Upper Motor Neuron vs Lower Motor Neuron: The Complete COMLEX Guide
Master neurological localization with (Pre)Meducated's proven approach to understanding UMN and LMN lesions.
If you've ever struggled to differentiate upper motor neuron (UMN) from lower motor neuron (LMN) lesions, you're not alone. This is one of the most frequently tested—and commonly misunderstood—concepts in neurology for COMLEX Level 1 and Level 2.
At (Pre)Meducated, we've helped thousands of DO students master neurological localization through our interactive Office Hours and expert 1-on-1 tutoring. In this comprehensive guide, we'll break down everything you need to know about UMN and LMN lesions using the same systematic approach our tutors use in live sessions.
Table of Contents
Understanding the Anatomy: Where Does One End and the Other Begin?
The key to mastering UMN vs LMN differentiation is understanding exactly where the "dividing line" exists in your nervous system.
The Upper Motor Neuron Pathway
The upper motor neuron is a single, continuous neuron that originates in your motor cortex and travels all the way down through your central nervous system. Here's the journey:
Motor cortex (precentral gyrus)
Internal capsule (where fibers converge)
Brainstem (through the pyramids)
Decussation at the inferior medulla (where most fibers cross)
Spinal cord (lateral corticospinal tract)
Finally synapsing at the anterior horn cell
This entire pathway—from cortex to anterior horn cell—constitutes the upper motor neuron. Any lesion along this path produces UMN signs.
The Lower Motor Neuron Pathway
The lower motor neuron begins at the anterior horn cell and includes:
Anterior horn cell (in the spinal cord)
Nerve root (exiting the spinal cord)
Peripheral nerve
Neuromuscular junction
Muscle
Any lesion from the anterior horn cell onward produces LMN signs.
The Critical Dividing Line
Key Point: The anterior horn cell is where the transition happens. Think of it as the "handoff point" between UMN and LMN systems. A lesion affecting the anterior horn cell itself (like in ALS or polio) produces LMN signs because it's the first neuron in the lower motor pathway.
Pro Tip from (Pre)Meducated Office Hours: Students often get confused about spinal cord lesions. Remember: if you're still IN the spinal cord (above the anterior horn cell), you're dealing with UMN signs. Once you EXIT the spinal cord, you're in LMN territory.
Key Clinical Differences: How to Tell Them Apart
The most important skill for COMLEX is recognizing the pattern of signs that distinguish UMN from LMN lesions. Let's break this down systematically.
Complete Comparison Table
| Feature |
Upper Motor Neuron (UMN) |
Lower Motor Neuron (LMN) |
|---|---|---|
| Muscle Tone |
Increased (spasticity) |
Decreased (flaccidity) |
| Deep Tendon Reflexes |
Hyperreflexia (increased) |
Hyporeflexia or areflexia (decreased/absent) |
| Babinski Sign |
Present (upgoing toe) |
Absent (downgoing toe) |
| Muscle Atrophy |
Minimal (disuse only) |
Significant (denervation atrophy) |
| Fasciculations |
Absent |
Present |
| Distribution |
Larger territories, multiple muscle groups |
Localized to specific nerve/root |
| Clonus |
May be present |
Absent |
Feature Upper Motor Neuron Lower Motor Neuron Muscle Tone Increased (spasticity) Decreased (flaccidity) Deep Tendon Reflexes Hyperreflexia (increased) Hyporeflexia or areflexia (decreased/absent) Babinski Sign Present (upgoing toe) Absent (downgoing toe) Muscle Atrophy Minimal (from disuse only) Significant (denervation atrophy) Fasciculations Absent Present Distribution Often affects multiple muscles/limbs May be localized to specific nerve/root distribution Clonus May be present Absent
Why These Differences Exist
Understanding the why behind these signs helps you remember them:
UMN Lesions (Loss of Inhibition):
The upper motor neuron normally provides both excitatory AND inhibitory signals
When damaged, you lose the inhibitory control over reflexes
Result: reflexes become hyperactive (hyperreflexia, Babinski, increased tone)
LMN Lesions (Loss of Connection):
The lower motor neuron is the final pathway to the muscle
When damaged, muscles lose all innervation
Result: muscles become weak and atrophic with absent reflexes
The Babinski Sign: Your Most Reliable UMN Indicator
The Babinski sign deserves special attention because it's one of the most specific indicators of UMN pathology and appears frequently on COMLEX.
What Is the Babinski Sign?
Technique: Run a pointed object (reflex hammer handle) along the lateral sole of the foot from heel to toes.
Normal response (negative Babinski):
Toes curl downward (plantar flexion)
This is the normal response in adults
Abnormal response (positive Babinski):
Big toe extends upward (dorsiflexion)
Other toes may fan outward
Indicates UMN lesion
Clinical Pearl
The Babinski sign is testing the corticospinal tract integrity. A positive Babinski means there's damage somewhere along the UMN pathway—from motor cortex down to the spinal cord. It does NOT tell you exactly where the lesion is, just that there IS an UMN lesion.
Important Exception: Infants normally have a positive Babinski (upgoing toe) until the corticospinal tract fully myelinates around 12-24 months of age. This is not pathological in babies!
COMLEX Application
When you see a vignette describing "upgoing toe on plantar stimulation" or "extensor plantar response," immediately think: This is an UMN lesion. Then work to localize WHERE in the UMN pathway.
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Deep Tendon Reflexes: The Pattern Tells the Story
Deep tendon reflexes (DTRs) are graded on a scale, and understanding this scale is crucial for COMLEX:
DTR Grading Scale
0 = Absent (no reflex)
1+ = Trace (decreased)
2+ = Normal
3+ = Brisk (increased)
4+ = Hyperactive with clonus
Reflex Patterns by Level
Reflex Nerve Root How to Test Biceps C5-C6 Tap biceps tendon with elbow flexed Brachioradialis C5-C6 Tap brachioradialis with forearm semi-pronated Triceps C7-C8 Tap triceps tendon with elbow flexed Patellar (knee) L3-L4 Tap patellar tendon with knee flexed Achilles (ankle) S1-S2 Tap Achilles tendon with foot dorsiflexed
Clinical Interpretation
Hyperreflexia (3+ or 4+) = UMN lesion
Loss of descending inhibition
Reflexes become exaggerated
May have clonus (rhythmic oscillations)
Hyporeflexia or Areflexia (0 or 1+) = LMN lesion
Reflex arc is interrupted
No response or minimal response
Common in peripheral neuropathy, nerve root compression, anterior horn cell disease
Case Example from (Pre)Meducated Office Hours
Patient presents with:
Weakness in lower extremities (3/5 strength)
DTRs: Absent at knees and ankles
DTRs: Diminished in biceps and triceps
Sensation intact
Progressive symptoms over 5 days
Recent diarrheal illness
Question: Is this UMN or LMN pathology?
Answer: LMN pathology! The absent and diminished reflexes are the key finding. This pattern is classic for Guillain-Barré syndrome (GBS), which affects peripheral nerves (LMN). The ascending pattern from legs to arms is another clue.
Notice how systematic pattern recognition helps you localize quickly? This is exactly what we teach in (Pre)Meducated Office Hours.
Common Disease Examples: Connecting Pathophysiology to Clinical Presentation
Understanding which diseases cause UMN vs LMN signs helps you prepare for both COMLEX and clinical practice.
Classic UMN Diseases
1. Stroke (Cerebrovascular Accident)
Location: Cortex, internal capsule, brainstem, or spinal cord
Presentation: Acute onset weakness with hyperreflexia and positive Babinski
Key Feature: Contralateral to lesion (for cortical/subcortical strokes)
Example: Middle cerebral artery (MCA) stroke causing right-sided weakness
Right arm and leg weakness
Hyperreflexia on right side
Positive Babinski on right
If left MCA: also expect aphasia (cortical sign!)
2. Multiple Sclerosis (MS)
Location: Central demyelination (brain and spinal cord)
Presentation: Relapsing-remitting neurological symptoms with UMN signs
Key Feature: Lesions separated in space and time
3. Spinal Cord Compression
Location: Spinal cord (above anterior horn cells)
Presentation: Below the level of compression, you see UMN signs
Example: Thoracic cord compression from metastases
Bilateral lower extremity weakness
Hyperreflexia in legs
Bilateral positive Babinski
Sensory level (e.g., decreased sensation below T4)
Classic LMN Diseases
1. Guillain-Barré Syndrome (GBS)
Location: Peripheral nerves (demyelination)
Presentation: Ascending weakness with areflexia
Key Features:
Recent infection (Campylobacter is classic)
Symmetric weakness starting in legs
Absent or severely diminished reflexes
Albumino-cytologic dissociation on lumbar puncture (elevated protein, normal cell count)
2. Radiculopathy (Nerve Root Compression)
Location: Nerve root exiting spinal cord
Presentation: Dermatomal pain/weakness with decreased reflex at affected level
Example: L5 radiculopathy from herniated disc
Weakness in ankle dorsiflexion (foot drop)
Decreased sensation in L5 distribution
Normal or decreased ankle reflex
3. Peripheral Neuropathy
Location: Peripheral nerves
Presentation: Distal weakness and sensory loss ("stocking-glove" pattern)
Common Causes: Diabetes, alcohol, B12 deficiency, chemotherapy
Key Feature: Typically affects longest nerves first (feet before hands)
The Exception: ALS (Amyotrophic Lateral Sclerosis)
ALS is unique because it affects BOTH upper and lower motor neurons simultaneously.
Why both?
Affects anterior horn cells (LMN) → fasciculations, atrophy, weakness
Also affects lateral corticospinal tract (UMN) → hyperreflexia, positive Babinski
Classic presentation:
Muscle weakness and atrophy (LMN)
WITH hyperreflexia and Babinski (UMN)
This combination is the hallmark of ALS
From (Pre)Meducated Office Hours: "When you see fasciculations WITH hyperreflexia, think ALS. That mixed picture is pathognomonic."
COMLEX Study Strategy: Systematic Approach to Any Localization Question
At (Pre)Meducated, we teach a systematic framework that works for every neurological localization question. Here's the approach:
Step 1: Identify the Signs and Symptoms
List out everything the vignette tells you:
Motor findings (weakness, tone)
Reflex findings (hyper/hypo/absent)
Sensory findings
Special signs (Babinski, fasciculations, atrophy)
Associated symptoms (bowel/bladder, pain pattern)
Step 2: Determine UMN vs LMN
Use the comparison table above. Ask yourself:
Are reflexes increased or decreased?
Is there a Babinski sign?
Is tone increased (spastic) or decreased (flaccid)?
Are there fasciculations?
Step 3: Localize the Level
If UMN:
Cortex? (Look for cortical signs: aphasia, neglect, visual field defects)
Subcortical — like the internal capsule or thalamus? (Pure motor or sensory without cortical signs)
Brainstem? (Cranial nerve involvement + crossed signs)
Spinal cord? (Sensory level, bilateral symptoms)
If LMN:
Anterior horn cell? (Fasciculations prominent)
Nerve root? (Dermatomal pattern)
Peripheral nerve? (Specific nerve distribution)
Neuromuscular junction? (Fatigability)
Muscle? (Proximal weakness, normal reflexes initially)
Step 4: Consider the Time Course
Acute (seconds to hours): Think vascular (stroke)
Subacute (days to weeks): Think inflammatory (GBS, transverse myelitis)
Chronic (months to years): Think degenerative (ALS, MS) or compressive
Episodic: Think MS, myasthenia gravis
Step 5: Confirm with Associated Features
Look for clues that point to specific diagnoses:
Recent infection → GBS
Visual symptoms → MS
Back pain → Spinal cord compression
Dysphagia + weakness → Myasthenia gravis or brainstem lesion
Practice Application
Let's use this framework on a sample question:
Vignette: A 65-year-old man presents with 3 months of progressive weakness in his right leg. He has difficulty climbing stairs. On examination, you find 3/5 strength in right hip flexion and knee extension, 4+/4 reflexes in the right patellar and Achilles tendons, positive Babinski on the right, and decreased pain/temperature sensation on the left leg below L1.
Step 1 - Identify signs:
Right leg weakness (UMN pattern - pyramidal weakness)
Hyperreflexia right leg
Positive Babinski right
Contralateral sensory loss (left side)
Step 2 - UMN or LMN?
Hyperreflexia + Babinski = UMN lesion
Step 3 - Localize:
Crossed signs (motor right, sensory left) = Spinal cord lesion
Why crossed? Motor tracts have already decussated (crossed) at the medulla, but spinothalamic (pain/temp) decussates one or two levels above where it enters the spinal cord
Location: Likely right hemicord lesion around L2-L3
Step 4 - Time course:
Progressive over 3 months = chronic, likely compressive or neoplastic
Step 5 - Confirm:
Brown-Séquard syndrome (hemicord lesion)
Need MRI to rule out tumor, abscess, or demyelination
This systematic approach is what separates students who struggle with neurology from those who excel. It's the same methodology taught in every (Pre)Meducated Office Hours session.
Practice Questions
Test your understanding with these COMLEX-style questions:
Question 1
A 28-year-old woman presents with sudden onset left arm and leg weakness that began 4 hours ago. Examination shows 3/5 strength in the left upper and lower extremities, 3+ reflexes throughout the left side, and an upgoing toe on the left plantar reflex. The right side is normal. Which of the following best describes this presentation?
A) Lower motor neuron lesion affecting left cortical spinal tract
B) Upper motor neuron lesion affecting right internal capsule
C) Lower motor neuron lesion affecting multiple nerve roots
D) Upper motor neuron lesion affecting left motor cortex
——- Don’t scroll down until you’re ready to see the answer——-
Answer: B - Upper motor neuron lesion affecting right internal capsule
Explanation: The hyperreflexia and positive Babinski indicate an UMN lesion. The left-sided weakness means the lesion is on the RIGHT side of the brain (motor pathways cross at the medulla). The internal capsule is the most likely location because there are no cortical signs mentioned (like aphasia or neglect). This would be a pure motor stroke from the lenticulostriate arteries.
Question 2
A 45-year-old man presents with 5 days of progressive weakness that started in his feet and is now affecting his hands. He had a diarrheal illness 2 weeks ago. Examination shows 3/5 strength in bilateral lower extremities and 4/5 in upper extremities. Deep tendon reflexes are absent at the ankles and knees, and diminished at the biceps and triceps. Plantar reflexes are downgoing bilaterally. What is the most likely diagnosis?
A) Multiple sclerosis
B) Amyotrophic lateral sclerosis
C) Guillain-Barré syndrome
D) Myasthenia gravis
——- Don’t scroll down until you’re ready to see the answer——-
Answer: C - Guillain-Barré syndrome
Explanation: The absent reflexes and downgoing toes indicate LMN pathology. The ascending pattern of weakness after a recent infection is classic for GBS, which is a peripheral nerve demyelinating disease. MS and ALS would show UMN signs (hyperreflexia, positive Babinski). Myasthenia gravis presents with fatigable weakness and typically affects ocular and bulbar muscles first.
Question 3
A 70-year-old man with a history of smoking presents with back pain and bilateral lower extremity weakness for 2 weeks. He has difficulty urinating. Examination shows 3/5 strength bilaterally in the legs, 4+ reflexes at the knees and ankles, bilateral Babinski signs, and decreased sensation below the T6 level. X-ray shows lytic lesions in the thoracic vertebrae. What is the most appropriate next step?
A) Start physical therapy
B) Administer IV dexamethasone
C) Order EMG/NCS
D) Start dual antiplatelet therapy
——- Don’t scroll down until you’re ready to see the answer——-
Answer: B - Administer IV dexamethasone
Explanation: This patient has spinal cord compression from metastatic disease (likely lung cancer given smoking history). The UMN signs (hyperreflexia, bilateral Babinski) with a sensory level confirm cord compression. This is a neurological emergency. IV steroids (dexamethasone) should be given immediately to reduce cord edema while arranging urgent MRI and consultation with neurosurgery/radiation oncology. EMG/NCS tests peripheral nerves (LMN), which isn't indicated here.
Ready to Master Neurology for COMLEX?
Understanding UMN vs LMN is just the beginning. At (Pre)Meducated, we help DO students master all the high-yield neurology topics through:
✅ Interactive Office Hours with expert tutors
✅ Systematic frameworks for every localization question
✅ COMLEX-specific strategies from tutors who've taken the exam
✅ Real case-based learning like the examples in this guide
✅ Community support from fellow DO students
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Key Takeaways
🎯 Upper Motor Neuron Lesions:
Hyperreflexia, positive Babinski, increased tone
Lesion anywhere from motor cortex to spinal cord (before exiting)
Examples: Stroke, MS, spinal cord compression
🎯 Lower Motor Neuron Lesions:
Hyporeflexia/areflexia, absent Babinski, decreased tone, fasciculations
Lesion from anterior horn cell through peripheral nerve
Examples: GBS, radiculopathy, peripheral neuropathy
🎯 The Critical Dividing Line:
Anterior horn cell is where UMN ends and LMN begins
Inside the spinal cord = UMN
Outside the spinal cord = LMN
🎯 COMLEX Strategy:
Use systematic approach: Signs → UMN/LMN → Localize → Time course → Confirm
Practice pattern recognition with multiple cases
Understand the WHY behind clinical signs
Additional Resources
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This guide was created by (Pre)Meducated, a DO-founded COMLEX tutoring platform built for osteopathic medical students. Our mission is to help every osteopathic medical student achieve their best possible board scores through expert tutoring, proven strategies, and community support.
References:
Blumenfeld H. Neuroanatomy through Clinical Cases. 2nd ed. Sunderland, MA: Sinauer Associates; 2010.
Ropper AH, Samuels MA, Klein JP. Adams and Victor's Principles of Neurology. 10th ed. New York, NY: McGraw-Hill; 2014.
Patten J. Neurological Differential Diagnosis. 2nd ed. London: Springer-Verlag; 1996.
(Pre)Meducated Office Hours Session: Neurology Review with Dr. David, December 2024.
Last updated: December 2025