Upper Versus Lower Motor Neuron Lesions
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Direct answer
Upper versus lower motor neuron lesions are separated by the site of damage. Upper motor neuron lesions affect the corticospinal pathway above the anterior horn cell and cause spasticity, brisk reflexes and an extensor plantar response without marked wasting. Lower motor neuron lesions affect the anterior horn cell, root, plexus or nerve and cause flaccidity, areflexia, wasting, fasciculations and a flexor plantar response.
What you must remember
- Tone: Upper motor neuron lesions cause spasticity with clasp-knife resistance, while lower motor neuron lesions cause flaccidity or hypotonia.
- Reflexes: Upper lesions give exaggerated reflexes, clonus and a positive Hoffmann sign; lower lesions give reduced or absent reflexes in the affected muscles.
- Wasting: Upper lesions produce only disuse atrophy, whereas lower lesions produce true neurogenic wasting from denervation.
- Fasciculations: Seen only in lower motor neuron disease, usually in the tongue, limbs or trunk, and absent in upper motor neuron disease.
- Plantar response: An upper lesion gives an extensor (Babinski) response, while a lower lesion gives a flexor response.
- Spinal shock: A fresh cord transection starts flaccid and areflexic, mimicking a lower lesion, before upper motor neuron signs develop over days to weeks.
Localising by four bedside signs
The examiner separates the two lesion types by comparing a few bedside signs. Each sign has a reliable direction, so a single assessment of tone, reflexes, wasting and plantar response usually places the lesion correctly.
| Feature | Upper motor neuron | Lower motor neuron |
|---|---|---|
| Tone | Spastic, clasp-knife | Flaccid or hypotonic |
| Reflexes | Brisk, clonus may be present | Reduced or absent |
| Plantar | Extensor (Babinski) | Flexor |
| Wasting | Mild, disuse only | Marked, neurogenic |
| Fasciculations | Absent | Present |
| Weakness pattern | Pyramidal (arm extensors, leg flexors) | Myotomal or nerve territory |
| Common causes | Stroke, cord compression, multiple sclerosis | Anterior horn disease, neuropathy, root lesion |
Clasp-knife spasticity with brisk reflexes points upward in the neuraxis. Wasting with fasciculations points to the anterior horn, root or nerve, and a mixture of both sets of signs in one patient suggests motor neuron disease such as amyotrophic lateral sclerosis. Record the distribution of weakness as well, because a pyramidal pattern supports an upper lesion, while a myotomal or nerve-territory pattern supports a lower one.
Where the exam tries to catch you
Most lost marks come from misreading wasting and cranial nerve patterns.
- Trap: Calling post-stroke limb wasting neurogenic Correct: wasting after a stroke is mild and reflects disuse, so it does not localise to the lower motor neuron.
- Trap: Placing a lower face weakness in the upper motor neuron group without checking the forehead Correct: Bell's palsy, a lower motor neuron facial palsy, involves the forehead, while an upper lesion spares it.
- Trap: Attributing tongue fasciculation to pseudobulbar palsy Correct: tongue wasting and fasciculation indicate bulbar lower motor neuron disease, whereas pseudobulbar palsy is upper motor neuron with a brisk jaw jerk and emotional lability.
Frequently asked questions
Why is the plantar response extensor in an upper motor neuron lesion?
An extensor plantar response, or Babinski sign, appears in upper motor neuron lesions because loss of corticospinal inhibition unmasks a primitive withdrawal reflex. The great toe dorsiflexes while the other toes fan out when the sole is stroked. A flexor response is normal in adults and is expected in lower motor neuron disease.
Does wasting always indicate a lower motor neuron lesion?
Wasting does not always indicate a lower motor neuron lesion, because disuse atrophy after a stroke or long immobilisation can look similar. True neurogenic wasting, with fasciculations and reduced reflexes, points to denervation from an anterior horn, root or nerve lesion. Examiners expect you to combine wasting with fasciculation before localising the lesion.
Which features distinguish bulbar palsy from pseudobulbar palsy?
Bulbar palsy is a lower motor neuron lesion of the medullary cranial nerve nuclei, causing tongue wasting, fasciculations, nasal speech and dysphagia. Pseudobulbar palsy is an upper motor neuron lesion of the corticobulbar pathways, with spastic dysarthria, emotional lability and a brisk jaw jerk. The jaw jerk is the bedside discriminator, being normal or absent in bulbar palsy and brisk in pseudobulbar palsy.
How does facial nerve palsy differ between upper and lower motor neuron lesions?
A lower motor neuron facial palsy, such as Bell's palsy, involves the forehead as well as the lower face. An upper motor neuron lesion above the facial nucleus, typically a cortical or internal capsule stroke, spares the forehead because the frontalis receives bilateral cortical supply. This forehead sparing is the key clinical difference.
Why do upper motor neuron signs appear late after a spinal cord transection?
Spinal shock causes immediate flaccidity and areflexia below a complete transection of the cord, mimicking a lower motor neuron lesion. Spasticity, hyperreflexia and an extensor plantar response appear over the following days to weeks as spinal reflex excitability returns. Early examination therefore cannot reliably localise the lesion.