Upper Motor Neuron vs Lower Motor Neuron: Signs, Lesions, Assessment & Physio Notes

Upper Motor Neuron vs Lower Motor Neuron: Differences, Signs, Lesions & Physio Notes

Understanding the difference between an Upper Motor Neuron (UMN) lesion and a Lower Motor Neuron (LMN) lesion is one of the most frequently tested neuro topics in physiotherapy exams, viva and clinical postings. This post gives you an exam-ready, clinically useful and visually clear comparison with MCQs, mnemonics and a small interactive tool for students and clinicians.

1. Definitions & Basic Concept

• Upper Motor Neuron (UMN): Motor neurons that originate in the cerebral cortex or brainstem and whose axons form the descending tracts (like corticospinal tract) that modulate the activity of lower motor neurons.
• Lower Motor Neuron (LMN): Final common pathway to the muscle. Includes anterior horn cells, motor nerve roots, peripheral nerves, neuromuscular junction and muscle fibers.

In simple language: UMN = “command wires coming from brain & spinal cord” LMN = “final cable from spinal cord to muscle”.

2. UMN vs LMN – High-Yield Comparison Table

Feature	UMN Lesion	LMN Lesion
Common sites	Cortex, internal capsule, brainstem tracts, spinal cord tracts	Anterior horn cell, nerve root, plexus, peripheral nerve, NMJ, muscle
Muscle tone	↑ Increased (spasticity, velocity-dependent)	↓ Decreased (hypotonia / flaccidity)
Tendon reflexes	Hyperreflexia (brisk, exaggerated)	Hyporeflexia or Areflexia (reduced/absent)
Plantar response	Babinski positive (upgoing big toe)	Normal (downgoing) or absent
Muscle bulk	Normal initially; late disuse atrophy	Early, marked neurogenic atrophy
Fasciculations	Absent	Often present (visible twitching of muscle fibers)
Weakness pattern	Patterned (e.g., hemiparesis, paraparesis, pyramidal distribution)	Segmental or peripheral nerve distribution; specific muscles
Clonus	May be present	Absent
Typical causes	Stroke, spinal cord injury, MS, brain tumor	Polio, peripheral neuropathy, radiculopathy, motor neuron disease (LMN component)

3. How to Localize – Clinical Logic

• Spasticity + hyperreflexia + Babinski (+/- clonus) = classic UMN pattern.
• Flaccid weakness + severe early wasting + fasciculations + areflexia = classic LMN pattern.
• Dermatomal or peripheral nerve distribution of weakness/sensory loss = LMN (root/nerve).
• Bilateral UMN signs below a level (e.g., both legs spastic) = spinal cord lesion.

4. Clinical Examination – Step by Step

4.1 Motor Examination

• Bulk: note wasting, asymmetry.
• Tone: move joints slowly then quickly; spastic catch vs floppy limb.
• Power (MMT 0–5): pattern of weakness helps localization.

4.2 Reflexes & Special Signs

• Deep tendon reflexes: biceps, triceps, knee, ankle.
• Superficial reflexes: abdominal, plantar.
• Plantar response: upgoing big toe → UMN.
• Clonus: sustained ankle clonus → UMN.
• Fasciculations: LMN; look especially in tongue, deltoid, quadriceps.

4.3 Sensory & Coordination

• UMN lesion may have accompanying sensory or cerebellar signs (depending on level).
• LMN peripheral neuropathy → “glove and stocking” sensory loss.

5. Important Clinical Scales for UMN/LMN

Tool / Scale	Used For	Relevance
Modified Ashworth Scale (MAS)	Grading spasticity (UMN)	Stroke, SCI, CP – track spasticity changes with treatment.
Modified Tardieu Scale (MTS)	Spasticity assessment with angle of catch	More objective than MAS; distinguishes contracture vs spasticity.
MMT (Manual Muscle Testing)	Muscle strength grading	Both UMN & LMN; check patterns + progression.
EMG & Nerve Conduction Study (NCS)	Electrophysiology	Gold standard for LMN/peripheral nerve lesion characterization.
ASIA Impairment Scale	SCI motor & sensory scoring	UMN lesions below level in spinal cord injury.

6. Pathophysiology – Why Are Signs Different?

UMN lesion: loss of inhibitory control from cortex → spinal motor neurons become hyperexcitable → ↑ stretch reflex → spasticity, hyperreflexia and Babinski. Muscle remains innervated, so atrophy is due to disuse, not denervation.

LMN lesion: direct damage to motor neuron/axon → muscle fibers lose innervation → fibrillation potentials, fasciculations, rapid neurogenic atrophy, areflexia and flaccid paralysis.

7. Visual Summary (Clean & Clear)

🧠 UMN vs LMN — One Look Summary

Feature	UMN Lesion	LMN Lesion
Tone	↑ Increased (Spastic)	↓ Decreased (Flaccid)
Reflexes	Hyperreflexia	Hypo/Areflexia
Plantar Response	Babinski positive	Normal or absent
Atrophy	Late, mild (disuse)	Early, severe (neurogenic)
Fasciculations	Absent	Present
Typical pattern	Hemiplegia, paraplegia, quadriplegia	Root/nerve distribution; localized

Quick Clinical Flowchart

Step 1: Patient presents with weakness.

Step 2 – Check Tone:
• If ↑ increased / spastic → follow UMN path
• If ↓ decreased / flaccid → follow LMN path

UMN path:
• Hyperreflexia
• Babinski positive
• Possible clonus
→ Suggests brain or spinal cord lesion

LMN path:
• Areflexia
• Fasciculations
• Early muscle wasting
→ Suggests anterior horn cell, root or peripheral nerve lesion

8. Mnemonics to Remember UMN & LMN

UMN mnemonic — “SPASTIC”

• S – Spasticity (↑ tone)
• P – Plantar up (Babinski +)
• A – Active reflexes (hyperreflexia)
• S – Slight atrophy (late, disuse)
• T – Tracts (corticospinal affected)
• I – Inhibitory control lost
• C – Clonus may be present

LMN mnemonic — “FLAP”

• F – Fasciculations
• L – Low tone (flaccid)
• A – Atrophy (early, marked)
• P – Peripheral pattern (nerve/root)

9. Differential Diagnosis & Investigations

• Suspected UMN: MRI brain/spine, CT (acute stroke), MS work-up (MRI + CSF), evaluate for tumor/trauma.
• Suspected LMN: EMG/NCS, MRI spine (radiculopathy), blood tests (B12, glucose, thyroid), autoimmune and infectious screening.
• Mixed UMN+LMN signs: think of Motor Neuron Disease (e.g., ALS) and refer urgently to neurology.

10. Physiotherapy Management – Overview

10.1 UMN Lesions (Stroke, SCI, CP, MS)

• Spasticity management: prolonged stretches, weight-bearing, positioning, serial casting, splints.
• Motor control: task-specific training, balance training, constraint-induced movement therapy, treadmill/BWSTT.
• Use MAS/MTS periodically to monitor spasticity.
• Prevent secondary complications: contractures, pressure sores, deconditioning.

10.2 LMN Lesions (Peripheral neuropathy, polio, nerve injuries)

• Maintain ROM and prevent contractures with regular stretching.
• Strengthening of partially innervated muscles; avoid overwork in severely denervated muscles.
• NMES/FES where appropriate in incomplete denervation.
• Orthoses (AFO, wrist splints, KAFO) to support weak muscles and improve function.
• Sensory retraining for peripheral nerve injuries.

Clinical pearl: UMN = treat spasticity + train motor control & function. LMN = protect joints, support with orthoses, and strengthen what’s left.

11. Interactive UMN vs LMN Recognizer Tool

Tick the observed signs for a patient and click Classify to get a quick, teaching-only suggestion (not a diagnosis).

Increased tone / spasticity
Hyperreflexia / brisk tendon reflexes
Positive Babinski (upgoing plantar)
Fasciculations present
Early marked muscle atrophy
Dermatomal / peripheral nerve sensory loss

12. One-Page Student Notes (Revision)

UMN: spasticity, hyperreflexia, Babinski positive, late mild atrophy, no fasciculations, patterned weakness (hemi/para/quadriplegia).
LMN: flaccidity, hyporeflexia/areflexia, early severe atrophy, fasciculations, segmental/peripheral pattern of weakness.
Key tests: MAS/MTS (spasticity), MMT (strength), EMG/NCS (LMN), MRI brain/spine (UMN).
Mnemonics: UMN = SPASTIC, LMN = FLAP.

13. FAQs (Exam & Viva Style)

Q1. Why does an UMN lesion cause Babinski positive?

Because corticospinal (pyramidal) tract inhibition on the spinal reflex arc is lost. The primitive extensor plantar response reappears, seen as upgoing big toe with fanning of other toes.

Q2. Can a patient show both UMN and LMN signs?

Yes. Classic example is Motor Neuron Disease (ALS), which affects both corticospinal tracts (UMN) and anterior horn cells (LMN). Chronic UMN lesions can also have disuse atrophy, which may confuse beginners.

Q3. Which is more painful – UMN or LMN lesions?

Pain is more common with LMN/peripheral lesions (radiculopathy, neuropathy) due to nerve root/nerve inflammation. UMN lesions like stroke may have central pain but not always present.

Q4. How does physio approach differ between UMN and LMN?

UMN: focus on spasticity reduction, motor control and functional training. LMN: protect joints, use orthoses, prevent contractures and strengthen partially innervated muscles without overwork.

14. 10 Practice MCQs (With Answers)

Q1. A positive Babinski sign indicates involvement of:

Answer: A) Upper motor neuron.

Q2. Fasciculations are a hallmark of:

Answer: B) LMN lesion.

Q3. Velocity-dependent increase in tone is called:

Answer: A) Spasticity — typical of UMN.

Q4. Early and severe muscle wasting suggests:

Answer: B) LMN lesion.

Q5. Which of the following is not a typical sign of an UMN lesion?

Answer: C) Fasciculations — LMN sign.

Q6. Clonus is most frequently associated with:

Answer: A) UMN lesion.

Q7. A patient with foot drop and absent ankle jerk most likely has:

Answer: B) Common peroneal nerve lesion — LMN lesion.

Q8. Which investigation is most useful to differentiate peripheral neuropathy from myopathy?

Answer: B) EMG/NCS.

Q9. Mixed UMN + LMN features classically suggest:

Answer: A) ALS.

Q10. Which is the most appropriate early physiotherapy goal in a pure UMN spastic hemiplegic patient?

Answer: A) Prevent contractures & manage spasticity.

15. Small Clinical Cases (For Viva)

• Case 1: 60-year-old with right-sided facial, arm and leg weakness, hyperreflexia and Babinski on right → Left cortical stroke (UMN).
• Case 2: 35-year-old with wasting and fasciculations in one limb, areflexia and normal plantar response → Peripheral LMN lesion (root/nerve/anterior horn cell).
• Case 3: 52-year-old with both hyperreflexia and fasciculations → think Motor Neuron Disease (mixed UMN+LMN).

References

• DeJong, R. N. (2013). The Neurologic Examination. Lippincott Williams & Wilkins.
• Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2013). Principles of Neural Science. McGraw-Hill.
• O’Sullivan, S. B., Schmitz, T. J., & Fulk, G. (2019). Physical Rehabilitation (7th ed.). F.A. Davis.
• Preston, D. C., & Shapiro, B. E. (2012). Electromyography and Neuromuscular Disorders. Elsevier.
• Misulis, K. E., & Head, T. (2019). Essentials of Clinical Neurology. Oxford University Press.