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in the lateral corticospinal tract, where does decussation occur?
medulla (pyramids)
in the spinothalamic tract, where does decussation occur?
at the level of the spinal cord it enters
in the dorsal column, where does decussation occur?
medulla
what causes a central cord lesion?
extension injury → sensory and motor loss
motor issues are more common in upper or lower extremities?
upper
what kind of distribution does sensory issues tend to have?
shawl or cape-like
likely has loss of pain/temp
light touch/vibration intact
in the lateral corticospinal tract [MOTOR pathway], from most medial to outward?
cervical
thoracic
lumbar
sacral
if there is a central lesion, because cervical is more medial, it makes sense there is more issues with motor on UE
for the sensory pathways, from medial to lateral?
sacral
lumbar
thoracic
cervical
what causes an anterior cord lesion?
hyperflexion of the neck or spinal artery injury (usually surgery)
what is preserved in an anterior cord lesion?
posterior column functions, everything else is lost below the level of injury
what are the manifestations of an anterior cord lesion and what parts does it affect?
affects 2/3 of the cortex, including spinothalamic and corticospinal tract → impacts motor, gross touch, pain, and temp bilaterally
dorsal column tract still intact
injuries to the dorsal column tract lead to what?
paraplegia or quadriplegia
what kind of lesion is brown-seguard syndrome?
unilateral cord lesion
what is brown-seguard syndrome?
damage to half of the spinal cord
IPSILATERAL SIDE (and below): loss of vibration, motor function, deep touch, and position
CONTRALATERAL SIDE (and below damage): loss of pain, temp, and light touch (motor is ok tho)
spinothalamic tract lesions (damge to half of cord) (brown-seguard syndrome)
below the level of injury on the ipsilateral side of injury, touch, pain, and temp are intact, @ the injury tho, these are affected
contralateral: the information can come in, and can cross over, but when it tries to go up, there’s the lesion, so touch, pain temp on the CONTRALATERAL side is lost on that level and ALL The way down (B/C THE REST WILL CROSS OVER AND KEEP HITTING THE LESION)
remember it crosses right at the spinal level - contralateral
dorsal column lesion (brown-seguard syndrome)
if damage to half of the cord, ie thoracic. b/c info comes in at the level of the cord, it will be affected by the lesion, and BELOW and ipsilateral will have issue. above is still fine
however, the other side, the dorsal column nerves don’t ever touch the lesion b/c they decussate in the medulla
the only place you lose the dorsal column is on ipsilateral side of injury
corticospinal tract lesion pathway manifestation (brown-seguard syndrome)
if damage to the R half of cord, at the level of injury, corticospinal tract on that side (R) will be affected, and lost motor function at this level and below (no motor info can get from brain → at and below injury)
the contralateral (L) side is not impaired b/c it decussates in the medulla
what does central cord syndrome affect?
affects upper extremities more than lower
what is anterior cord syndrome? (image a bowl shape)
motor, pain, temp, and gross touch lost below injury
vibration, light touch, and proprioception preserved
a pt presents with loss of pain and motor function below the nipple line, with normal extremity function. what spinal cord level is likely injured? what type of spinal cord injury did the pt have?
T4 (nipple)
motor = corticospinal, pain = spinothalamic pathway, and no mention of vibration, light touch, of proprioception
this question sounds like bilateral, motor and spinothalamic pathways = anterior cord syndrome
what is a transverse thoracic cord lesion?
disruption of bilateral sensory and motor pathways below the level of the lesion
what causes a transverse thoracic cord lesion?
trauma
tumors
multiple sclerosis
effects of transverse thoracic cord lesion
dorsal columns cannot go up and send messages bilaterally
corticospinal tract cannot transmits the motor neurons from brain to below the lesion bilaterally (enters at the level of spinal cord, it does decussate at the level but it doesn’t matter b/c the lesion is transverse)
spinothalamic tract cannot transmit pain, temp, or gross touch to the sensory cortex at and below level of injury (enters at the level of spinal cord)
you are assessing pt who has a mets to the spinal cord. has a tumor to the R side of the spine at C4 level. when assessing the strength in the UE, there is significant waeakness and spasticity to R arm. what would you expect to find when assessing strength of legs on same side?
LMN tends to be flaccid, UMN is spastic
tumor is in the cord, so this would probably be UMN
tumor is mainly affecting corticospinal tract
spastic paralysis in the RL extremity
what are the LMN lesion findings?
flaccid paralysis
decreased deep tendon reflexes
atrophy
possible fasculations
babinski reflex no present
what are lesions at the spinal roots noted to have that is related to a specific nerve root/dermatome?
weakness and atrophy
what is mononeuropathy (peripheral)?
weakness and atrophy in peripheral nerve distribution (at individual peripheral nerve)
compression neuropathy is most common
what is polyneuropathy (periphery)?
weakness and atrophy more prominent distal compared to proximal
stocking glove-distribution (seen with DM, drugs, HIV, vitamin deficiencies)
upper vs. lower MN, in which would atrophy be more common to be seen earlier?
LMN lesion (if UMn would be more d/t disuse)
what are examples of nerve entrapment?
UE: carpal tunnel syndrome (median nerve is compressed under the fascial sheath of the flexor retinaculum)
LE: meralgia paresthetica (lateral femoral cutaneous nerve is compressed when leaving pelvis)
what is an example of peripheral neuropathy?
b12 deficiency (causes megaloblastic anemia and neurologic causes) → degeneration of dorsal (posterior) and antero-lateral spinal columns → symmetrical sensory neuropathy, legs > arms
paresthesia and ataxia
loss of vibration and position sense
progressing to severe weakness, spasticity, clonus, paraplegia, and incontinence
CNS symptoms of degeneration of dorsal (posterior) and antero-lateral spinal columns (caused by b12 def)
cerebellar ataxia, memory loss, irritability, and dementia (and atrophic glossitis)
what are causes of b12 def?
malabsorption (pernicious anemia, gastrectomy, atrophic gastritis, h. pylori infection, alcoholism)
drugs: BPPIs, metformin
vegetarian and vegan diets (only dietary source is meet)