Spinal Motor Tracts and

Motor Neurons
Dr Sikes
OT 532
Division of Occupational Therapy
Shenandoah University
Objectives
• Understand top-down control of voluntary movement
• Describe and recall definitions of upper motor neurons (UMN) and
lower motor neurons (LMN), as well as functional importance of both
• Describe function of alpha (αMNs) and gamma motor neurons (γMNs)
• List and describe the motor tracts of the spinal cord
• Identify and recall the movements associated with myotome
distributions from C5 – T1
• Define paresis, paralysis, hypotonia, flaccidity, spasticity, hypertonia,
and rigidity
 Top-down motor control
• Neural activity begins with a decision
made in the frontal lobe
• Next, motor planning areas are activated
along with control circuits in the
cerebellum and basal ganglia
• Then, motor tract activity is initiated and
sends information to
• Spinal interneurons and
• Motor neurons
• Then, the command makes it to the
skeletal muscle and elicits contraction
 Motor tracts from the cortex
• Lateral corticospinal tract (holds
90% of the tract)**
• Voluntary motor control &
fractionation on contralateral side
• Decussates at the medulla
• Most important pathway for
controlling voluntary movement
• Anterior corticospinal tract
• Voluntary motor control on ipsilateral
side
• Only about 10% of the motor
information travels along this path
 Motor tracts from the cortex: Lesions
• Lesions along corticospinal pathway
• In the primary motor area
• Contralateral loss of voluntary movement
• Hyperactive reflexes
• UMN damage -> spasticity of distal musculature below lesion level
• Internal capsule lesion
• Contralateral spastic paralysis
• Hyperactive reflexes
• Unilateral lesion in brainstem above decussation
• Contralateral spastic paralysis
• Unilateral lesion in spinal cord below decussation
• Ipsilateral loss of voluntary control
• Spasticity in distal musculature below lesion level
• Flaccidity at lesion level
• Hyperactive reflexes
• Complete severance
• Bilateral loss of voluntary control
• Spasticity below and flaccidity at lesion level
Corticospinal tract specifics
• Damage to the corticospinal tracts results in decorticate rigidity
• Upper extremities are in a spastic flexed position
• Lower extremities are in a spastic extended position
• This happens because there is no information from the cortex actually making it
do the periphery in order to control the tone
• More accurate to call it rigidity, and is characterized by higher tone on one side
of the joint
Motor tracts from the Midbrain
• Rubrospinal
• Small and makes minor contribution to UE distal extensor motor control
Motor Tracts for Posture
• Reticulospinal
• Bilateral postural muscles
• Medial and lateral vestibulospinal
• Medial: neck control
• Lateral: postural muscles
• Medial corticospinal
• Neck, shoulder, and trunk muscles
“Nonspecific” motor tracts
• Ceruleospinal & Raphespinal
• Both of these tracts are
activated during intense
emotions
• Motor effects of both tracts
are general, are not related to
specific movements
• May contribute to poorer
motor performance when
anxiety is high
 Main Ones for You
• Lateral corticospinal
• Voluntary motor control & fractionation on contralateral side
• Most important pathway for controlling voluntary movement
• Dorsal column
• Motor function: proprioception from here is helpful
• Comes from contralateral side
• Lateral spinothalamic
• Pain and temperature can create a reflexive motor action
• Comes from contralateral side
• Spinocerebellar
• Proprioception (unconscious) from LE
• Vestibulospinal
• Facilitates extensor tone
• Really important to assess this one after neurologic injury
 Motor tract syndromes
• Chronic MT syndromes experience contractures and weakness
due to structural changes of the muscle itself (weak actin-myosin
bonds)
• Adult-onset MT syndromes, paresis or paralysis is primary cause
of impaired motor function
• Cerebral MT syndrome, reticulospinal tract is overactive and that
is primary cause of impaired motor function
• In SCI, muscle stretch hyperreflexia contributes largely to motor
dysfunction
• Spastic CP, brainstem MT overactivity, abnormal co-contractions,
and abnormal muscle development interfere with motor function
• Abnormal co-contraction only occurs in developmental spasticity
Upper motor neurons (UMN)
• Upper MNs are located in the pre-
motor and primary motor regions
• Typical clinical symptoms of
impairment with upper MNs:
• Uncontrolled movement(s)
• Decreased sensitivity to reflex
stimulation
• Flaccidity at the level of lesion
• Loss of muscle tone
• Spasticity below lesion level
• Increase in muscle tone with associated
inability to voluntarily control muscle
Lower motor neurons (LMN)
• Lower MNs are located in nuclei of the
brainstem and in ventral horn
• Located in CNS like the UMNs, but they have axonal
extension + connections outside the CNS
• Lower MNs get information from upper MNs, sensory
neurons and interneurons
• Typical clinical symptoms of impairment with
lower MNs:
• Paralysis
• Flaccidity
• Hyporeflexia
• Muscle atrophy with resultant fibrillations and
fasciculations*
Compare/contracts UMN and LMN
Upper MN Lower MN

Location Cortex of brain Brainstem and Spinal Cord

Neurotransmitter Glutamate ACh

Targets Inside CNS (ex: tracts) Outside CNS (ex: muscles)

Clinical sign of damage Spasticity below lesion Paralysis

Flaccidity at lesion Flaccidity at and below lesion
 Types of lower MNs
• Branchial (i)
• Located in the brainstem
• Pair up with sensory neurons to form cranial nerves/nuclei
• Innervate muscles of face and neck (CN VII, V, IX, X, XI)
• Visceral (ii)
• Part of the ANS
• Control smooth muscle (heart and arteries) and glands
• Somatic (iii)
• Located in brainstem and spinal cord
• Innervate skeletal muscles for muscles
• Split into 3 groups: alpha, beta, and gamma MNs according to the muscle fiber type they
innervate
• ”Motor Unit” is the single lower MN and all of the muscle fibers it innervates
alpha (αMNs)& gamma motor neurons (γMNs)
• Alpha (αMNs)
• Large and myelinated
• Connect to extrafusal skeletal
muscle and branches to activate
multiple terminals
• Can usually release enough ACh
that every muscle fiber innervated
contracts on activation
• Gamma (γMNs)
• Medium and myelinated
• Connect to the intrafusal fibers
within the muscle spindle
alpha (αMNs)& gamma motor neurons (γMNs)
• αMNs & γMNs work together (“Coactivation”)
• The dual relationship allows the muscle spindle to
maintain the stretch sensitivity while the
extrafusal muscle fibers are contracted
• Keeps inside portion ‘taught’ so you recognize the
stretch
• This coactivation is required for you to recognize the
muscle activity and change in muscle status
• Knee jerk reflex example
Knee Jerk Reflex (“phasic stretch reflex”)
 Cutaneous Reflex: Withdrawal Reflex
• Cutaneous stimulation can also
elicit reflexive movements
• Circuitry responsible for the
withdrawal reflex is also located
within the spinal cord

• Abnormal cutaneous reflex would

be a + Babinski sign
• Indicates corticospinal tract
damage in people >6 months
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Most Common Abnormal Reflexes
• After SCI or some MT lesions, we often see:
• Phasic stretch hyperreflexia
• Excessive response to phasic stretch (Ex: Knee jerk reflex)
• Clonus
• Involuntary, repeating, rhythmic, reflexive contractions of a single muscle group
• Occurs in SCI after placing foot on wheelchair frequently, but occurs in neurotypical
people as well (‘unsustained’ clonus)
• Clasp-knife response
• Paretic muscle is being slowly and passively stretched, but suddenly drops all resistance.
Occurs in paretic muscles, especially biceps brachii.
Motor Neuron vs. Motor Tract Lesion
Motor neuron lesion
Structures CN or SC motor neurons
Pathologies Guillain Barre, peripheral nerve injury,
neuropathy, polio, radiculopathy
Motor tract lesion
Tracts in the brain, brainstem, or SC
CP, SCI, TBI, MS, certain kinds of CVA

Voluntary Weak or absent Impaired or absent; some may present with abnormal
movement muscle synergies
Strength Ipsilaeral paresis or paralysis; follows Paresis or paralysis below level of lesion
peripheral nerve or myotome
distribution

Muscle bulk Neurogenic atrophy: rapid, severe Disuse atrophy: not as severe as neurogenic atrophy.
wasting in a peripheral nerve or Occurs in the same distribution as hemiplegia, paraplegia,
myotome distribution or tetraplegia

Reflexes Decreased or absent Increased with hyperreflexia. + Babinski skin, muscle

stretch hyperreflexia, clonus, exaggerated cutaneous and
autonomic reflexes
Muscle tone Decreased (hypotonia) or absent Increased: velocity dependent hypertonia (spasticity)
(flaccidity)
Myotomes
• “Myotomes” is the term we use to
describe the distribution of the
group of muscles innervated by a
single spinal nerve
• Useful in determining expected
level of function following a SCI
• Usually, there is a period of “spinal
shock” after a SCI in which the client
has limited control and true impact of
SCI is unknown
Myotome charts can be
annoying
• C1/2: neck flexion/extension
• C3: neck lateral flexion
• C4: Shoulder elevation
• C5: Shoulder abduction + Biceps and Deltoid (a little)
• Flex elbow
• C6: Biceps, Deltoids and Extensor Carpi
• Extend wrist and stronger elbow flexion
• C7: Triceps, wrist flexors and finger extensors
• Extend elbow, flex wrist, extend fingers
• C8: Palmar interossei
• Finger flexion and finger adduction
• T1: Dorsal interossei
• Finger abduction
Involuntary Muscle Contractions
• Muscle cramps
• Severe, painful muscle contractions lasting seconds to minutes.
• Fasciculations
• Quick twitches of all muscle fibers in a single motor unit
• Myoclonus
• A brief, involuntary contraction of a muscle or group of muscles
• Fibrillations
• Random, spontaneous, brief contractions of single muscle fibers not visible on
the surface of skin
• Tremors
Copyright © 2018 by Elsevier, Inc. All rights reserved. 24
Tremors
• Involuntary, rhythmic movements of a body part
• Physiologic tremors can be enhanced by anxiety,
stress, fatigue, medications, metabolic disorders,
caffeine, or alcohol withdrawal.
• Action tremors:
• Postural: maintained against gravity
• Orthostatic: only when standing in trunk/LB
• Intention: voluntary movement and more severe as
target is approached
• Resting tremors are most active while person is
at rest and not actively moving

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Tremors (Cont.)
• In Parkinson’s disease, tremor is typically a
resting tremor affecting mainly hands and
lower limb
• Cerebellar tremors are usually intention
tremors
• Cerebellar tremors are most severe during the
final part of the movement to press an elevator
button

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Muscle Tone: Resistance to Passive Stretch
• Muscle tone is the resistance to
stretch in a resting muscle
• Clinically, passive range of motion is
used to assess muscle tone
• When muscle tone is normal,
resistance to passive stretch is
minimal
• Normal resting muscle tone is
provided by titin and weak actin-
myosin bonds
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Muscle tone
Muscle Tone Terms & Conditions
• Terminology:
• Hypertonia -> Rigidity: velocity-independent increase in resistance to stretch
• Occurs in: BG disorders and lesions in midbrain/above midbrain
• Hypertonia -> Spasticity: velocity-dependent increase in resistance to stretch
• Chronic motor tract lesions like SCI, spastic CP, TBI, CVA, ALS, and MS
• “Normal”: resistance to stretch in a resting, typically innervated muscle
• Typical muscular systems
• Hypotonia: atypically low muscular resistance to passive stretch
• Developmental disorders (CP, Trisomy 21, MD) and temporarily during neural shock
• Flaccidity: complete loss of muscle tone, no resistance to stretch
• MN disorders, more severe forms of SB , “floppy infant syndrome” (severe hypotonic CP)
Spasticity
• Rigidity is velocity independent, and causes increased resistance across all
muscles involved
• Decerebrate: rigid extension of limbs & trunk, and plantar flexion
• Decorticate: rigid flexion of UE, extended neck and lower limbs, and plantarflexion
• Spasticity is velocity dependent, and can be functional for some
populations
• When the muscle contraction is assisting with postural control, mobility, muscle
mass maintenance and bone mineralization, assists with decreasing edema and
prevents DVTs.
• Needs treatment if it interferes with function, reduces participation, or causes pain
Some extra videos
• Video on Spasticity demonstrating brief spastic ROM in client with CP
and example of clonus, as well as a brief image of contracture
• Dr. Gooch talks further on difference between
spasticity, dystonia, and rigidity
Measuring muscle tone
• Modified Ashworth Scale (MAS)
• Evidence kinda sucks, TBH
• Motor screening, p. 95 – 98 in Gutman Screening text
Grade Description
0 No increase in muscle tone
1 Slight increase in muscle tone manifested by a catch and release, or by minimal resistance at the
end of the ROM when the affected part is flexed or extended
2 Slight increase in muscle tone manifested by a catch followed by minimal resistance throughout
the remainder (less than half) of the ROM
3 More marked increase in muscle tone through most of the ROM, but affected part is easily
moved
4 Considerable increase in muscle tone, making passive movement difficult
5 Affected part rigid in flexion or extension