Upper Motor Neurones, Lower Motor Neurones, and Descending Tracts

Overview

The descending tracts are mainly motor. The cell bodies of motor neurones are found in the cerebral cortex, brain stem, or spinal cord. Motor neurones convey impulses from these areas to muscles and glands. Motor neurones are divided into:

• Upper motor neurones (UMNs):
  • Travel from the cerebral cortex through different tracts and synapse with lower motor neurones in the brainstem or spinal cord
• Lower motor neurones (LMNs):
  • Transmits signals from UMNs to the effector muscles to perform a movement

UMN and LMN signs play an important role in working out where a neurological lesion is.

Tracts

Nervous impulses involved in movement are conveyed through tracts, which describe pathways consisting of white matter made of myelinated axons.

UMN tracts can be divided into:

• Pyramidal tracts:
  • Form a direct pathway from the cerebral cortex to the spinal cord and brainstem
  • Responsible for the voluntary control of muscles in the body and face
• Extrapyramidal tracts:
  • Form a pathway from the brainstem to the spinal cord
  • Responsible for involuntary control of muscles (e.g. tone, balance, posture etc.) 

The Pyramidal Tracts

Overview

The pyramidal tracts convey UMNs from the cerebral cortex to the spinal cord and brainstem and are involved in the voluntary control of muscles in the body and face. They divide into:

• The corticospinal tract – UMNs from the cerebral cortex synapse with spinal nerves:
  • Supplies muscles of the body
• The corticobulbar tract – UMNs from the cerebral cortex synapse with cranial nerves:
  • Supplies muscles of the head and neck

The corticospinal tract

UMNs from the cerebral cortex descend through the midbrain, ventral pons, and the medulla. At the bottom of the medulla:

• Most (90%) of the corticospinal tracts decussate (cross over):
  • These UMNs continue their descent on the contralateral side to where they originated from.
  • These UMNs form the lateral corticospinal tract.
  • These UMNs synapse with LMNs involved in controlling the distal extremities (e.g. the fingers and hands)
• Around 10% do not decussate:
  • These UMNs continue their descent ipsilateral to where they originated from.
  • These UMNs form the anterior corticospinal tract.
  • The anterior corticospinal tract is involved in axial muscles (e.g. muscles of the trunk, neck, and shoulders)
  • Most of these UMNs decussate in the cervical and upper thoracic levels of the spinal cord instead.
  • Some of these UMNs do not decussate at all
    • These UMNs are involved in controlling axial muscles to maintain body posture.

The corticobulbar tract

UMNs from the cerebral cortex synapse with cranial nerve nuclei in the brainstem. Most corticobulbar tracts decussate above each cranial nerve nucleus (except the trochlear nerve which decussates within the brainstem before emerging) and most of the cranial nerve nuclei receive bilateral UMN innervation except for:

• CN VII (facial nerve):
  • The CN VII nucleus is divided horizontally in half:
    • The superior half represents the superior half of the face and is bilaterally innervated
    • The inferior half represents the inferior half of the face is contralaterally innervated
• CN XII (hypoglossal nerve):
  • UMNs for CN XII only provide contralateral innervation

Clinical significance

Lesions to the pyramidal tracts can have serious consequences. The sites of decussation and whether UMNs or LMNs are affected can help localise where the pathology is based on symptoms. In general:

• Lesions above the level of decussation lead to contralateral symptoms
• Lesions below the level of decussation lead to ipsilateral symptoms

The trochlear nerve decussates within the brainstem, therefore lesions of the trochlear nerve after it emerges from the brainstem lead to ipsilateral symptoms, whereas lesions to the trochlear nerve nucleus lead to contralateral symptoms.

Upper and motor neurone signs are discussed below.

Upper Motor Neurone Signs

Upper motor neurone signs

Signs and symptoms of UMN lesions can be divided into:

• Negative symptoms:
  • Weakness
  • Decreased control
  • Easily fatigued
• Positive symptoms:
  • Spasticity – velocity-dependent increased tone to passive stretch:
    • Quick movements of an affected limb result in increased tone
  • Clonus – rhythmic, involuntary muscle contractions when abrupt muscle stretch is applied
    • E.g. quick dorsiflexion of the foot leads to involuntary plantarflexion rhythmic movements
  • Hyperreflexia – brisk reflexes:
    • This is because UMNs are involved in providing inhibitory signals to LMNs
  • Pathological reflexes – such as:
    • The Babinski sign: stroking the sole of the foot leads to the extension of the large toe and fanning of the other toes – a positive Babinski sign
      • A normal response in adults is plantarflexion
    • The Hoffman sign: holding the patient’s middle finger and flicking the fingernail downward leads to flexion and adduction of the thumb – a positive Hoffman sign
      • This is seen in degenerative cervical myelopathy

Upper motor neurone signs in cranial nerves

Since most cranial nerves are bilaterally innervated, they show signs when both UMNs are damaged. When both UMNs are damaged, this is known as pseudobulbar palsy and can manifest with:

• Dysphagia
• Dysarthria
• A brisk jaw-jerk reflex
• Tongue spasticity
• Pseudobulbar affect – emotional imbalance (e.g. excessive crying or laughing)

The exceptions to this are cranial nerves VII (the facial nerve) and XII (the hypoglossal nerve):

• CN VII:
  • Unilateral UMN lesions result in a lower facial droop away from the side of the lesion
    • The upper half is unaffected as it is bilaterally innervated
  • LMN lesions would affect the ipsilateral side and involve both the upper and lower face
  • A patient presenting with a UMN lesion of the face, where only the lower face is affected, should raise suspicion of stroke
• CN XII:
  • Unilateral UMN lesions result in tongue deviation away from the side of the lesion

Lower Motor Neurone Signs

Overview

Although both UMN and LMN lesions result in weakness. LMN lesions have the following signs:

• Decreased reflexes – reflexes may be absent
• Decreased tone – muscles are weak or may be floppy
• Muscle atrophy – muscles are wasting/thinning
• Fasciculations – involuntary, rapid muscle twitches
• Flaccid paralysis – paralysis and decreased tone

Since LMNs do not decussate, they cause ipsilateral signs. 

The Extrapyramidal Tracts

Overview

The extrapyramidal tracts convey UMNs from the brainstem to the spinal cord and are involved in the involuntary control of the muscles, including their tone, balance, posture, and locomotion.

The extrapyramidal tracts include:

• The vestibulospinal tracts – from the vestibular nuclei to the spinal cord:
  • Control balance and posture
  • Subdivided into medial and lateral vestibulospinal pathways
  • Do not decussate – provide ipsilateral innervation
• The reticulospinal tracts – from the reticular formation in the brainstem to the spinal cord:
  • Subdivided into:
    • The medial reticulospinal tract – arises from the pons and facilitates voluntary movement and increases muscle tone
    • The lateral reticulospinal tract – arises from the medulla and inhibits voluntary movement and decreases muscle tone
  • Do not decussate – provide ipsilateral innervation
• The rubrospinal tracts – from the red nucleus in the midbrain to the spinal cord:
  • Exact function unclear, thought to be involved in the control of fine hand movements
  • They do decussate – provide contralateral innervation
• The tectospinal tracts – from the superior colliculus in the midbrain to the spinal cord:
  • The superior colliculus receives signals from the optic nerve
  • Involved in coordinating head movements in response to vision
  • They do decussate – provide contralateral innervation

Clinical significance

Degenerative disorders (e.g. Parkinson’s disease) and drugs (such as drugs that antagonise dopamine D2 receptors including antipsychotics and antiemetics such as metoclopramide) can lead to extrapyramidal symptoms (EPS). These are characterised by:

• Acute dystonic reactions – painful muscular spasms of the jaw, neck, back, limbs, eyes etc.
  • Oculogyric crisis is a type of acute dystonic reaction where there is a prolonged involuntary upward deviation of the eyes
  • May be treated with procyclidine (an anticholinergic drug)
• Akathisia – severe restlessness:
  • May manifest as an inability to sit still, pacing, or anxiety
• Parkinsonism – features of Parkinson’s disease, which can be remembered with TRAP:
  • Tremors
  • Rigidity
  • Akinesia/bradykinesia – slowing of movements which may progress as movement goes on 
  • Postural instability
• Tardive dyskinesia – involuntary movements of the muscles of the lower face and distal extremities:
  • Examples are chewing and pouting of the jaw
  • Tardive – presents later, either due to a chronic condition or long-term drug use
  • May be treated with tetrabenazine