Lower Motor Neuron Syndrome
Anatomy and physiology
•Location: anterior horn of the spinal cord + motor nuclei of cranial nerves
•Each LMN is connected (through arborization of the terminal part of its efferent fiber) to
a group of muscle fibers (few to 100) = MOTOR UNIT (MU)
•MU –central concept of peripheral nervous system organization and function
MU
•Variations in force, range, rate and type of movements are related to the numberand
sizeof the MU recruited in contraction and to the sequence and frequency of firing into
each MU
•Muscles are innervated according to the segments of the spinal cord in a “metameric “
distribution.
•Motor nerve fiber of each ventral root participate together with the neighboring roots to
the plexuses formation
•So each large muscle can be innervated by 2 or more roots
•But a single peripheral nerve innervates completely a muscle or a group of muscles
1
, •Tendon reflex activity and muscle tone are controlled by
–large (alpha) motor neurons
–Muscle spindles
–Afferent fibers of the muscle spindles
–Small anterior horn cell (gamma) motor neurons –axons are connected with the
spindles.
Myotatic stretch reflex
•Tap on the tendon –activates nuclear bag fibers inside the spindles
•Afferent projections synapse with the alpha motor neurons (in the same and adjacent
segments)
•Impulses to skeletal muscles –monosynaptic muscle contraction = strech reflex
•Antagonist muscles are inhibited through disynaptic connections in the same time
LMN lesion –clinical picture
1-Motor deficit –restricted to the muscle fibers that are innervated by the injured LMNs
2-Diminished or loss of muscle tone –hypotonia in the same territory._
3-Muscle fibers amyotrophic changes -refers to the muscle fibers part of the affected MU
–we can have “group amyotrophy”
4-Tendon and cutaneous reflexes controlled by the injured LMNs–diminished or lost
5-Fasciculations–involuntary rippling of muscles without moving segments due to
pericarional and axonal membrane instability and generation of spontaneous, aberrant,
action potentials (very prominent in pericarional and radicular lesions)
Radicular syndrome
•Motor deficit –metameric segmental
2
Anatomy and physiology
•Location: anterior horn of the spinal cord + motor nuclei of cranial nerves
•Each LMN is connected (through arborization of the terminal part of its efferent fiber) to
a group of muscle fibers (few to 100) = MOTOR UNIT (MU)
•MU –central concept of peripheral nervous system organization and function
MU
•Variations in force, range, rate and type of movements are related to the numberand
sizeof the MU recruited in contraction and to the sequence and frequency of firing into
each MU
•Muscles are innervated according to the segments of the spinal cord in a “metameric “
distribution.
•Motor nerve fiber of each ventral root participate together with the neighboring roots to
the plexuses formation
•So each large muscle can be innervated by 2 or more roots
•But a single peripheral nerve innervates completely a muscle or a group of muscles
1
, •Tendon reflex activity and muscle tone are controlled by
–large (alpha) motor neurons
–Muscle spindles
–Afferent fibers of the muscle spindles
–Small anterior horn cell (gamma) motor neurons –axons are connected with the
spindles.
Myotatic stretch reflex
•Tap on the tendon –activates nuclear bag fibers inside the spindles
•Afferent projections synapse with the alpha motor neurons (in the same and adjacent
segments)
•Impulses to skeletal muscles –monosynaptic muscle contraction = strech reflex
•Antagonist muscles are inhibited through disynaptic connections in the same time
LMN lesion –clinical picture
1-Motor deficit –restricted to the muscle fibers that are innervated by the injured LMNs
2-Diminished or loss of muscle tone –hypotonia in the same territory._
3-Muscle fibers amyotrophic changes -refers to the muscle fibers part of the affected MU
–we can have “group amyotrophy”
4-Tendon and cutaneous reflexes controlled by the injured LMNs–diminished or lost
5-Fasciculations–involuntary rippling of muscles without moving segments due to
pericarional and axonal membrane instability and generation of spontaneous, aberrant,
action potentials (very prominent in pericarional and radicular lesions)
Radicular syndrome
•Motor deficit –metameric segmental
2
