USMLE Step 1Neuroanatomy and lesion localisationEP 01 of 16

Upper vs lower motor neuron lesions: signs and localisation

Weak is weak, but the muscle tells you which neuron broke. Learn the signs of upper and lower motor neuron lesions and use them to place the damage.

  • 5:08 video
  • 3 min read
  • 11 sources
  • Published 15 Nov 2026
Chapters (8)
By the end of this lesson

Distinguish upper from lower motor neuron lesions by tone, reflexes, plantar response, fasciculations and atrophy, and say on which side of the body the signs appear for a lesion above or below the pyramidal decussation.

The short version

  1. Voluntary movement needs two neurons: the upper motor neuron in the central nervous system and the lower motor neuron that touches the muscle.
  2. A lower motor neuron lesion gives flaccid weakness, reduced or absent reflexes, fasciculations and then wasting, in a local pattern.
  3. An upper motor neuron lesion gives weakness with spasticity, brisk reflexes and a Babinski sign, without fasciculations or marked wasting.
  4. Above the pyramidal decussation, upper motor neuron signs appear on the opposite side; in the cord they stay on the same side. Lower motor neuron signs are usually on the side of the lesion.
  5. Upper and lower signs together mean both neurons are involved.

Same weakness, opposite signs

Two patients come to clinic with the same complaint: a weak right foot. In the first, the leg is stiff, the knee jerk is brisk, and stroking the sole sends the big toe upward. In the second, the leg is floppy, the ankle jerk is gone, and the calf is thin and twitching.

Same weakness, opposite signs. This lesson is about upper vs lower motor neuron lesions: how each one changes tone, reflexes, the plantar response, fasciculations and wasting, and how the signs help you place the damage.[2][8][9]

The chain of two neurons

Voluntary movement needs a chain of two neurons. The upper motor neuron starts in the primary motor cortex of the frontal lobe, and its axon runs down the corticospinal tract.[1][2]

Most of its fibres cross to the opposite side at the pyramidal decussation, at the bottom of the medulla, then descend in the lateral column of the cord.[1][2]

The lower motor neuron has its cell body in the ventral horn of the cord, or in a cranial nerve motor nucleus, and its axon runs in a peripheral nerve to the muscle.[1][2]

So the upper neuron lies wholly inside the central nervous system, while the lower neuron sends its axon out to touch the muscle. The lower neuron keeps muscle tone and runs the reflex arc, and the upper neuron's descending input modifies it.[2][7]

Lower motor neuron lesion signs: the muscle loses its wire

Cut the lower motor neuron and the muscle loses its wire. The result is flaccid paralysis.[2][4][8]

  • Low tone
  • Reflexes reduced or absent
  • Fasciculations (and fibrillations on EMG)
  • Then wasting of the muscle

The weakness follows the damaged segment or nerve, so it is local. Think of poliovirus in ventral horn cells, or a crushed nerve.[4][8]

That is the second patient from the opening: floppy leg, absent ankle jerk, thin and twitching calf.

Upper motor neuron lesion signs: spasticity and the Babinski sign

Cut the upper motor neuron instead. The lower neuron and its reflex arc are still intact, but have lost descending control. The result is weakness with spasticity, brisk reflexes and a Babinski sign.[2][3][9]

Spasticity is raised tone, worse with a fast stretch, that can give way suddenly like a pocket knife closing: the clasp-knife response.[2][7][9]

The Babinski sign is the big toe extending, with the other toes fanning, when the sole is stroked. It is normal in infants, but in an adult it points to damage of the corticospinal tract.[1][2][9]

The lower neuron still feeds the muscle, so there are no fasciculations and no marked wasting. That is the first patient.[2][3]

Upper vs lower motor neuron lesion signs
SignUpper motor neuronLower motor neuron
WeaknessYesYes, local to the segment or nerve
ToneSpastic, clasp-knifeLow, flaccid
ReflexesBriskReduced or absent
Plantar responseBabinski signNo Babinski sign
FasciculationsNonePresent
WastingNo marked wastingWasting follows

Place the lesion: capsule, cord and spinal shock

The signs also help you place the lesion. Because most corticospinal fibres cross at the pyramidal decussation, the side of the upper motor neuron signs depends on whether the damage is above or below it. Lower motor neuron signs are usually on the same side as the lesion.[1][2][9][10]

  • A stroke in the left internal capsule hits fibres that have not yet crossed, so the signs, with spasticity once the acute phase passes, appear in the right arm and leg.
  • A lesion in the cord is below the crossing, so the signs stay on the same side.

Some diseases damage both neurons, giving upper and lower signs together. Amyotrophic lateral sclerosis is diagnosed clinically from both upper and lower motor neuron signs in a patient with progressive muscle weakness.[3][5]

Three things to keep

  1. Upper vs lowerUpper means weak, spastic, brisk, Babinski, no wasting. Lower means weak, floppy, reduced reflexes, fasciculations, wasting.
  2. Which sideAbove the pyramidal decussation, upper motor neuron signs are on the opposite side; in the cord, the same side.
  3. Both togetherUpper and lower signs together mean both neurons are involved.

Practice question

Original · USMLE style
Your turnQB-MS-S1-NEURO-010-01

A 66-year-old man has had 4 months of progressive weakness. On examination, the muscles of his right hand are thin, with visible fasciculations. His legs are stiff, with brisk knee and ankle reflexes, and both plantar responses are extensor. Sensation is normal.

Which of the following best describes the primary site of this disorder?
Pick one option. Your answers stay on this device.

Common questions

What is the difference between an upper and a lower motor neuron lesion?

A lower motor neuron lesion gives flaccid weakness with low tone, reduced or absent reflexes, fasciculations and wasting. An upper motor neuron lesion gives weakness with spasticity, brisk reflexes and a Babinski sign, without fasciculations or marked wasting.

What is the Babinski sign?

It is the big toe extending, with the other toes fanning, when the sole is stroked. It is normal in infants, but in an adult it points to damage of the corticospinal tract.

On which side do the signs appear in an upper motor neuron lesion?

Above the pyramidal decussation, such as a stroke in the left internal capsule, the signs appear on the opposite side. A lesion in the cord is below the crossing, so the signs stay on the same side.

What is spinal shock?

Right after a sudden cord injury, the limbs below can be flaccid and areflexic. This is called spinal shock, so spasticity may take time to appear.

Why does a lower motor neuron lesion cause wasting but an upper one does not cause marked wasting?

The lower neuron is the one that feeds the muscle. When it is cut, the muscle wastes. In an upper motor neuron lesion the lower neuron still feeds the muscle, so there are no fasciculations and no marked wasting.

Transcript

Read the full narration, by chapter714 words

0:00Same weakness, opposite signs?

Two patients come to clinic with the same complaint: a weak right foot. In the first, the leg is stiff, the knee jerk is brisk, and stroking the sole sends the big toe upward. In the second, the leg is floppy, the ankle jerk is gone, and the calf is thin and twitching. Same weakness, opposite signs. What does that tell us? Today: tell an upper from a lower motor neuron lesion, and use the signs to place the damage.

0:28The chain of two neurons

Voluntary movement needs a chain of two neurons. The upper motor neuron starts in the primary motor cortex of the frontal lobe, and its axon runs down the corticospinal tract. Most of its fibres cross to the opposite side at the pyramidal decussation, at the bottom of the medulla, then descend in the lateral column of the cord. The lower motor neuron has its cell body in the ventral horn of the cord, or in a cranial nerve motor nucleus, and its axon runs in a peripheral nerve to the muscle. So the upper neuron lives inside the central nervous system, and the lower neuron is the one that touches the muscle. The lower neuron keeps muscle tone and runs the reflex arc, and the upper neuron's descending input modifies it. Now break each link in turn.

1:18Cut the lower motor neuron

Cut the lower motor neuron, and the muscle loses its wire. The result is flaccid paralysis: low tone, reflexes reduced or absent, fasciculations and fibrillations, and then wasting of the muscle. The weakness follows the damaged segment or nerve, so it is local. Think of poliovirus in ventral horn cells, or a crushed nerve. That is our second patient.

1:44Cut the upper motor neuron

Now cut the upper motor neuron instead. The lower neuron and its reflex arc are still intact, but have lost descending control. The result is weakness with spasticity, brisk reflexes, and a Babinski sign. Spasticity is raised tone, worse with a fast stretch, that can give way suddenly like a pocket knife closing: the clasp-knife response. The Babinski sign is the big toe extending, with the other toes fanning, when the sole is stroked. It is normal in infants, but in an adult it points to damage of the corticospinal tract. The lower neuron still feeds the muscle, so there are no fasciculations and no marked wasting. That is our first patient.

2:28Place the lesion: capsule, cord, spinal shock

The signs also help you place the lesion. A stroke in the left internal capsule hits fibres that have not yet crossed, so the signs, with spasticity once the acute phase passes, appear in the right arm and leg. A lesion in the cord is below the crossing, so the signs stay on the same side. One caution: right after a sudden cord injury, the limbs below can be flaccid and areflexic, called spinal shock, so spasticity may take time. Some diseases damage both neurons, giving upper and lower signs together.

3:04Your turn: a practice question

Your turn. A 66-year-old man has four months of progressive weakness. The muscles of his right hand are thin, with visible fasciculations. His legs are stiff, with brisk knee and ankle reflexes, and both plantar responses are extensor. Sensation is normal. Which of the following best describes the primary site of this disorder? A, upper motor neurons only. B, lower motor neurons only. C, upper and lower motor neurons. D, the neuromuscular junction itself. E, the skeletal muscle itself. Pause here and decide. A is out: upper motor neuron damage alone causes no fasciculations or marked wasting. B is out: a lower motor neuron lesion lowers reflexes and tone, with no extensor plantars or brisk reflexes. D is out: a junction disorder cannot produce spasticity or Babinski. E is out: muscle disease explains no upper motor neuron signs, and fasciculations are not its feature.

4:18The answer

So the answer is C. Wasting and fasciculations in the hand mean the lower neuron is damaged, and stiff legs with brisk reflexes and extensor plantars mean the upper neuron is damaged too.

4:32Three things to keep, and the next lesson

Three things to keep. One: upper means weak, spastic, brisk, Babinski, no wasting. Lower means weak, floppy, reduced reflexes, fasciculations, wasting. Two: above the pyramidal decussation, signs are on the opposite side; in the cord, the same side. Three: upper and lower signs together mean both neurons are involved. Next, the ascending sensory pathways: dorsal column versus spinothalamic.

Sources

Numbers in the text, e.g. [1], point here
  1. OpenStax Anatomy and Physiology 2e, 14.3 Motor Responses. openstax.org/books/anatomy-and-physiology-2e/pages/14-3-motor-responses
  2. OpenStax Anatomy and Physiology 2e, 16.4 The Sensory and Motor Exams. openstax.org/books/anatomy-and-physiology-2e/pages/16-4-the-sensory-and-motor-exams
  3. Europe PMC PMC8151104 (primary lateral sclerosis, the pure upper motor neuron phenotype). europepmc.org/article/PMC/PMC8151104
  4. Europe PMC PMC5529975 (differentiating lower motor neuron syndromes). europepmc.org/article/PMC/PMC5529975
  5. Europe PMC PMC7540334, Amyotrophic lateral sclerosis: a clinical review, Eur J Neurol 2020. europepmc.org/article/PMC/PMC7540334
  6. Europe PMC PMC8710452, Management of Acute Traumatic Spinal Cord Injury, Front Surg 2021 (spinal shock). europepmc.org/article/PMC/PMC8710452
  7. Europe PMC PMC8071570, Muscle Tone Physiology and Abnormalities, 2021. europepmc.org/article/PMC/PMC8071570
  8. Wikipedia, Lower motor neuron lesion. en.wikipedia.org/wiki/Lower_motor_neuron_lesion
  9. Wikipedia, Upper motor neuron lesion. en.wikipedia.org/wiki/Upper_motor_neuron_lesion
  10. Wikipedia, Brown-Sequard syndrome. en.wikipedia.org/wiki/Brown-S%C3%A9quard_syndrome
  11. Wikipedia, Anterior spinal artery syndrome. en.wikipedia.org/wiki/Anterior_spinal_artery_syndrome

The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.

Image credits. Gray's Anatomy plates 764, 689 and 688 (Henry Vandyke Carter), public domain, via Wikimedia Commons, recoloured and outlined. Illustrations: Servier Medical Art (smart.servier.com), CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/), adapted (recoloured, outlined, labelled): "Foot", "Spinal cord section". Original diagrams: the leg, hammer, muscle, body and reflex sketches, the spinal-shock strip and the cards. No AI-generated teaching images.

Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-NEURO-010.

For exam study only, not medical advice. Read the medical disclaimer.

  1. EP 01Upper vs lower motor neuron lesions: signs and localisation5:08
  2. EP 02Dorsal column vs spinothalamic tract: where each pathway crosses5:01
  3. EP 03Spinal cord syndromes compared: rebuild each from three tracts5:06
  4. EP 04Cranial nerve nuclei: a brainstem map by level and position5:10
  5. EP 05Brainstem crossed findings: the localisation rule4:50
  6. EP 06Medial vs lateral medullary syndrome: artery, structures and signs5:30
  7. EP 07Facial nerve palsy: why the forehead tells you the lesion4:59
  8. EP 08Stroke syndromes by artery: ACA, MCA and PCA4:41
  9. EP 09Lacunar stroke syndromes: pure motor, pure sensory and more4:54
  10. EP 10Visual pathway lesions and field defects4:42
  11. EP 11Basal ganglia direct and indirect pathways: D1, D2 and movement5:19
  12. EP 12Cerebellar lesion localisation: vermis vs hemisphere4:42
  13. EP 13Brain herniation syndromes: what is squeezed, and where4:56
  14. EP 14CSF flow and hydrocephalus: where the flow fails5:12
  15. EP 15Corticospinal tract: from cortex to anterior horn4:59
  16. EP 16Hypothalamic nuclei and their functions5:24