CH 9: Lesions of peripheral nerves, spinal nerve roots & SC

Question 1

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:

Answer 1

wallerian degeneration

for several weeks after the injury, the Nissl bodies in the cell undergo CHROMATOLYSIS

Question 2

what is chromatolysis

Answer 2

a process in which the ribosomes (RNA )lose their staining characteristics and seem to dissolve in the surrounding cytoplasm

Question 3

in the PNS, completely severed nerves have some capacity to:

Answer 3

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

Question 4

in the CNS, completely severed nerve fibers:

Answer 4

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

Question 5

injury of an individual peripheral nerve leads to :

Answer 5

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

Question 6

polyneuropathy:

Answer 6

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

Question 7

LMN refers to:

Answer 7

anterior horn cells of the SP (innervate skeletal muscles ) and motor nerve cels of the brain stem (innervate muscles suppled by CNs)

Question 8

destruction of LMN, their axons in ventral roots or motor fibers of peripheral nerves abolishes :

Answer 8

both the voluntary and reflex responses of muscles

muscles show: paralysis, hypotonia, absence of DTRs

Question 9

hypotonia=

Answer 9

diminished resistance to passive manipulation of the limbs

Question 10

more profound atrophy occurs in:

Answer 10

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

Question 11

muscles undergoing early stages of atrophy display:

Answer 11

fibrillation potentials= fine twitching of single muscle fibers that generally can’t be seen on exam

Question 12

fasiculation potentials=

Answer 12

brief contractions of motor units that can be seen

don’t necessarily indicate motoneuron disease

Question 13

herniation of nucleus pulposus frequently injuries:

Answer 13

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

Question 14

dorsal root lesions also cause:

Answer 14

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

Question 15

UMN referes to:

Answer 15

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

Question 16

+ babinski sign indicates:

Answer 16

lesion of corticospinal tract

lesion rostrall to decussation in lower medulla causes contralateral spasticity, muscle weakness, hyperreflexia,

lesion caudal to decussation causes ipsilateral symptoms

Question 17

hemiplegia=

Answer 17

paralysis affecting the arm and leg of one side of the body

Question 18

paraplegia=

Answer 18

paralysis of both legs

Question 19

monoplegia=

Answer 19

paralysis of a single extremity

Question 20

quadriplegia=

Answer 20

paralysis that includes all 4 extremities

Question 21

paresis=

Answer 21

weakness w/out total paralysis

Question 22

paralysis=

Answer 22

complete loss of motor function

Question 23

+ hoffman sign=

Answer 23

prompt reflexive adduction of the thumb and flexion of the index finger

associated w/ injury of corticospinal tract but also sometimes normal

Question 24

complete transection of the SC causes:

Answer 24

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

Question 25

after acute spinal transection:

Answer 25

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

Question 26

lateral hemisection of the SC causes:

Answer 26

brown-sequard syndome

Question 27

lateral column damage results in:

Answer 27

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

Question 28

dorsal column damage results in:

Answer 28

loss of position sense, vibration sense, tactile discrimination on SAME side below level.

Question 29

damage to anteriolateral system results in:

Answer 29

loss of sensations of pain and temp on side OPPOSITE to lesion beginning 1 or 2 segments below level of injury

Question 30

simple touch sensation may be intact because:

Answer 30

it exists in both the dorsal columns on ipsilateral side AND the anterolateral system on the contralateral side

Question 31

irritation of fibers in the dorsal root zone leads to :

Answer 31

paresthesias or radicular pain in a band over the affected dermatomes

Question 32

destruction of dorsal roots results in:

Answer 32

a band of anesthesia (sensory loss) over the dermatomes supplied by involved roots

Question 33

destruction of ventral roots evokes:

Answer 33

a flaccid paralysis affecting only the muscles innervated by fibers that have been destroyed

Question 34

brown sequard syndrome results more often from:

Answer 34

lesions compressing the SC from the outside than from lesions within it

Question 35

sacral sparring=

Answer 35

sensation below the level of a lesion is lost, except in the sacral dermatomes

Question 36

syringomyelia=

Answer 36

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

Question 37

sensory dissociation =

Answer 37

loss of some sensory modalities with preservation of others

Question 38

ALS=

Answer 38

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

Question 39

combined system disease=

Answer 39

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