in minimal weakness although contralateral placing deficits may occur. 

Below is a summary of the major descending UMN tracts. Included is information on their beginning, ending and function. 

Corticospinal and Corticobulbar Tracts

Beginning: both are from the cerebral cortex.

Ending: the corticobulbar tract innervates the nuclei of cranial nerves in the brain stem (bilaterally, but mainly contralaterally).

The Corticospinal tract continues to the medullary pyramids where 75-90% of the axons decussate and continue as the lateral corticospinal tract (LCST). In the dog, 50% of LCST axons terminate in the cervical grey matter, 20% in thoracic grey matter and 30% in lumbosacral grey matter where they influence LMNs of distal musculature via interneurons.

Those axons that don’t decussate continue as the ventral corticospinal tract on the ipsilateral side. These synapse with motor neurons of the axial and proximal limb muscles.

Function: not very important in domestic animals.

Extrapyramidal System

These neurons originate in the cerebral cortex, including the motor area. These fibres travel to the brain stem directly or via subcortical nuclei and synapse with additional neurons along the way. The fibres pass through the spinal cord and don’t cross at the pyramids. These are usually multisynaptic pathways.

Rubrospinal Tract

This is the most important lateral descending pathway in animals.

Beginning: It originates in the red nucleus which receives afferent axons from an ipsilateral (same side) area of the cerebral cortex.

Ending: lateral grey matter of spinal cord, influencing LMNs of flexor muscles of the thoracic and pelvic limbs.

Function: Since it is found in the lateral part of the spinal cord it is involved with conscious, voluntary, skilled movement.

Vestibulospinal Tracts

This is involved mainly with the maintenance of posture and balance and consists of lateral and medial tracts.

Lateral Vestibulospinal Tract:

Beginning: vestibular nuclei which receives input from the vestibular apparatus and inhibitory input from cerebellum.

Ending:  descends ipsilaterally and terminate mainly on interneurons which activate LMNs of the trunk and limbs.

 

Function: This facilitates extensors and inhibits flexors and is involved in the maintenance of posture and balance.

Medial Vestibulospinal Tract

Beginning: rostral, medial and caudal vestibular nuclei

Ending: contains crossed and uncrossed fibres and terminates in the cervical and cranial thoracic spinal cord segments.

Function: adjusts head and neck position in response to change in posture.

Tectospinal Tract

Beginning: the visual tectum of midbrain (superior colliculus)

Ending:  crosses to the contralateral side and projects to the cervical and upper thoracic spinal cord.

Function: influences LMN circuits which work to control the axial musculature of the neck. This tract is important in the reflex co-ordination of head and eye movements in response to visual stimuli.

Reticulospinal Tracts

There are two reticuolspinal tracts: the medullary (lateral) reticulospinal tract and the pontine (medial) reticulospinal tract (RST). 

Beginning: Originate in the Reticular formation which receives projections from the cerebellum, spinal cord and higher levels of the brain including extrapyramidal nuclei. 

Ending: all levels of the spinal cord.

Function: The medullary RST projects bilaterally and supresses extensor spinal reflex activity. The proximal RST projects ipsilaterally and facilitates the extensor spinal reflex activity. 

The diagram below shows the arrangement of these tracts on a cross-section of the spinal cord. 

Spinal Tracts. Source

Damage to the Descending Pathways

Damage to upper motor neurons is common and is characterised by:

• Paresis: this is weakness due to interference with the ability of the upper motor neurons to initiate gait generation. This paresis is different to that seen in LMN damage which interferes with the ability to support weight not to initiate gait. UMN disorders result in a delay or absence of protraction of the limb with attempts to walk or hop. 
• Hypertonia: The inhibition of gamma motor neurons, which innervate muscle spindles, is lost. This is most evident in antigravity extensor muscles. Thus the increased firing of gamma motor neurons, especially to chain fibres which detect length, causes them to shorten and this increases the firing of Type 1a and Type 2 sensory fibres. This leads to a reflex increases in the firing of alpha motor neurons which shortens the muscle to a new length and increases muscle tone. 
• Spasticity: This refers to an increased muscle tone when the limbs are moving. UMN damage results in the loss of gamma motor innervation to the nuclear bag fibres of the muscle spindles which causes them to shorten. At rest, there is no increase in the firing of type 1a primary fibres. It is only when the muscle is lengthened that there is greatly increased Type 1a firing and excessive contraction. This is found predominantly in the extensors of the pelvic and thoracic limbs. 
•  Hyperreflexia: Because the UMNs are damaged, the LMNs are no longer inhibited. This leads to an increased force and amplitude of spinal reflexes which is especially evident in the patellar tendon reflex. 

That's all for this post, see you next time :)