Clinical Disorders of the Motor System

Disorders of the motor system can manifest themselves by changes in any one or a combination of what

Muscle strength and bulk
Muscle contraction
Muscle tone
Reflexes
Movement efficiency and speed
Postural control

Changes in muscle strength and bulk

Paralysis
Paresis/plegia
Atrophy

Paralysis

Complete loss of voluntary muscle contraction

Paresis/plegia

Partial loss
Hemiplegia(paresis), paraplegia, tetraplegia

Atrophy

Disuse vs. neurogenic

Assessment of muscle strength and bulk

MMT/dynamometry
Tape measure

Involuntary muscle contractions

Muscle spasms and cramps
Fasciculations
Fibrillations
Hyperkinetic disorders

Muscle spasms

Sudden involuntary contractions of muscles

Cramps

Severe painful muscle spasms

Fasciculations

Quick twitches of muscle fibers of single motor unit
Visible on surface but no joint movement

Fibrillations

Brief contraction of single motor fiber, not visible
Always abnormal, can be caused by upper or lower motor neuron problems

Hyperkinetic disorders

Generally associated with basal ganglia disorders
Tremor, athetosis, chorea, ballismus

Muscle tone

Hypotonia
Hypertonia
Damage almost anywhere in the motor system can alter muscle tone
UMN lesion, initial CNS shock
Decerebrate rigidity: UE/LE extension (severe midbrain lesion)
Decorticate rigidity: UE flexion and LE extension (severe lesions above midbrain)

Hypotonia

Abnormally low resistance to passive stretch
Flaccidity (no tone)

Hypertonia

Abnormally high resistance to passive stretch
Spastic (velocity dependent) and rigid (velocity independent) forms
Clonus

What tracts are bias towards extension

Pontine (medial) reticulospinal
Lateral vestibulospinal

What tracts are bias towards flexion

Medullary (lateral) reticulospinal (inhibits extensors) too much extension without cortical influence
Rubrospinal (facilitates upper extremity flexors) too much UE flexion without cortical influence

How do you assess muscle tone

Passive ROM
Modified Ashworth Scale
Tardieu Scale (V1, V2, V3)

Reflexes: cutaneous

Babinski
Flexor withdrawal
Abdominal
Glabellar

Reflexes: Deep Tendon Reflexes (DTR)

Bicep
Brachioradialis
Triceps
Knee
Ankle

Movement efficiency and speed (coordination): observation

Finger to nose
Rapid alternating movement
Heel-to-shin

Postural control: observation

Rhomberg
Tinetti
Berg Balance Scale
Biodex Balance Master
Gait (heel toe, on toes, on heels)

Disorders of motor system divided into 4 broad categories

Lower motor neuron
upper motor neuron (pyramidal)
Basal ganglia (extrapyramidal)
Cerebellar (extrapyramidal)

Clinical manifestations of LMN disorders: muscle strength and bulk

Decreased
Flaccid paralysis

Clinical manifestations of LMN disorders: muscle contraction

Fibrillations

Clinical manifestations of LMN disorders: muscle tone

Decreased

Clinical manifestations of LMN disorders: reflexes

Absent

Clinical manifestations of LMN disorders: movement efficiency and speed

Impaired

Clinical manifestations of LMN disorders: postural control

Impaired due to strength and sensation deficits of LE’s

Examples of lower motor neuron disorders

Guillain-Barre Syndrome
Poliomyelitis
Radiculopathy
Peripheral neuropathy
Neuropathy gait

Clinical manifestations of UMN disorders: muscle strength

Decreased but not as severe as LMN, paresis

Clinical manifestations of UMN disorders: muscle contraction

Fibrillations
Spasms
Cramps

Clinical manifestations of UMN disorders: muscle tone

Increased tone and spasticity
Clonus
SCI: decreased tone but with spasticity

Clinical manifestations of UMN disorders: reflexes

Increased
Abnormal cutaneous and primitive

Clinical manifestations of UMN disorders: movement efficiency and speed

Impaired, abnormal timing of muscle activation loss of fractionation

Clinical manifestations of UMN disorders: postural control

Impaired depending on lesion

Abnormal cutaneous reflexes

Babinski sign
Muscle spasm/flexor withdrawal reflex to innocuous stimuli

Abnormal timing of muscle activation

Initiation of movement
Rate of force development
Muscle contraction time prolonged
Activation of agonist/antagonist

Co-contraction

Temporal overlap of agonist and antagonist muscle contraction
Normal under certain circumstances

Contracture

Adaptive shortening of muscle
Loss of sarcomeres
Increased cross linking between fibers
A component of myoplastic hyperstiffness

Myoplastic hyperstiffness

Excessive resistance to muscle stretch due to structural changes within the muscle due to changes in neuromuscular activity
Contracture and increased weak actin-myosin bonding
Selective atrophy of type II muscle fibers
Common in stroke

Muscle overactivity

Muscle contraction that is excessive for the task

What causes muscle overactivity

Excessive neural input to the muscle(s)
May be due to lack of skill in performing the task, anxiety, or pain

Muscle tone

Amount of tension in resting muscle
Hyper/hypotonia
UMN (spastic hypertonia) vs. basal ganglia (rigid hypertonia)

How is muscle tone examined

Passively
Not velocity dependent

Paresis

Partial loss of strength and movement
Occasionally paralysis (complete SCI)

Spasticity/Hyperrelexia

“Velocity dependent” resistance to passive muscle strength

Clonus

Repeated stretch included contractions due to spasticity

Examples of UMN disorders

Spinal cord injury
Stroke
Multiple sclerosis
Spastic cerebral palsy
Traumatic brain injury