Upper and lower motor neuron

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Upper Motor Neuron (UMN) vs Lower Motor Neuron (LMN)

Overview

The distinction between UMN and LMN lesions is one of the most fundamental concepts in clinical neurology, forming the backbone of motor system localization.

Upper motor neurons project from the cerebral cortex (and brainstem) down to the anterior horn of the spinal cord (or cranial nerve motor nuclei). This pathway is the corticospinal (pyramidal) tract, together with corticobulbar fibers.
Lower motor neurons project from the anterior horn cells of the spinal cord (or cranial nerve motor nuclei) via peripheral nerves to skeletal muscle. They are the "final common pathway."

Anatomy

UMN Pathway

Originates mainly in Brodmann area 4 (primary motor cortex), area 6 (premotor cortex), and supplementary motor cortex, with contributions from parietal cortex
Fibers descend through the corona radiata → internal capsule (posterior limb) → cerebral peduncle → basis pontis → medullary pyramids
~85% decussate at the pyramidal decussation in the medulla, then travel as the lateral corticospinal tract in the contralateral spinal cord
The remaining ~15% travel uncrossed as the anterior corticospinal tract
Somatotopic organization: face (anterior) → arm (central) → leg (posterior) in the internal capsule

LMN Pathway

Alpha motor neurons in the anterior horn of the spinal cord (or motor nuclei of cranial nerves V, VII, IX, X, XI, XII)
Axons exit via ventral roots → spinal nerves → peripheral nerves → neuromuscular junction → skeletal muscle
Each lower motor neuron innervates a group of muscle fibers = a motor unit

Signs: UMN vs LMN Lesions

This is the classic comparison table from multiple textbooks:

Sign	UMN Lesion	LMN Lesion
Weakness	Yes	Yes
Muscle atrophy	Mild (disuse only)	Marked (up to 70% of bulk)
Fasciculations	Absent	Present
Muscle tone	Increased (spasticity)*	Decreased (flaccidity)
Deep tendon reflexes	Hyperreflexia*	Hyporeflexia / areflexia
Plantar response (Babinski)	Extensor (upgoing)*	Flexor (normal) or absent
Clonus	May be present	Absent
Superficial abdominal reflexes	Absent	Present
Distribution of weakness	Groups of muscles, never individual	Individual muscles may be affected
EMG	Normal nerve conduction; no denervation potentials	Abnormal nerve conduction; fibrillations, positive sharp waves, fasciculations

With acute UMN lesions (e.g., spinal shock, acute stroke), reflexes and tone may initially be decreased - the hyperreflexia and spasticity develop over hours to months.

Key Features Explained

Spasticity (UMN)

Spasticity is not caused by damage to the corticospinal tract alone - experimental lesions restricted to the pyramidal tract cause an initial flaccid hemiplegia with considerable recovery. Spasticity arises from damage to descending inhibitory pathways (particularly corticoreticulospinal pathways) that travel alongside the corticospinal tract. Loss of these inhibitory influences increases excitability of anterior horn alpha and gamma motor neurons, causing hyperreflexia and increased tone. - Adams and Victor's Principles of Neurology, 12th Ed.

Babinski Sign (UMN)

In adults: dorsiflexion of the great toe + fanning of the other toes on scratching the lateral sole = positive (pathological)
Indicates a corticospinal tract lesion at any level
Normal in infants with immature corticospinal tracts; its persistence or re-emergence after infancy is always pathological
Physiologically represents a "release" of a spinal flexion/withdrawal reflex from cortical inhibition - Adams and Victor's Principles of Neurology, 12th Ed.

Clonus (UMN)

Rhythmic involuntary contractions at 5-7 Hz in response to sustained stretch stimulus (e.g., ankle clonus)
Requires hyperexcitability of alpha and gamma motor neurons (suprasegmental effect)

Fasciculations (LMN)

Spontaneous, visible muscle twitches caused by spontaneous firing of entire motor units
A benign example: eyelid twitching from fatigue or caffeine
In pathology, indicate denervation or irritation of the anterior horn cell or its axon

Atrophy (LMN)

Profound ("amyotrophic") - muscles lose up to 70% of bulk because they are denervated and lose trophic support from the nerve
In UMN lesions, only mild disuse atrophy occurs since the muscle still receives LMN input

Localization by Level

Level of UMN Lesion	Clinical Pattern
Motor cortex (area 4)	Mainly distal weakness, hypotonia
Premotor cortex (area 6)	Weakness + spasticity
Internal capsule	Pure motor hemiplegia (face + arm + leg equally)
Cerebral peduncle	Contralateral hemiplegia
Midbrain/Pons	Hemiplegia ± cranial nerve signs (crossed syndrome)
Cervical cord	Ipsilateral arm + leg weakness (quadriplegia if bilateral)
Thoracic cord	Paraplegia (legs)

Key rule: A UMN lesion causes contralateral weakness (because the tract has decussated), except when the lesion is below the pyramidal decussation (spinal cord), where weakness is ipsilateral.

Combined UMN + LMN: ALS

Amyotrophic Lateral Sclerosis (ALS) is the prototype disease with BOTH UMN and LMN signs simultaneously:

LMN signs: muscle atrophy, fasciculations, weakness, hyporeflexia in affected segments
UMN signs: spasticity, hyperreflexia, Babinski sign, jaw jerk
The presence of BOTH in the same patient, without sensory involvement, is the hallmark
Involves progressive degeneration of alpha motor neurons; ~40% of familial cases have SOD-1 mutation on chromosome 21
Treatment: riluzole (modestly slows progression); baclofen or tizanidine for spasticity - Ganong's Review of Medical Physiology, 26th Ed.

Facial Nerve (CN VII) - Special Case

The facial nucleus has bilateral cortical input to its upper division (forehead) but predominantly contralateral input to its lower division.

UMN facial palsy (central, above the pons): Lower face weakness only (forehead spared), because the forehead muscles receive bilateral cortical input
LMN facial palsy (CN VII nucleus or nerve itself): Entire ipsilateral face weakness including forehead - Neuroanatomy through Clinical Cases, 3rd Ed.

Quick Memory Mnemonic

UMN = USHH - Upgoing plantar, Spasticity, Hyperreflexia, Hypertonia
LMN = FAAH - Fasciculations, Atrophy, Areflexia/hyporeflexia, Hypotonia/flaccidity

Sources:

Neuroanatomy through Clinical Cases, 3rd Ed. - Section 6.1, Table 6.4
Adams and Victor's Principles of Neurology, 12th Ed. - Chapter 3, Table 3-1
Ganong's Review of Medical Physiology, 26th Ed. - Section on Lower vs Upper Motor Neuron Damage
Harrison's Principles of Internal Medicine, 22nd Ed.

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