Unit 4 spinal cord vascular supply and lesions Flashcards

(49 cards)

1
Q

What is the vascular supply?

A

PICA
Vertebral
Posterior spinal
Anterior Spinal

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2
Q

What does the anterior spinal arteru supply?

A

ventral surface of the spinal cord

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3
Q

what does the posterior spinal arteries (2) supply?

A

the dorsal surface of the spinal cord (may also be from some of the PICA)

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4
Q

What are the spinal radicular arteries? What do they supply?

A
  • Arise from segmental spinal arteries
  • Supply the meninges, roots of spinal nerves, and dorsal root ganglion
  • 6-10 of the larger radicular arteries can reach and anastomose with anterior spinal artery and posterior spinal artery.
  • Larger radicular arteries are crucial for supplying blood to the lower spinal cord where main arteries are insufficient on their own.
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5
Q

What is the great radicular artery of adamkiewicz?

A
  • a radicular artery arising between T9 and T12; provides the major blood supply to the lumbar and sacral cord; susceptible to infarction from episodes of hypotension.
  • Can cause spinal stroke. Primary artery for the spinal stroke
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6
Q

Cross Section PIC

A

A. Anterior view showing principal sources of blood supply: the anterior spinal artery from the vertebral arteries, and radicular branches farther caudally.

B. Cross-sectional view through the spinal cord showing paired posterior spinal arteries and a single anterior spinal artery.

C. Cross section of the arteries in the cervical spinal cord. There are numerous variations in the vascular supply.

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7
Q

anterior spinal artery

A
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8
Q

posterior spinal artery

A
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9
Q

What are the traumatic cuases of SCI

A
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10
Q

what are the non-traumatic causes of SCI?

A
  • tumors
  • myelomenigeocele
  • viral and bacterial infections
  • prolapsed disc, vertebral subluxation
  • vascualr problems
  • spinal stenosis
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11
Q

What are the common misdiagnoses of SCI?

A
  • Non-traumatic SCI is often misdiagnosed as a musculoskeletal condition
  • Happens when primary complaint is back pain; thorough exam may reveal changes in reflexes below level of pain or changes in bowel/bladder
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12
Q

pathophys

What is the primary injury of the spinal cord?

A
  • Spinal cord is protected by the surrounding bone of the vertebrae, but in severe trauma, the vertebrae fracture or dislocate.
  • Fracture, dislocation, and/or subluxation of the vertebrae are the most common causes of SCI.
  • The damaged bony segments impinge the spinal cord and immediately cause a lesion.
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13
Q

What is the secondary spinal cord injury toxic enviorment created by the initial injury?

A
  • Red blood cells flood the gray matter, and the iron and hemoglobin they contain are toxic to neurons that were not initially damaged
  • As bystander neurons die, they release neurotoxins and glutamate that go on to kill other neurons beyond the primary injury site.
    Free radicals, reactive oxygen species, and peroxidases are produced which degrade myelin, cell membranes and cause further cell death.
  • With this necrotic cell death, edema increases and the damaged blood vessels are sealed a few segments away from the primary injury, causing ischemia.
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14
Q

What is the secondary spinal cord injury neuroinflamtion?

A
  • Activated microglia produce high levels of proinflammatory cytokines and chemokines
  • Reactive astrocytes create a glial scar that acts as a physical barrier to regenerating axons & produce chemical inhibitory barriers (CSPGs)
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15
Q

what is the timeline (phases) of the secondary spinal cord injury?

A
  1. Phase 1: lasts up to 24 hours; areflexia below the level of injury; ends with return of polysynaptic reflexes
  2. Phase 2: brief; injured neurons become more responsive to neurotransmitter release into the synapse, a condition known as denervation hypersensitivity; this promotes the return of monosynaptic cutaneous reflexes (initial reflex return).
  3. Phase 3: can last up to four weeks; new synapses begin to grow in the damaged areas, with local interneurons dominating. (early hyper-reflexia UMN presentation)
  4. Phase 4: spinal shock resolves into a classic upper motor neuron presentation as newly developed local circuits are accompanied by loss of cortical inhibition. (late hyper-reflexia)
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16
Q

What is the process for identifying likely lesion effects?

A
  1. Where is the lesion? Right / left / dorsal / ventral / central
  2. Which white matter tracts are damaged?
  3. Which areas of gray matter are damaged?
  4. What is the function of those areas?
  5. Do those tracts decussate?
    * Is the lesion above or below that area of decussation?
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17
Q

C?

A

Loss of sensation AT the level of the lesion.

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18
Q

B?

A

Loss of light touch sensation AT and BELOW the level of the lesion.

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19
Q

D?

A

Loss of motor function AT the level of the lesion.

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20
Q

A?

A

Loss of motor function AT and BELOW the level of the lesion

lateral corticospinal tract

21
Q

Transverse cord lesions.
what is damaged?

A

all sensory and motor pathways are either partially or completely interrupted.

22
Q

Transverse cord lesions.
what function(s) are lost?

A
  • sensory: a;; forms of sensation are diminished bilaterally; at and bellow the level of lesion.
  • Motor: bilateral weakness (UMN signs); at and bellow the level of the lesion (lateral cortical spinal tract is the UMN before it goes to the dorsal root ganglia) (and LMN)
23
Q

transvers cord lesion
what are common causes?

A
  • trauma
  • tumors
  • MS
  • transceres myelitis
24
Q

Brown Sequard Syndrome/ Hemicord Lesion
What is damaged?

A

Dorsal Columns DCML
Anterolateral/ spinothalamic tracts
lateral Corticospinal tract

25
Brown Sequard Syndrome/ Hemicord Lesion What fucntions are lost?
Sensory: * Ipsilesional loss of light touch, vibration, joint position; at and below the level of lesion * Contralesional loss of pain and temperature; 1-2 segments below the level of lesion and below * Ipsilesional strip of pain/temp loss of 1-2 segments; at the level of the lesion Motor: * Ipsilesional motor weakness (UMN signs); at and below the level of injury
26
Brown Sequard Syndrome/ Hemicord Lesion Common causes?
* penetrating injury (stab wound) * closed injury with bony fracture
27
Central Cord Syndrome What is damaged?
* Spinothalamic fibers crossing in ventral/anterior while commissure * Ventral horn cells (LMN) * Large Lesion: maybe posterior columns / anterolateral columns / lateral CST
28
Central Cord Syndrome What function(s) are lost?
Sensory * Bilateral loss of pain and temp; at 1-2 levels below the level of the lesion * maybe: bilat reduction of light touch, vibration, proprioception; at and below lesion * maybe: bilat reduction of pain and temp; at and below level of injury except sacral sparing Motor: * Bilateral loss of volitional movement (LMN signs); only at the level of the lesion * maybe: Bilateral weakness (UMN signs); at and below the level of the lesion.
29
Central Cord Syndrome Common causes?
* Degenerative narrowing of spinal canal * Severe neck hyperextension injury
30
If there were a large central cord lesion and part of the lateral corticospinal tract was damanged... Would the UMN signs be more pronounced in the UE or LE? WHY?
UE It would get more of the cervical and thoracic region rather than the lumbar or sacral more then the LE due to this region
31
Anterior spinal cord syndrome what is damaged?
* Spinothalamic tract * Ventral horns * Large Lesion: maybe lateral corticospinal tract
32
Anterior spinal cord syndrome What function(s) are lost?
Sensory: * Bilateral loss of pain and temp; at and below level of lesion Motor: * Bilateral loss of volitional movement (LMN signs); at the level of lesion * Maybe: Bilateral weakness (UMN signs); at and below the level of the lesion. (corticospinal tract)
33
Anterior spinal cord syndrome what causes?
* Anterior spinal artery infarct * Traumatic: flexion injury (common < 35yo) * Multiple sclerosis
34
Posterior spinal cord syndrome What's damaged?
* dorsal columns DCML * large lesion: maybe encroach on lateral corticospinal tract
35
Posterior spinal cord syndrome what functions are lost?
* Sensory: Bilateral loss of light touch, vibration, proprioception; at and below the level of the lesion. * Motor: Maybe: Bilateral weakness (UMN signs); at and below the level of the lesion.
36
Posterior spinal cord syndrome Common causes?
Vascular disruption of posterior spinal arteries from trauma or disease
37
Conus Medullaris
* Injury at the L1 vertebral level, where the spinal cord ends. * Affects nerves that originate from this part of the cord and nerves that travel through this space. * These problems have a sudden onset and usually a bilateral presentation.
38
Conus Medullaris presentation
* deep aching pain in the low back * numbness in the groin, thigh, leg, or foot * urinary retention, bowel dysfunction * bilateral lower limb weakness mucg UMN involvment, some LMN involvement
39
Cauda Equina (hourse tail)
Simultaneous compression of multiple lumbosacral nerve roots below the level of the conus medullaris; (below the L2 vertebral level)
40
Cauda equina presentation
* severe, stabbing (radicular) pain along dermatomal patterns * “saddle anesthesias” sensory disturbance * weakness in distribution of nerve root (LEs) * symptoms usually unilateral Only LMN involvement
41
What injurys are these?
1. transverse cord lesion 2. hemicord lesion 3. central cord syndrome
42
spinal subdural/ epidural hematoma
Accumulation of blood in subdural or epidural space that can mechanically compress the spinal cord.
43
multiple sclerosis
Chronic autoimmune disease, typically progressive. Involves damage to the myelin sheaths of nerve cells in the brain and spinal cord. Symptoms may include numbness, impairment of speech and of muscular coordination, blurred vision, and severe fatigue.
44
Degenerative disk disease
Condition in which the discs between vertebrae lose structure, fragmentation and herniation, often related to aging. Symptoms: back or neck pain; sometimes weakness, numbness, and hot, shooting pains in the arms or legs (radicular pain).
45
46
Transverse myelitis
Inflammation the spinal cord. Myelin damage. Etiology includes infections and immune systems disorders. There is often a band-like sensation across the trunk of the body, with sensory changes below. Symptoms include pain, sensory problems, weakness in the, bladder and bowel problems; may develop suddenly (hours) or over days or weeks.  
47
Amyotrophic lateral sclerosis
Progressive neurodegenerative disease that causes damage to motor neurons and subsequent loss of motor control. Early symptoms include muscle twitches/cramps, weakness or stiffness, gradually all muscles are affected and difficulty speaking, swallowing and breathing occur.
48
Spina Bifida
Spina bifida is a birth defect that occurs when the spine and spinal cord don't form properly. It's a type of neural tube defect. Symptoms depend on the severity but could include none, bladder and bowel dysfunction, walking and mobility problems, orthopedic complications, hydrocephalus, etc.
49
Spinal muscular atrophy
Spinal Muscular Atrophy refers to a group of hereditary diseases that damages and kills motor neurons in the brain and spinal cord. Symptoms may include reduced movement, contractures, reduced muscle tone, lack of tendon reflexes, problems swallowing and feeding. Life expectancy depends on which SMA type an individual has.