Topic 11: Localizing Lesions (UMN vs LMN, Lateral vs Medial)

Weakness (Paresis/Paralysis)

Follows descending tract patterns and may involve large regions depending on tract damage.

Monoplegia

Weakness affecting one limb.

Paraplegia

Weakness affecting both legs.

Quadriplegia

Weakness affecting all four limbs.

Hemiplegia

Weakness affecting one side of the body.

Spasticity (Hypertonia)

Muscle tone increases, especially in antigravity muscles.

Increased DTR Reflexes

Exaggerated due to removal of inhibitory descending input when UMN are lesioned.

Hypereflexia

Exaggerated deep tendon reflexes resulting from UMN lesions.

Clonus

Rhythmic muscle contractions triggered by a quick stretch.

Babinski Sign (Pathological Reflex)

Dorsiflexion of great toe with fanning of others upon sole stimulation, indicating corticospinal tract damage.

Features of UMN Lesions

1. Large areas of involvement 2. Spastic muscle tone 3. Hyperreflexia/Clonus 4. Pathological Reflexes 5. Mild Disuse Atrophy 6. Absent Fasciculations.

Pathologies associated with UMN

Includes stroke, multiple sclerosis, TBI, ALS, and spinal cord injury.

Spasticity (Increased Muscle Tone / Hypertonicity)

Velocity-dependent resistance to passive ROM due to loss of inhibitory control from UMNs.

Resistance to Passive ROM

Spasticity primarily resists movement in one direction (unidirectional).

Knife-Clasp Phenomenon

Initial high resistance to passive stretch, followed by a sudden release.

Differential: Spasticity vs Rigidity

UMN spasticity is unidirectional and velocity-dependent, while Parkinsonian rigidity is bidirectional and constant.

Hyperreflexia

Increased Deep Tendon Reflexes (DTRs) due to loss of UMN inhibition.

Pathological Reflexes

Return of primitive/infantile reflexes due to loss of UMN inhibition.

Normal Babinski Sign

Stroking lateral sole in infants results in great toe extension and fanning of other toes.

Abnormal Babinski Sign

Indicates UMN lesion in adults.

Clonus (Prolonged Hyperreflexia)

Repetitive, rhythmic muscle contractions triggered by a quick stretch.

Ankle Clonus

Rapid stretch into dorsiflexion results in rhythmic plantarflexion contractions.

Wrist Clonus

Rapid stretch into wrist extension results in repetitive wrist flexion contractions.

What are the locations where LMN lesions can occur?

LMN lesions can occur at the brainstem, spinal cord, or along the axon from its origin to the neuromuscular junction.

Which cranial nerves are involved in LMN lesions?

Cranial nerves III-VII and IX-XII, which have motor components.

What spinal levels are associated with LMN lesions?

Anterior horn cell, anterior root, spinal nerve, plexus, or peripheral nerves.

What is the primary effect of LMN damage on motor function?

It affects motor unit output, resulting in characteristic motor dysfunction localized to specific myotomes or peripheral nerve distributions.

What is the nature of weakness caused by LMN lesions?

Weakness (paresis or paralysis) is localized to muscles innervated by the damaged LMN and is not widespread.

Provide an example of weakness due to C5-6 radiculopathy.

Weakness in the deltoid, biceps, and infraspinatus.

What is the effect of LMN lesions on muscle tone?

Decreased muscle tone (hypotonicity/flaccidity) due to disrupted intrafusal fiber innervation.

How do LMN lesions affect muscle stretch reflexes?

They cause decreased muscle stretch reflexes or DTRs (hyporeflexia or areflexia) due to disruption of the reflex arc.

What is the difference in muscle atrophy between LMN and UMN lesions?

LMN atrophy is more rapid and severe than UMN atrophy due to loss of trophic support to muscle fibers.

What are fasciculations and what causes them?

Visible muscle twitches caused by spontaneous depolarization of unstable, denervated motor units.

What clinical implications do fasciculations have?

They may reflect ongoing denervation and are considered an SOS signal from denervated muscle units.

What happens if the LMN cell body survives after denervation?

The axon may regrow at approximately 1 inch per month, potentially restoring function.

What occurs if the LMN cell body dies?

Collateral reinnervation from nearby surviving LMNs may occur, leading to 'giant' motor unit potentials on EMG.

What is denervation atrophy?

Visible muscle wasting resulting from loss of LMN input.

How do LMN lesions affect the sensitivity of muscle spindles?

Damage to gamma motor neurons disrupts intrafusal fiber innervation, impairing muscle spindle sensitivity.

What is the contrast between LMN and UMN lesions regarding muscle tone?

LMN lesions cause hypotonicity/flaccidity, while UMN lesions cause spasticity (increased tone).

Which common reflexes are affected by LMN lesions?

Commonly tested reflexes such as biceps, triceps, patellar, and Achilles reflexes may be diminished.

What is the significance of fibrillations in LMN lesions?

Fibrillations are spontaneous single-muscle fiber contractions that are not visible on the skin but detectable on needle EMG.

What is the role of collateral reinnervation in LMN lesions?

It may occur from nearby surviving LMNs if the original LMN cell body dies, aiding in recovery.

What is the typical recovery rate for axon regrowth after LMN damage?

Axon regrowth occurs at approximately 1 inch per month.

What is the primary cause of muscle atrophy in LMN lesions?

Loss of trophic support to muscle fibers due to the absence of LMN input.

Lateral Motor System

Controls movement of the extremities/limbs and facilitates fine motor control, especially distal limbs.

Primary tracts of Lateral Motor System

Lateral corticospinal tract and Rubrospinal tract.

Decussation of Lateral Motor System

Fibers cross at the pyramidal decussation in the caudal medulla; spinal cord lesions affect the ipsilateral side, while brain or brainstem lesions affect the contralateral side.

Medial Motor System

Controls axial/trunk musculature and is important for posture, balance, and gait.

Primary tracts of Medial Motor System

Tectospinal tract, Reticulospinal tract, and Vestibulospinal tract.

Decussation of Medial Motor System

Varies by tract: Vestibulospinal is largely ipsilateral, Tectospinal has contralateral decussation in the midbrain, and Reticulospinal has mixed decussation.

Spinal Cord Lesion (Unilateral)

UMN signs appear on the ipsilateral side due to the lateral corticospinal tract having already crossed at the medulla.

Effects of Spinal Cord Lesion

Limb weakness (especially distal muscles) on the same side as the lesion; trunk posture/movement may be more preserved due to bilateral medial system input.

Brain or Brainstem Lesion (Supraspinal)

UMN signs appear on the contralateral side because the descending lateral corticospinal tract has not yet crossed.

Effects of Brain or Brainstem Lesion

Facial and limb weakness often contralateral; may also see cranial nerve involvement, depending on lesion level.

Clinical Takeaway for Lateral System

Fine, distal control; decussates in medulla; ipsilateral spinal lesion effects.

Clinical Takeaway for Medial System

Postural, axial control; often bilateral or uncrossed; more diffuse or bilateral deficits.

Distinguishing UMN vs LMN and Lesion Location

Use pattern of weakness, reflex and tone findings, and lesion side.

Lateral corticospinal tract

A primary tract in the lateral motor system responsible for fine motor control.

Rubrospinal tract

A primary tract in the lateral motor system that influences limb movement.

Tectospinal tract

A primary tract in the medial motor system that coordinates head and eye movements.

Reticulospinal tract

A primary tract in the medial motor system that influences posture and locomotion.

Vestibulospinal tract

A primary tract in the medial motor system that helps maintain balance.

UMN lesion

A lesion affecting upper motor neurons, characterized by signs such as hyperreflexia, spasticity, and positive Babinski sign.

LMN lesion

A lesion affecting lower motor neurons, characterized by signs such as hyporeflexia, flaccid paralysis, and severe muscle atrophy.

Neuromuscular junction (NMJ) disorder

A condition affecting the transmission of signals from motor neurons to muscles, leading to weakness.

Primary muscle disease (myopathy)

A disorder that directly affects muscle fibers, resulting in weakness.

Reflexes in UMN lesion

Hyperreflexia (increased deep tendon reflexes).

Reflexes in LMN lesion

Hyporeflexia or areflexia.

Tone in UMN lesion

Spasticity, increased tone.

Tone in LMN lesion

Flaccid paralysis, decreased tone.

Muscle Atrophy in UMN lesion

Mild atrophy from disuse.

Muscle Atrophy in LMN lesion

Severe atrophy from denervation.

Fasciculations in UMN lesion

Rare.

Fasciculations in LMN lesion

Common.

Babinski Sign in UMN lesion

Positive (toes extend).

Babinski Sign in LMN lesion

Negative.

Clonus in UMN lesion

May be present.

Clonus in LMN lesion

Absent.

UMN Overview

Upper motor neurons are located entirely within the CNS and modulate lower motor neurons.

LMN Overview

Lower motor neurons are the final common pathway to muscles, with cell bodies in the anterior horn or cranial nerve nuclei.

Corticospinal tract

A descending tract that controls limbs and trunk.

Corticobulbar tract

A descending tract that projects to cranial nerve nuclei in the brainstem.

Rubrospinal tract

A tract that arises in the brainstem and modulates motor control.

Reticulospinal tract

A tract that arises in the brainstem and modulates posture and reflexes.

Vestibulospinal tract

A tract that arises in the brainstem and helps maintain balance.

Tectospinal tract

A tract that arises in the brainstem and coordinates head and eye movements.

Localization Tips for UMN lesion

Increased reflexes, spastic tone, and positive Babinski sign suggest UMN lesion.

Localization Tips for LMN lesion

Decreased or absent reflexes, atrophy, and fasciculations suggest LMN lesion.

CN VII (Facial Nerve) involvement in UMN lesion

Contralateral lower facial weakness with upper face spared.

CN VII (Facial Nerve) involvement in LMN lesion

Ipsilateral entire facial weakness.

Key Factors in Lesion Localization

Distribution of weakness, associated findings on exam, and clinical history are considered to identify the source of weakness.

Role of Special Studies

EMG, nerve conduction studies, and imaging may be needed for further localization when physical findings are inconclusive.

Cerebellum

Involved in coordination and balance. Lesions may cause ataxia, intention tremor, and dysmetria (inaccurate range of movement).

Basal Ganglia

Involved in movement initiation and regulation. Lesions may cause bradykinesia (slowness), rigidity, tremor, and involuntary movements (e.g., chorea, athetosis).

Somatosensory System

Supplies proprioceptive feedback necessary for fine movement control. Lesions may cause clumsy or uncoordinated movement (sensory ataxia) and positive Romberg sign (unsteady when eyes are closed).

Lateral Motor System

Controls movement of the extremities/limbs. Facilitates fine motor control, especially distal limbs.

Primary tracts of Lateral Motor System

Lateral corticospinal tract and rubrospinal tract.

Decussation in Lateral Motor System

Fibers cross at the pyramidal decussation in the caudal medulla. Therefore, spinal cord lesions affect the ipsilateral side; brain or brainstem lesions affect the contralateral side.

Medial Motor System

Controls axial/trunk musculature. Important for posture, balance, and gait. Coordinates gross movements of midline muscles.

Primary tracts of Medial Motor System

Tectospinal tract, reticulospinal tract, and vestibulospinal tract.