What type of neurons are upper motor neuron

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Here is a complete answer drawn from authoritative neuroanatomy textbooks:

Upper Motor Neurons (UMNs) - Neuron Type

Upper motor neurons are multipolar neurons. More specifically, the largest and most distinctive among them are the Betz cells - giant multipolar pyramidal neurons located in layer V of the primary motor cortex (Brodmann area 4).

Key Details

Cell type and location:

UMNs are large projection neurons with their cell bodies in layer V of the primary motor cortex (precentral gyrus, Brodmann area 4), as well as the premotor and supplementary motor cortex (area 6), and in the parietal cortex (areas 3, 1, 2, 5, 7)
The Betz cells (the largest neurons in the human CNS) are the classic UMNs, but they number only ~25,000-35,000, while the medullary pyramid contains ~1 million axons - so most UMN axons arise from non-Betz cortical neurons
Brainstem UMNs (bulbospinal neurons) arise from the red nucleus, vestibular nuclei, reticular formation, and tectum

What "upper motor neuron" actually encompasses: The term UMN is broader than just the corticospinal (pyramidal) tract. It includes all descending motor pathways:

Corticospinal tract (pyramidal) - direct cortex to spinal cord
Corticobulbar tract - cortex to brainstem motor nuclei
Bulbospinal pathways (extrapyramidal): rubrospinal, reticulospinal, vestibulospinal, tectospinal

UMN Signs (vs LMN):

Feature	UMN Lesion	LMN Lesion
Tone	Spasticity (increased)	Flaccidity (decreased)
Reflexes	Hyperreflexia	Hyporeflexia/absent
Plantar response	Babinski sign (extensor)	Flexor (normal)
Wasting/atrophy	Absent	Present
Fasciculations	Absent	Present
Weakness	Present (often proximal)	Present (often distal)

In summary: UMNs are multipolar neurons (specifically large pyramidal/Betz cells in the motor cortex) that originate in the cortex and brainstem and synapse on lower motor neurons or spinal interneurons. They do NOT directly innervate muscle.

Harrison's Principles of Internal Medicine 22E, Fig 26-1 and accompanying text
Adams and Victor's Principles of Neurology, 12th Ed, Chapter 3: "The Upper Motor Neuron"

UMN VS LMN LESION

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Here is a thorough comparison of UMN vs LMN lesions from authoritative sources:

UMN vs LMN Lesion - Complete Comparison

Quick Reference Table

Feature	UMN Lesion	LMN Lesion
Tone	Increased (spasticity)	Decreased (flaccidity)
Reflexes	Hyperreflexia	Hyporeflexia / absent
Plantar response	Extensor (Babinski sign +)	Flexor (normal)
Clonus	Present	Absent
Hoffmann sign	Present	Absent
Weakness pattern	Pyramidal distribution*	Segmental / peripheral nerve distribution
Muscle wasting / atrophy	Absent (or minimal, late)	Prominent, early
Fasciculations	Absent	Present
Fibrillations (on EMG)	Absent	Present
Clasp-knife phenomenon	Present	Absent
Abdominal reflexes	Lost	Normal
Jaw jerk	Brisk (if bilateral lesion above pons)	Reduced/absent
Onset of atrophy	Disuse atrophy only (mild, late)	Rapid denervation atrophy

*Pyramidal distribution = extensors weak in UL, flexors weak in LL (i.e., arm hangs down, leg circumducts)

UMN Lesion - Features in Detail

Spasticity (the hallmark)

Spasticity reflects altered alpha motoneuron firing due to loss of descending inhibitory input. There is excess excitatory neurotransmission (serotonin, norepinephrine, glutamate) and reduced inhibitory (GABA, glycine) activity. Clinically, you feel a sudden "catch" on passive stretch that then releases - the clasp-knife phenomenon.

Pathological Reflexes

Babinski sign: Extension of the great toe + fanning of other toes on stroking the lateral plantar surface. This is the most important UMN sign.
Hoffmann sign: Flicking the nail of the middle finger causes flexion of the thumb and index finger (upper limb equivalent of Babinski)
Clonus: Rhythmic involuntary contractions, especially at the ankle
Loss of abdominal reflexes: Superficial reflexes disappear

Pseudobulbar Palsy (bilateral UMN lesion of corticobulbar tracts)

Dysarthria (spastic type), dysphagia, brisk jaw jerk
Emotional lability (pathological crying/laughing) - distinguishes it from true bulbar palsy
No tongue wasting or fasciculations

Weakness Pattern

Weakness follows a "pyramidal distribution":

Upper limb: Extensors (triceps, wrist/finger extensors) weaker than flexors
Lower limb: Flexors (hip flexors, knee flexors, ankle dorsiflexors) weaker than extensors
This gives the classic hemiplegic posture: flexed arm, extended leg

LMN Lesion - Features in Detail

Flaccidity

Loss of all tonic input to muscle. Tone is reduced or absent.

Muscle Wasting and Fasciculations

Denervation atrophy begins within days-weeks of LMN damage
Fasciculations = spontaneous firing of entire motor units (visible twitching under the skin)
On EMG: fibrillation potentials and positive sharp waves (denervation activity)

Bulbar Palsy (LMN involvement of CN IX, X, XI, XII nuclei)

Dysarthria (flaccid/nasal type), dysphagia, hoarse/nasal voice
Tongue wasting and fasciculations - key distinguishing feature from pseudobulbar palsy
Depressed/absent gag reflex
No emotional lability

Key Distinguishing Scenarios

Scenario	Localizes to
Hemiplegia + Babinski + spasticity	Contralateral cortex or internal capsule (UMN above decussation)
Hemiplegia + flaccidity + fasciculations	Ipsilateral anterior horn / LMN
Tongue wasting + fasciculations + nasal speech	LMN (bulbar palsy)
Brisk jaw jerk + emotional lability + spastic speech	UMN (pseudobulbar palsy)
Hyperreflexia + clonus + extensor plantar	UMN (spinal cord or above)
Areflexia + atrophy + fasciculations	LMN (anterior horn or peripheral nerve)

Important Caveat - Acute UMN Lesions

In the acute phase of a UMN lesion (e.g., acute stroke, spinal cord injury), reflexes may actually be reduced or absent and tone may be flaccid - this is called spinal/cerebral shock. Hyperreflexia and spasticity develop over days to weeks. This is why a fresh hemiplegic patient may initially appear "LMN-like."

Bradley and Daroff's Neurology in Clinical Practice - Box 97.2
Harrison's Principles of Internal Medicine, 22E - Chapter 26
Goldman-Cecil Medicine - Chapter 387
Rosen's Emergency Medicine - Box 93.9

What is fasciculation What is clasp knife phenomenon

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Here are detailed explanations of both phenomena, sourced directly from neurology and physiology textbooks:

1. Fasciculation

Definition

A fasciculation is the spontaneous, involuntary contraction of all the muscle fibers belonging to a single motor unit (or part of a unit). It appears as a brief, visible twitch or dimpling under the skin.

Mechanism

Caused by spontaneous, ectopic firing of a motor axon at a site of irritability - usually at the level of the anterior horn cell or along the motor root/axon
The exact site of origin is debated: originally thought to be the anterior horn cell, but nerve block experiments showed fasciculations persist even after blocking, suggesting distal axonal generation is more common
The fired impulse travels down the entire motor unit and contracts all its muscle fibers simultaneously - this is why it is visible (unlike a fibrillation, which is a single fiber firing and not visible to the naked eye)

On EMG

Fasciculation potential: polyphasic (3-5 phases), duration 5-15 ms, amplitude several millivolts
Combination of fibrillations + fasciculations = active denervation + chronic reinnervation

Clinical Significance

Type	Features	Meaning
Benign fasciculations	Occasional, no weakness, no wasting, consistent location (calves, hands, periocular)	Normal variant - no disease
Pathological fasciculations	Widespread, every examination, associated with weakness and atrophy	Denervating disease - especially anterior horn cell disease (e.g., ALS, SMA, polio)

"Fasciculations that are widespread and seen on every examination may indicate denervating disease, particularly anterior horn cell disease." - Bradley and Daroff's Neurology in Clinical Practice

Key Point

Fasciculations alone (without wasting or weakness) = benign. They become significant only when accompanied by weakness and muscle atrophy.

2. Clasp-Knife Phenomenon

Definition

The clasp-knife phenomenon is a velocity-dependent form of spasticity seen in UMN lesions. On passive stretching of a spastic limb:

There is initial high resistance ("catch")
Followed by a sudden release and give-way as the movement continues

The analogy is a pocket knife: it initially resists closing, then suddenly snaps shut.

Mechanism

The clasp-knife reflex is an exaggerated Golgi Tendon Organ (GTO) reflex (Ib afferents):

When passive stretch continues, tension rises in the muscle
This activates Golgi tendon organs (Ib sensory fibers)
Ib fibers synapse on inhibitory interneurons in the spinal cord
This inhibits alpha motor neurons → sudden muscle relaxation → the limb "gives way"

Physiologically:

Normal GTO reflex = protective mechanism to prevent muscle damage from excessive tension
Clasp-knife = pathological exaggeration of this reflex due to loss of descending UMN inhibitory control

How to Elicit

Ask the patient to relax
Rapidly extend the forearm at elbow (flexors will catch then give way)
OR rapidly flex the knee (extensors catch then give way)
It is velocity-dependent - slow stretching may show little resistance

Clasp-Knife vs Rigidity (important distinction)

Feature	Clasp-Knife (Spasticity)	Rigidity (Parkinsonism)
Velocity dependence	Yes - worse with fast stretch	No - same resistance at any speed
Direction	Directional (flexors in UL, extensors in LL)	Uniform in all directions
Give-way	Yes - sudden release	No give-way (lead-pipe) or ratchety (cogwheel)
Pathway	UMN / corticospinal lesion	Extrapyramidal (basal ganglia)
Reflex change	Hyperreflexia	Normal or slightly reduced reflexes
Babinski	Present	Absent

Summary Diagram

FASCICULATION
  LMN / Anterior Horn Cell Irritation
  ↓
  Spontaneous ectopic firing of motor axon
  ↓
  Entire motor unit contracts
  ↓
  Visible twitch under skin (≠ fibrillation which is microscopic)

CLASP-KNIFE
  UMN Lesion → Loss of descending inhibition
  ↓
  Spastic limb passively stretched rapidly
  ↓
  Initial catch (stretch reflex) → continued tension
  ↓
  GTO (Ib) activated → inhibitory interneuron
  ↓
  Sudden release / give-way

Adams and Victor's Principles of Neurology, 12th Ed - The Abnormal EMG; Spasticity section
Costanzo Physiology, 7th Ed - Golgi Tendon Reflex / Clasp-Knife Reflex
Bradley and Daroff's Neurology in Clinical Practice - Fasciculations and UMN Signs

Dont you think fasciculation must occur in umn lesion and not in lmn lesion

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Actually, the opposite is true - and your intuition has it backwards. Here is the correct reasoning, backed by multiple textbooks:

Why Fasciculations = LMN, NOT UMN

The Logic You Might Be Thinking

You may be reasoning: "In a UMN lesion, the LMN is intact and still firing below the lesion - so shouldn't those LMNs produce fasciculations?"

This is understandable, but incorrect. Here is why:

What Fasciculations Actually Require

A fasciculation requires a motor axon that is irritable or unstable - it fires spontaneously without any voluntary or descending command. This happens when:

The anterior horn cell (LMN cell body) itself is diseased - e.g., ALS, poliomyelitis, spinal muscular atrophy
The motor root or peripheral nerve is irritated - e.g., radiculopathy, entrapment neuropathy, polyneuropathy
The axon terminal is unstable due to ongoing denervation and attempted reinnervation

In all these cases, the LMN itself is damaged or irritated - this is an LMN process.

Why UMN Lesions Do NOT Cause Fasciculations

In a pure UMN lesion (e.g., stroke, internal capsule lesion, spinal cord injury above the anterior horn):

The LMN (anterior horn cell) is completely intact and anatomically normal
Its axon is intact, its neuromuscular junction is intact, its muscle fibers are intact
There is no irritability or instability in the motor axon
Therefore no spontaneous ectopic firing occurs → no fasciculations

The LMN simply receives fewer/altered descending commands, but it is not diseased, damaged, or irritated itself.

"UMN signs: clonus, Babinski sign, brisk tendon reflexes, hypertonia, loss of dexterity. LMN signs: atrophy, weakness, fasciculation."

Goldman-Cecil Medicine

"Fasciculation potentials are most common in diseases of anterior horn cells but also occur in radiculopathies, entrapment neuropathies, and peripheral polyneuropathies."

Bradley and Daroff's Neurology in Clinical Practice

Simple Way to Remember

Question	Answer
Is the motor axon damaged/irritated?	Only in LMN lesions
Does the LMN fire spontaneously/ectopically?	Only when it is diseased (LMN lesion)
In a UMN lesion, is the LMN axon diseased?	NO - it is structurally intact
Therefore, fasciculations occur in...?	LMN lesions only

The Analogy

Think of the LMN as a car engine:

UMN lesion = the driver (UMN) is not controlling the car, but the engine itself is fine - it does not sputter or misfire spontaneously
LMN lesion = the engine itself is faulty - it sputters and misfires on its own (= fasciculations)

One Important Exception - ALS

In Amyotrophic Lateral Sclerosis (ALS), you see both UMN and LMN signs together, including fasciculations. This is because ALS damages BOTH upper and lower motor neurons simultaneously. But the fasciculations in ALS come from the LMN component of the disease, not the UMN component.

Goldman-Cecil Medicine - ALS diagnostic criteria (Awaji-Shima)
Bradley and Daroff's Neurology in Clinical Practice - EMG findings
Adams and Victor's Principles of Neurology, 12th Ed

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