UMN Lesions Signs Flashcards
UMN syndrome: structures involved
- UMN’ s in cerebral cortex
- descending brainstem tracts
- CST of spinal cord
CST= corticospinal tract
UMN syndrome: distribution of abnormalities
how are structures typically affected
- Muscles that are supplied by motor nuclei below the level of the lesion are affected in groups
- Contralateral limb muscles are affected when lesions are above decussation
- ispilateral muscles are affected when the lesion is below the decussation
LMN syndrome: Structures involved
- Spinal cord or brainstem alpha motor neurons (LMN)
- PNS: motor neurons in all spinal nerves and cranial nerves (axons of LMNs)
LMN syndrome: distribution of abnormalities
- effects are always segmental and limited to muscles innervated by damaged Alpha motor neurons or their axons
- individual muscles or groups of muscles are affected
UMN
Location of lesions
- brain
- brainstem
- corticospinal tracts
- spinal cord
UMN: diagnosis/pathogies
- CVA
- TBI
- SCI
- MS
- CP
UMN lesions: tone and reflexes
- hypertonia/velocity dependent
- hyperreflexia,
- clonus,
- exaggerated cutaneous reflexes
- (+) babinski
UMN syndrome
Involuntary movements
Muscle spasms
flexor or extensor
UMN lesions
Strength/muscle bulk
Strength:
- weakness or paralysis
- unilateral or bilateral distribution; never focal
Muscle bulk:
- disuse atrophy
- variable
- widespread distribution
UMN syndrome
Voluntary movements
- impaired or absent
- obligatory mass synergies
LMN Lesion
Location of lesion
- CN nuclei/nerves
- Ventral horn cells
- spinal roots
- peripheral nerves
LMN Lesion
Diagnosis/pathologies
- polio
- Guillian barre
- peripheral nerve injury
- peripheral neuropathy
- radiculopathy
LMN Lesion
Tone&reflexes
- hypotonia, flaccidity
- not velocity dependent
- hyporeflexia or absent
Paresis vs paralysis
- Paresis: Occurs in UMN tract lesions as consequence of inadequate facilitation of LMNs
- Paralysis: Occurs in muscles innervated by LMNs below the level of a complete spinal cord lesion
What is an abnormal synergy
- abnormal coupling of movements at adjacent joints due to stereotyped coactivation of muscles
- ex; shoulder abduction and ER combined with elbow flexion when patient is attempting to reach forward
- Mechanism: loss of cortical inhibition of reticulospinal tracts
- Loss of cortical inhibition of reticulospinal tracts (disruption of selective movements)
abnormal synergies example
- UE flexion synergy: shoulder ABD + ER, elbow flexion, forearm supination, wrist and finger flexion.
- LE flexion synergy: hip ER + ABD + flexion, knee flexion, ankle DF and INV, DF of toes.
- LE extension synergy: hip IR + ADD + extension, knee extension, ankle PF and INV, PF of toes
Normal phasic stretch reflex
- quick stretch of a muscle, elicited by striking the muscle’s tendon, stimulates type 1a affernets from the muscle spindle
- activity of type 1a afferents causes monsynaptic excitation of alpha motor neurons to the stretched muscle resulting in an abrupt contraction of the muscle fibers
- UMN influence spinal reflexes by adjusting background level of neural activity in SC
Normal babinski’s sign
- stroking from heel to ball of foot along lateral sole
- then across the ball of the foot normally causes the toes to flex
- seeing nothing is okay
Developmental or pathological babinski
- in people with CST lesions or in children <2 the great toe extends
- although the other toes may fan out their movement is not required for babinski
Abnormal Clonus
- Involuntary repeating rhythmic contractions of a single muscle group
- can be elicited by muscle stretch, cutaneous and noxious stimuli
- most common at the ankle
- sustained clonus repeating more than 5 times is always pathological
*tremor is not the same = alternaing agonist/anatgonist contractions
muscle tone
- Resistance to stretch in resting muscle
- muscle tone is categorized on a continuum
Muscle Tone
Resistance ranges from
flaccid: lack of resistance
hypotonia: abnormally low
normal:
spasticity: velocity-dependent hypertonia; abnormally high resistance that increases with faster movements
rigidiy: velocity-independent hypertonia
some basal ganglion disorders cause rigidity typically in more severe cases
Spasticity
- velocity dependent hypertonia
- in spasticity the amount of resistance to passive movement depends on the velocity of movement
- both cahnges in muscle tissue and neuromuscular overactivity contribute to velocity-dependent hypertonia
- two mechanisms produce neural overactivity: hyperreflexia, reticulospinal tract overactivity
