Upper vs Lower Motor Neurone Lesions

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Table of Contents

Introduction

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

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)

**Figure 2**. An example of the Babinski sign with extension of the big toe.

Lower motor neurone leisions

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

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

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

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Upper motor neurone lesions present with hypertonia and spastic paralysis, whereas lower motor neurone lesions are usually associated with hypotonia and 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 muscles leading to constant contraction of muscles.

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

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

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

	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 of conditions	Ischaemic or haemorrhagic stroke (including brainstem strokes) Amyotrophic lateral sclerosis Multiple sclerosis	Peripheral nerve trauma/compression Spinal muscular atrophy Amyotrophic lateral sclerosis Guillain-Barré syndrome Poliomyelitis