Upper and Lower Motor Neuron Lesions
1) Summary
- STORM Baby
Tone
- depends on gamma motor neuron
Reflex
- hyperreflexia (loss of UMN comand)
Mass
- disuse atrophy
- denervation atrophy (loss of continuous ACh release)
Babynski
- child (normal - UMN are not till myelinated)
Fasciculations (Denervation hypersensitivity)
- loss LMN --> loss ACh release --> muscle increase production of ACh receptors (any hit can cause fasciculations)
2) UMN lesions
Acute manifestations
- Spinal shock
- Relative sparing trunk
Late manifestations
- Babinski sign
- Spasticity
- Hyporeflexia of superficial reflexes
- Contralateral or ipsilateral involvement
- Involvement below the lesion
- Decorticate posture
- Decerebrate posture
3) Spinal shock
- Hypotonia and loss of all reflexes on contra-lateral side
- Gamma-motor neurons by stretching muscle spindle bodies, activate alpha-motor neurons leading to extrafusal muscle contraction.
- In upper motor neuron lesion, supraspinal excitatory input to gamma-neurons is lost.
4) Relative sparing of trunk muscles
- Trunk muscles are bilaterally innervated by anterior corticospinal tract, so that a lesion of one side of the tract has minimal/ imperceptible manifestations.
- Distal muscles, fingers, toes, fine articulations and flexors more than extensors are handled by lateral corticospinal tract and affected more.
5) Babinski sign
- It is a primitive response present normally in newborns.
- The extensor response is modified to flexor response by developing corticospinal tract.
- Upper motor neuron lesion results in reappearance of primitive extensor response.
6) Spasticity
- Increased muscle tone, hyperactive stretch reflexes, and clonus.
- Due to removal of inhibitory influences exerted by cortex on postural centers of vestibular nuclei and reticular formation.
7) Hyporeflexia of superficial reflexes
- Superficial reflexes are absent in infants and appear after about 6 months to 1 year.
- Their appearance may depend upon the myelination of the corticospinal tract.
- Hence, in upper motor neuron lesion, superficial reflexes may be lost.
- It may even be absent in normal individuals, hence, correlation with other corticospinal signs is necessary.
8) Contralateral or ipsilateral involvement
Pyramidal decussation occurs at the level of medulla-spinal cord junction.
Lesion above pyramidal decussation leads to contralateral signs.
Lesion below pyramidal decussation leads to ipsilateral signs.
Involvement below the lesion
Damage of UMN below the level of lesion
9) Decorticate posture
- Occurs in UMNL above the red nucleus – hence, rubrospinal tract still working.
- This leads to release of cortical inhibition of the rubro-, reticulo-, and vestibulospinal tracts. In this circumstance, the action of rubrospinal tract supercedes that of the reticulo- and vestibulospinal tracts, which results in arm flexion at the elbows and lower extremity extension, so-called decorticate posturing.
10) Decerebrate posture
- Occurs in UMNL below the red nucleus – hence, rubrospinal tract not working.
- This releases inhibition of the reticulo- and vestibulospinal tracts, which results in extension of the neck and all four limbs, so-called decerebrate posturing.
11) LMN lesions
- Ipsilateral involvement
- Involvement at the level of lesion
- Flaccid paralysis, loss of deep tendon reflexes, and hypotonia
- Muscle atrophy
- Fasciculations and fibrillations
12) Ipsilateral involvement
- Lower motor neuron comprises of motor neurons in the anterior neurons and the fibers originating from them, which innervates the skeletal muscles.
- These fibers go uncrossed to the same side.
13) Involvement at the level of lesion
- Damage of LMN at the level of lesion.
14) Flaccid paralysis, loss of deep tendon reflexes, and hypotonia
- Loss of efferent limb in monosynaptic stretch or deep tendon reflexes
- Information from motor cortex doesn’t reach muscles due to defect in Lower motor neuron – leading to flaccid paralysis
- Loss of gamma and alpha motor neurons lead to decrease in baseline Ia and alpha motor neuron discharge – leading to hypotonicity
15) Muscle atrophy
- Denervation (deprived of necessary trophic factors)
- Disuse
16) Fasciculations and fibrillations
- Damaged α-motor neuron → Spontaneous action potential → Motor unit fires → Visible twitching of muscle fibers group (fasciculations)
- Increased excitability of muscle fibers due to denervation → Spontaneous contraction of single muscle fiber visible in EMG (fibrillations)