Lower
motor neuron (LMN) lesions may arise from disease processes affecting the
anterior horn cell or the motor axon and/or its surrounding myelin.
Neuromuscular junction pathology and muscle disorders may mimic an LMN disorder
and form part of the differential diagnosis. In an LMN lesion, the muscle
becomes hypersensitive to neuro-transmitter as it is denervated. Similarly, the
damaged lower motor erratically discharges the neurotransmitter stored within
itself as the neuron degrades. So, both increased hypersensitivity and erratic
release of neurotransmitter cause fasciculations. However, in UMN lesions,
there is regular firing to prevent the atrophy of muscles. LMN syndromes are
clinically characterized by muscle atrophy, weakness, and hyporeflexia without
sensory involvement.
Neuromuscular
Junctions, the junction between a motor neuron and muscle fiber is a
specialized synapse. The motor neuron releases a flood of acetylcholine (Ach)
neurotransmitters upon stimulation from the axon terminals from synaptic
vesicles that bind with the post-synaptic receptors at the plasma membrane.
This response is contractile causing muscle contraction and inhibition does not
require a neurotransmitter release.
UMC
& LMN lesions cause very different clinical findings.
- UMN lesions are lesions anywhere from the cortex to the descending tracts. This lesion causes hyperreflexia, spasticity, and a positive Babinski reflex, presenting as an upward response of the big toe when the plantar surface of the foot is stroked, with other toes fanning out.
- LMN lesions are lesions anywhere from the anterior horn of the spinal cord, peripheral nerve, neuromuscular junction, or muscle. This type of lesion causes hyporeflexia, flaccid paralysis, and atrophy.
