CH 9: Lesions of peripheral nerves, spinal nerve roots & SC Flashcards
transection or permanent destruction of an axon leads to complete degeneration of the part that has been separated from the nerve cell body. this process is called:
wallerian degeneration
for several weeks after the injury, the Nissl bodies in the cell undergo CHROMATOLYSIS
what is chromatolysis
a process in which the ribosomes (RNA )lose their staining characteristics and seem to dissolve in the surrounding cytoplasm
in the PNS, completely severed nerves have some capacity to:
repair themselves
Schwann cells proliferate and attempt to bridge the gap with the distal end of the nerve
if suitably matched, connections can be reestablished and function can be restored. considerable recovery can occur with partial injury to peripheral nerves, provided the neurolemmal tubes remain intact
in the CNS, completely severed nerve fibers:
do NOT regenerate effectively
some partial injuries can prevent conduction of nerve impulses without causing irreversible fiber degeneration
the pressure of brain/SC tumors, herniated interveretebral discs, blood clots or swelling/edema
the prospect of recovery depends on the severity and duration of the pressure
injury of an individual peripheral nerve leads to :
paralysis of muscles and loss of sensation distal to the lesion involving only muscles and skin areas supplied by the inured nerve
muscles: flaccid, hypotonic, atrophy
sensation: lost
polyneuropathy:
widespread peripheral nerve disease
commonly bilaterally
distal parts of extremities
muscular weakness/atrophy
sensory los in glove and stocking distribution
common with diabetes, nutritional deficiencies
LMN refers to:
anterior horn cells of the SP (innervate skeletal muscles ) and motor nerve cels of the brain stem (innervate muscles suppled by CNs)
destruction of LMN, their axons in ventral roots or motor fibers of peripheral nerves abolishes :
both the voluntary and reflex responses of muscles
muscles show: paralysis, hypotonia, absence of DTRs
hypotonia=
diminished resistance to passive manipulation of the limbs
more profound atrophy occurs in:
muscle fibers deprived of their motoneurons than in muscles rendered inactive
because AHCs exert a trophic influence on muscle fibers that is essential for maintaing their normal state
muscles undergoing early stages of atrophy display:
fibrillation potentials= fine twitching of single muscle fibers that generally can’t be seen on exam
fasiculation potentials=
brief contractions of motor units that can be seen
don’t necessarily indicate motoneuron disease
herniation of nucleus pulposus frequently injuries:
dorsal roots by protruding laterall b/w adjacent vertebral bodies and compressing one or more dorsal roots
results: pain and paresthesias (numb, tingle)
decrease/loss of sensation in dermatomal distribution
dorsal root lesions also cause:
also disrupts stretch reflex pathway and causes hypotonia and loss of DTRs.
LMN intact; ms strength intact (unless disuse from pain); coordination may deteriorate bc of loss of sensory feedback
UMN referes to:
nerve cell bodies that originate in high levels of the CNS and send their axons into the BS or SC
these axons synapse, directly or indirectly on motor nuclei of the CNs and AHC in the SC
examples of UMN pathways: corticospinal corticobulbar reticulospinal vestibulospinal rubrospinal
+ babinski sign indicates:
lesion of corticospinal tract
lesion rostrall to decussation in lower medulla causes contralateral spasticity, muscle weakness, hyperreflexia,
lesion caudal to decussation causes ipsilateral symptoms
hemiplegia=
paralysis affecting the arm and leg of one side of the body
paraplegia=
paralysis of both legs
monoplegia=
paralysis of a single extremity
quadriplegia=
paralysis that includes all 4 extremities
paresis=
weakness w/out total paralysis
paralysis=
complete loss of motor function
+ hoffman sign=
prompt reflexive adduction of the thumb and flexion of the index finger
associated w/ injury of corticospinal tract but also sometimes normal
complete transection of the SC causes:
immediate loss of all sensation and all voluntary movement below the level of the lesion
preserved function above the level
if lesion occurs between C1 and C3- respiration stops
after acute spinal transection:
spinal shock appears: paralysis is flaccid, DTRs absent, plantar stim gives no response
signs of UMN lesion appear only after several weeks
eventually, +babinski
followed by gradual appearance of hyperactive DTR, clonus, spasticity
bladder/bowl function usually automatic
lateral hemisection of the SC causes:
brown-sequard syndome
lateral column damage results in:
paralysis of muscles on the SAME side below the injury spasticity hyperactive reflexes clonus loss of superficial reflexes Babinski sign
lateral corticospinal tract
rubrospinal tract
dorsal column damage results in:
loss of position sense, vibration sense, tactile discrimination on SAME side below level.
damage to anteriolateral system results in:
loss of sensations of pain and temp on side OPPOSITE to lesion beginning 1 or 2 segments below level of injury
simple touch sensation may be intact because:
it exists in both the dorsal columns on ipsilateral side AND the anterolateral system on the contralateral side
irritation of fibers in the dorsal root zone leads to :
paresthesias or radicular pain in a band over the affected dermatomes
destruction of dorsal roots results in:
a band of anesthesia (sensory loss) over the dermatomes supplied by involved roots
destruction of ventral roots evokes:
a flaccid paralysis affecting only the muscles innervated by fibers that have been destroyed
brown sequard syndrome results more often from:
lesions compressing the SC from the outside than from lesions within it
sacral sparring=
sensation below the level of a lesion is lost, except in the sacral dermatomes
syringomyelia=
progressive disorder of uncertain origin that produces tissue destruction w/ cavitation around the central canal of the SC (most common in cervical enlargement)
a small lesion interrupts the lateral spinothalamic fibers that pass through the ventral white commissure– results in loss of pain and temp in a segmental distribution affecting the UE on BOTH sides
as the lesion enlarges, degeneration often extends into the AHC– causes paralysis w/ atrophy of muscles innervated by the segments involved
sensory dissociation =
loss of some sensory modalities with preservation of others
ALS=
amyotrophic lateral sclerosis
progressive, fatal disease of unknown cause
neuronal degeneration in the motor nuclei of the CNs and in the AH of the SC
often see with pernicious anemia or nutritional deficiencies
degeneration of corticospinal and corticobulbar tracts bilaterally
sensation preserved
presents with limb weakness/atrophy, fasciculations of hand/arm
followed later by spastic paralysis of limbs, difficulty speaking/swallowing
combined system disease=
subacute degeneration of the SC
dorsal and lateral columns of SC degenerate but gray matter remains preserved
results:
- difficulty walking/tingling in feet
- loss of position & vibration sense (dorsal column)
- +Romberg (dorsal column)
UMN degeneration projectings in lateral columns leads to:
- leg weakness
- spasticity
- hyperactive muscle stretch reflexes
- bilateral babinski
later reflexes may disappear
