Upper limb neuro post pic

Upper vs Lower Motor Neurone Lesions

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Introduction

The neurological examination helps you localise a lesion in the nervous system.Β 

A helpful starting point can be differentiating between an upper (brain or spinal cord) or lower (anterior horn cell, motor nerve roots or peripheral motor nerve) motor neurone lesion.

Upper vs lower motor neurones
Figure 1. Upper motor neurons originating in the primary motor cortex synapse to lower motor neurons in the anterior horn of the spinal cord.1

Upper motor neurone leisions

An upper motor neurone (UMN) lesion will be in the central nervous system (brain and spinal cord).

On neurological examination, typical signs of an upper motor neurone lesion include:

  • Disuse atrophy (minimal) or contractures
  • Increased tone (spasticity/rigidity) +/- ankle clonus
  • Pyramidal pattern of weakness (extensors weaker than flexors in arms, and vice versa in legs)
  • Hyperreflexia
  • Upgoing plantars (Babinski sign)
An example of the Babinski sign
Figure 2. An example of the Babinski sign with extension of the big toe.
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Lower motor neurone leisions

A lower motor neurone (LMN) lesion affects anywhere from theΒ anterior horn cell to theΒ muscle.Β 

On neurological examination, typical signs of a lower motor neurone lesion include:

  • Marked atrophy
  • Fasciculations
  • Reduced tone
  • Variable patterns of weakness
  • Reduced or absent reflexes
  • Downgoing plantars or absent response

Upper vs lower motor neurone lesions

Upper motor neurone lesions present with hypertoniaΒ andΒ spastic paralysis, whereas lower motor neurone lesions are usually associated with hypotoniaΒ andΒ flaccid paralysis.

This is because of the impaired ability of motor neurons to regulate descending signals, giving rise to disordered spinal reflexes.

The central nervous system is involved in suppressing pathway activity. That is, the corticospinal tract helps in the conscious inhibition of muscle. If we damage UMNs, there is a loss of inhibitory tone of musclesΒ leading toΒ constant contraction of muscles.

This leads to the typical hypertonia,Β spastic paralysis and hyperreflexia seen when examining patients with UMN lesions.Β 

In contrast, if LMNs are damaged or lost, there is nothing to tell the muscles to contract, resulting in hypotoniaΒ andΒ flaccid paralysis.

Table 1. A summary of upper motor neurone (UMN) vs lower motor neurone (LMN) lesions.

Β  Upper motor neurone Lower motor neurone
Site of the lesion Cerebral hemispheres, cerebellum, brainstem, spinal cord Anterior horn cell, motor nerve roots, peripheral motor nerves
Inspection No fasciculations or significant wasting (however there may be some disuse atrophy or contractures) Wasting and fasciculation of muscles
Tone Increased (spasticity or rigidity) +/- ankle clonus Decreased (hypotonia, flaccid) or normal
Power Reduced with pyramidal pattern of weakness (extensors weaker than flexors in arms, and vice versa in legs) Reduced in distribution of affected motor root/nerve
Reflexes Exaggerated or brisk (hyperreflexia) Reduced or absent (hyporeflexia or areflexia)
Plantar reflex Upgoing/extensor (Babinski positive) Normal (downgoing/flexor) or no movement
Examples ofΒ  conditions
  • Ischaemic or haemorrhagic stroke (including brainstem strokes)
  • Amyotrophic lateral sclerosis
  • Multiple sclerosis
  • Peripheral nerve trauma/compression
  • Spinal muscular atrophy
  • Amyotrophic lateral sclerosis
  • Guillain-BarrΓ© syndrome
  • Poliomyelitis

References

  1. Rcchang16. UMN vs LMN. License: [CC BY-SA]

 

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