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spinal cord Flashcards

1
Q

SC circulation consists of

A

2 posterior spinal arteries
1 anterior spinal artery
6-8 radicular arteries

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2
Q

what supplies the anterior and posterior spinal arteries in the cervical region of the SC

A

vertebral arteries supply anterior and posterior spinal arteries in cervical region

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3
Q

what supplies the spinal arteries below the cervical region of the SC

A

spinal arteries are perfused by radicular and lumbar arteries

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4
Q

pathway of the two posterior spinal arteries
where they run on SC
what they perfuse

A

(cervical region) aorta->subclavian artery->vertebral a-> posterior spinal a
(below cervical region) aorta->segmental a->posterior radicular a->posterior spinal a
runs length of SC longitudinally on both sides of midline of posterolateral sulcus
perfuses posterior 1/3 of SC (green)

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5
Q

pathways of anterior spinal artery
where it runs on SC
what it perfuses

A

(cervical region) aorta–>subclavian a–>vertebral a–> anterior spinal a
(below cervical region) aorta->segmental a->anterior radicular a->anterior spinal a

runs length of SC longitudinally across anterior median fissure
perfuses anterior 2/3 of SC (blue)

ASA flow through thoracolumbar region of cord can be inconsistent, often making this region highly dependent on radicular flow

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6
Q

largest and most important artery

A

artery of adamkiewicz (great radicular artery)

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7
Q

artery of adamkiewicz (great radicular artery)
what it perfuses
where it originates

A

perfuses anterior SC in thoracolumbar region
most commonly originates from left side between T11-12
in 75% of the population, it originates between T8-12 and in another 10% it arises at L1-2

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8
Q

anterior spinal artery syndrome aka Becks syndrome
cause
classic s/sx

A

aortic x clamp placed above artery of adamkiewicz
s/sx: flaccid paralysis of LE’s, bowel and bladder dysfunction, loss of temperature and pain sensation, preserved touch and proprioception

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9
Q

perfusion of corticospinal tract

A

anterior blood supply
-this explains why patient presents with flaccid paralysis of LE’s in anterior spinal artery syndrome

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10
Q

perfusion of autonomic motor fibers

A

anterior blood supply
-this explains why the patient experiences bowel and bladder dysfunction in anterior spinal artery syndrome

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11
Q

perfusion of spinothalamic tract

A

anterior blood supply
-this explains why patient loses pain and temperature sensation in anterior spinal artery syndrome

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12
Q

perfusion of dorsal column

A

posterior blood supply
-this explains why touch and proprioception are preserved in anterior spinal artery syndrome

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13
Q

which anatomic structure is marked in this image

A

dorsal column

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14
Q

ID the structures in this image

A
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15
Q

define ganglion

A

collection of cell bodies that reside outside of CNS

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16
Q

what does the grey matter contain
outline the laminae

A

grey matter contains neuronal cell bodies. processes afferent signals that arrive from periphery.
subdivided into 10 laminae
1-6 reside in dorsal grey matter- sensory
7-9 reside in ventral grey matter- motor
10 resides around central canal. anterior and posterior commissures comprise lamina 10

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17
Q

the grey matter is larger in these 2 specific regions of the SC

A

the region of cervical enlargement (C5-7) contain cell bodies from neurons that supply UE’s
region of lumbar enlargement (L3-S2) contain cell bodies from neurons that supply LE’s

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18
Q

what does white matter contain and how is it divided

A

contains axons of ascending and descending tracts
-divided into dorsal, lateral, ventral columns

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19
Q

outline the 4 sensory tracts in the white matter and what info they transmit

A
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20
Q

outline the 2 motor tracts in the white matter and what info they transmit

A
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21
Q

where does the corticospinal tract travel and what kind of pathway is it

A

from cortex to spine, motor

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22
Q

where does the spinothalamic tract travel and what kind of pathway is it

A

from spine to thalamus, sensory

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23
Q

dorsal column- medial lemniscal system
sensations it transmits
discrimination
fiber type
how fast it transmits info

A

transmits mechanoreceptive sensations (fine touch, proprioception, vibration, pressure)
capable of two point discrimination- a high degree of localizing stimulus
consists of large myelinated rapidly conducting fibers
transmits sensory info faster than anterolateral system

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24
Q

dorsolateral column- medial lemniscal system (DC-LMS) pathway

A
  1. 1st order neuron enters through dorsal root ganglion, ascends on ipsilateral side, synapses with second order neuron in medulla
  2. crosses to contralateral side in medulla, then ascends towards thalamus via medial lemniscus. synapses with 3rd order neuron in thalamic relay station, the ventrobasal complex
  3. fibers pass through internal capsule and advance towards somatosensory cortex in post central gyrus in parietal lobe
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25
Q

dorsolateral column- medial lemniscal system (DC-LMS) first order neuron
nerve fiber type
where it enters
where it relays
where it ascends
where it synapses

A

usually A beta fiber
enters via DRG
relays from dorsal column to medulla
where it ascends (on ipsilateral side)
synapses with second order neuron in medulla (cuneate and gracile nuclei)

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26
Q

dorsolateral column- medial lemniscal system (DC-LMS) second order neuron
desiccation
what its joined by
where it synapses

A

crosses contralateral side in medulla after it synapsed, ascends towards thalamus via medial lemniscus
-joined by trigeminal nerve. recall that this nerve provides sensation to face and head
-synapses with 3rd order neuron in thalamic relay station- ventrobasal complex

27
Q

sensory pathway- anterolateral system-spinothalamic tract
what it transmits
how fast it transmits
fiber types
type of discrimination

A

-transmits pain, temperature, crude touch, tickle, itch, sexual sensation.
-transmits sensory info 1/2 to 1/3 as fast as dorsal column (medial lemniscal)
-consists of smaller myelinated and non myelinated slower conducting fibers
-two point discrimination is not present

28
Q

sensory pathway- anterolateral system-spinothalamic tract pathway

A
  1. first order neuron cell body is in dorsal root ganglion. may ascend or descend 1-3 levels on ipsilateral side in lissauer tract before synapsing with second order neuron
  2. pain neurons synapse with the second order neuron in the substantial gelatinosa- rexed lamina 2 or in dorsal horn laminae 1, 4, 5, 6
  3. then crosses to contralateral side of SC and ascends 2 ways: lateral spinothalamic (pain and temp) or anterior spinothalamic (crude touch/pressure). cell bodies reside in dorsal horn of SC.
  4. 2nd order neurons synapse with 3rd order neurons in RAS and thalamus
  5. most tactile signals are relayed to ventrobasal complex of thalamus. pass through internal capsule and advance through somatosensory cortex in post central gyrus in parietal lobe.
    -most pain fibers synapse with 3rd order neuron in RAS. from here, connects to thalamus.
29
Q

sensory pathway- anterolateral system-spinothalamic tract neuron fiber types

A

A delta (first) pain, mechanoreceptors
C fibers (slow) pain, polymodal nociceptors.

30
Q

injury above desiccation will cause

A

spastic paralysis on contralateral side

31
Q

injury below desiccation will cause

A

flaccid paralysis on ipsilateral side

32
Q

corticospinal tract is also called

A

pyramidal tract (because pyramids are formed by corticospinal neurons as they run through the medulla). for this reason, all motor pathways outside of this corticospinal (pyramidal) tract are collectively known as extrapyramidal tracts

33
Q

primary functions of corticospinal tract

A

voluntary fine motor control of limbs and coordination of posture

34
Q

corticospinal tract pathway

A

motor neurons exit pre central gyrus of frontal lobe, pass through internal capsule, then travel inferiorly through pyramids of medulla.

35
Q

lateral corticospinal tract

A

the fibers that innervate the limbs cross over to the contralateral side in the medulla. from here, they descend SC via lateral corticospinal tract

36
Q

ventral corticospinal tract

A

fibers that innervate the axial muscles remain on the ipsilateral side as they descend via ventral corticospinal tract.
-most of these fibers cross over to the contralateral side of SC when they reach cervical or upper thoracic area

37
Q

upper motor neurons
where they begin
where they synapse

A

begin in cerebral cortex
synapse with lower motor neurons in ventral horn of SC
-“pass messages from brain to SC”

38
Q

result of injury to upper motor neurons, the “why”, 2 examples

A

contralateral spastic paralysis and hyperreflexia
-spastic paralysis and hyperreflexia area result of inhibitory effects being blocked at level of injury which leads to over reactivity of the lower motor neurons.
ex) cerebral palsy, ALS

39
Q

significance of babinski sign/test

A

assesses integrity of corticospinal tract.
negative test (intact tract): firm stimulus to under side of foot produces a downward motion of all of the toes
positive test (damage to tract): firm stimulus to under side of foot produces upward extension of big toe with fanning of other toes.

40
Q

where do lower motor neurons begin and end

A

in the ventral horn and end at NMJ
“pass messages from SC to muscles”

41
Q

injury to lower motor neurons results in

A

ipsilateral flaccid paralysis/impaired reflexes.
(babinski sign would be absent with this injury)

42
Q

SSEP’s
which peripheral nerves are usually used
monitor the integrity of which column
what supplies this region of the SC?

A

via ulnar or tibial n
monitor integrity of dorsal column, medial lemniscus
supplied via posterior spinal arteries

43
Q

MEP’s
which peripheral nerves are usually used
monitor the integrity of which column
what supplies this region of the SC?

A

monitor integrity of corticospinal tract
perfused via anterior spinal artery

44
Q

most common site of SCI

A

C7

45
Q

complete SCI leads to
initially:
then:

A

-damage to upper motor neurons initially leads to flaccid paralysis and loss of sensation below level of injury. loss of bowel and bladder function occurs as well.
-after the acute phase, spinal reflexes return which leads to spasticity

46
Q

pathophysiology of neurogenic shock and sx triad, how long it can last

A

sympathectomy below level of injury
-bradycardia (impairment of cardioaccelerator fibers at T1-4, unopposed vagal tone, reduced inotropy as well),
HoTN (decreased SNS tone, venous pooling, decreased CO and BP) hypothermia (impairment of sympathetic pathways from hypothalamus to BV, cant vasoconstriction or shiver)
-can last 1-3w

47
Q

difference in sx of neurogenic versus hypovolemic shock

A

neurogenic: bradycardia, HoTN, hypothermia with warm peripheral extremities
hypovolemia shock: tachycardia, HoTN, cool/clammy extremities

48
Q

best pressor for a patient in neurogenic shock?

A

norepinephrine, restore SVR and inotropy

49
Q

major cause of morbidity and mortality for patients with cervical and upper thoracic lesions is

A

ineffective alveolar ventilation and inability to clear secretions

50
Q

describe when you should expect autonomic hyperreflexia, which SCI patients are at risk, and the pathophysiology

A

after the spinal shock phase ends (1-3w)
most patients with an injury above T6 will experience AH but its very unlikely if the injury is below T10
-there is a return of spinal sympathetic reflexes below level of injury. without inhibitory reflexes that would usually come from above, sympathetic reflexes below level of injury exist in an over reactive state. a profound* degree of vasoconstriction below the level of injury then occurs, which activates baroreceptor reflex in carotid sinus. body attempts to reduce afterload by vasodilation above level of injury. this is AH or “mass reflex”

51
Q

common events that cause AH include

A

stimulation of hollow organs (bladder, bowel uterus)
bladder catheterization
surgery (esp cysto or colonoscopy)
BM
cutaneous stimulation
childbirth

52
Q

classic presentation of autonomic hyperreflexia is (because of what reflex)

A

HTN and bradycardia–> baroreceptor reflex (carotid sinus)

53
Q

classic presentation of autonomic hyperreflexia is (because of what reflex)

A

HTN and bradycardia–> baroreceptor reflex (carotid sinus)

54
Q

other s/sx of AH

A

nasal stuffiness due to massive vasodilation above level of injury
HA and blurred vision d/t HTN
CVA, sz, LVF, dysrhythmias, pedema, MI d/t malignant HTN

55
Q

anesthetic management of a patient with AH

A

GA or spinal is best option for these patients- trying to prevent that stimulus in the first place
epidural can be used for laboring mother but doesn’t block sacral nerve roots to the same degree
HTN best tx with: remove stimulus, deepen anesthetic, rapid acting vasodilator such as nitrprusside
-tx brady with atropine or glyco
-AH may present in postop period as anesthesia effects wear off, FYI

56
Q

should you admin a positive chronotrope with vasoconstrictive properties to an AH patient

A

nah it will worsen HTN

57
Q

does lido jelly to the foley or cystoscope help with AH

A

nah fam we are past that

58
Q

pathophysiology of ALS

A

progressive degeneration of motor neurons in corticospinal tract
-astrocyte gliosis replaces affected motor neurons
-upper and lower motor neurons are affected
-etiology unknown

59
Q

ALS s/sx

A

-upper motor neuron involvement presents as spasticity, hyperreflexia, and loss of coordination
-lower neuron involvement presents as muscle weakness, fasciculations, and atrophy
-often begins in hands and over time spreads to rest of body including tongue, pharynx, larynx, chest
-ocular muscles are not affected
-autonomic dysfx is evidenced by orthostatic HoTN and resting tachycardia
-sensation remains intact

60
Q

only drug that reduces mortality of ALS

A

riluzole (NMDA receptor antagonist)

61
Q

most common cause of death for ALS patients

A

resp failure

61
Q

most common cause of death for ALS patients

A

resp failure

62
Q

anesthetic management of ALS patient
(succ? resp considerations?)

A

-no evidence supports clear benefit of any anesthetic technique
-lower motor neuron dysfx associated with extra junctional receptors aka NO succ
-bulbar muscle dysfunction increases the risk of pulmonary aspiration
-chest weakness reduces vital capacity and max MV
-consider postop MV

63
Q

ALS patient and NDNMB’s

A

increased sensitivity

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