Circulatory Disturbances and Traumatic Injuries of the Nervous System Flashcards

(69 cards)

1
Q

what is cerebrovascular disease?

A

stroke: any abnormality in the brain resulting from a pathologic process of the blood vessels

hallmark: sudden loss of neurologic function

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2
Q

you take a phone call from a client with an 8 year old dog that has acute onset of neurologic signs. they are not progressing. what is your first differential?

A

stroke

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3
Q

thrombosis and infarction

A
  • infarction less common in animals compared to humans (diet- atherosclerosis)
  • outcome depends on type and size of obstructed vessel, rapid onset of ischemia, vulnerability of the area of brain or spinal cord
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4
Q

what conditions could pre-dispose a patient to thrombosis or infarction?

A

atherosclerosis: causes in dogs include hypothyroidism, diabetes mellitus, hypercholesterolemia

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5
Q

what cell types are most susceptible to hypoxia?

A

neurons > oligodendrocytes > astrocytes > microglia > vascular endothelial cell

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6
Q

what cell is most susceptible to hypoxia?

A

neurons

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7
Q

ischemic infarcts

A
  • vascular (artery/arterioles) obstruction: thrombus or thromboembolism
  • gross lesion: well circumscribed area of yellow to tan discoloration and softening (malacia)
  • grey matter more susceptible (neurons in there)
  • with chronicity: see cavitation if large region or injury
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8
Q

what is the gross lesion of ischemic infarcts?

A
  • these are vascular obstructions
  • see well circumscribed area of tan to yellow discoloration = malacia
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9
Q

what are the 2 types of infarcts?

A
  1. ischemic
  2. hemorrhagic
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10
Q

hemorrhagic infarcts

A
  • vascular damage/rupture leading to leakage of RBCs
  • venous thrombosis
  • gross lesion: regional area of parenchymal hemorrhage
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11
Q

chronic infarcts leads to

A

cavitation

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12
Q

fibrocartilaginous emboli (FCE)

A
  • common in dogs, uncommon in other species
  • peracute (usually lateralized) spinal signs without pain
  • exact mechanism unknown: herniation of degenerative disk material (nucleus pulposus) Hansen type 1 –> vasculature –> occlusive emboli –> ischemic injury
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13
Q

what is the proposed pathogenesis of fibrocartilaginous emboli?

A

exact mechanism unknown: herniation of degenerative disk material (nucleus pulposus) Hansen type 1 –> vasculature –> occlusive emboli –> ischemic injury

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14
Q

fibrocartilaginous emboli is common in what species

A

dogs

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15
Q

edema

A

excess fluid accumulation in the CNS parenchyma: can be associated with most disease processes

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16
Q

what are the 3 types of cerebral edema?

A
  1. vasogenic edema: most common
  2. cytotoxic edema
  3. interstitial edema
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17
Q

vasogenic edema

A
  • most common
  • disruption of BBB
  • increased vascular permeability = ECF accumulation
  • white matter most affected (spongiosis)
  • common causes: trauma, neoplasia, inflammation and some toxic/metabolic conditions
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18
Q

what are common causes of cerebral edema?

A

trauma, neoplasia, inflammation

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19
Q

what cells are most affected by vasogenic edema?

A

white matter

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20
Q

cytotoxic edema

A
  • altered cellular metabolism = intracellular fluid accumulation
  • low O2 = interference with ATP dependent Na K pumps in cell membrane
  • swelling of neurons, glial and endothelial cells (grey and white matter affected)
  • common causes: hypoxia, neoplasia, toxic/metabolic conditions (ex salt poisoning in pigs, hepatic encephalopathy)
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21
Q

what causes cytotoxic edema?

A
  • altered cellular metabolism = intracellular fluid accumulation
  • low O2 = interference with ATP dependent Na K pumps in cell membrane
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22
Q

what are common causes of cytotoxic edema?

A

hypoxia, neoplasia, toxic/metabolic conditions (ex salt poisoning in pigs, hepatic encephalopathy)

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23
Q

what is the unique cell type seen with hepatic encephalopathy?

A

alzheimer type 2 astrocytes

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24
Q

what are the gross lesions with edema?

A
  • flattened gyri and shallow sulci
  • clear, watery fluid in leptomeninges
  • posterior shifting of brain: ie herniation thru foramen magnum
  • white matter may be soft, wet, pale yellow
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24
interstitial edema (hydrostatic)
- accumulation of fluid in the periventricular white matter associated with increased ventricular pressure (see with bad hydrocephalus or hydromyelia)
25
what bacteria causes focal symmetrical encephalomalacia?
clostridium perfringens type D (epsilon toxin)
26
pathogenesis of Clostridium perfringens type D
- degeneration of vascular endothelial tight junctions = swelling and rupture of perivascular astrocyte processes = leakage of fluid and increased intracerebral pressure = parenchymal necrosis systemic: see leakage of fluid in all sorts of places: abdomen, cardiac, pulmonary edema, petechiation
27
what is the classic animal for clostridium perfringens type D?
sheep and goats subacute and chronic cause FSE, acute and peracute is protein rich fluid around blood vessels brain involvement uncommon in goats and cattle. in these species with chronic issues, would see colitis
28
what is the big concern with edema
herniation
29
where can the brain herniate?
1. thru foramen magnum (foramenal herniation) 2. under tentorium cerebelli (transtentorial herniation) 3. under the falx cerebri (falcine herniation) 4. thru a defect in the skull (ex trauma/fracture)
30
transtentorial herniation
when the brain herniates under the tentorium cerebelli
31
traumatic injury of the nervous system
- external trauma: forces external to body. HBC, kicks, falls, gunshots, bites - internal injury: intrinsic physical disturbances. disc extrusion, vertebral abscesses, neoplasia, congenital malformation - less frequent in animals than in humans: not exposed to trauma causing situations as commonly. anatomic differences: brain volume to cranium volume ration is less in animals
32
what trauma patients are susceptible to what 2 phases of injury?
1. primary injury: direct trauma or forces acting on brain 2. secondary injury: series of events that lead to continued injury to neurons/glial cells (ie days after)
33
primary injury with TBIs
- direct trauma: fractures, hemorrhages, edema, direct injury to parenchyma - forces acting on brain: acceleration, deceleration, rotational forces
34
acceleration/deceleration and rotational forces cause what types of damage to the brain?
acceleration/deceleration: superficial grey matter (hemorrhages, contusion, tearing of neuronal tissue) rotational: deeper white matter (causing concussive injuries and axonal damage)
35
secondary injury with TBIs
series of events that lead to continued injury to neurons/glial cells major mediators: oxygen free radicals, excitatory amino acids, nitric oxides
36
what are the 2 big types of brain trauma?
1. concussion: diffuse but transient brain injury associated with temporary loss of consciousness. typically no lesions and minimal microscopic lesions. uncommon in animals 2. contusion: focal brain injury which may result in unconsciousness. usually grossly detectable and superficial area of brain hemorrhage. often associated with a skull fracture
37
what is a concussion?
diffuse but transient brain injury associated with temporary loss of consciousness. typically no lesions and minimal microscopic lesions. uncommon in animals
38
what is a contusion?
focal brain injury which may result in unconsciousness. usually grossly detectable and superficial area of brain hemorrhage. often associated with a skull fracture
39
contusions are often associated with
skull fractures
40
T/F: concussions typically have no gross lesions
true
41
what are the gross lesions of a contusion?
superficial area of brain hemorrhage, often associated with skull fracture
42
hemorrhage can be seen with a wide variety of causes, what are some examples of these
1. TRAUMA most common 2. DIC 3. damage to vessels/vasculitis (virus, septic, immune, neoplasia, etc
43
what is the most common site to see damage to following brain trauma?
subarachnoid hemorrhage
44
what is the common site of traumatic brain injury in. horses?
they rear and fall over on their back, break the basisphenoid bone displaced bone lacerates large vessels at base of brain hemorrhage becomes the dominant lesion
45
what is the dominant lesion of TBI in horses? what is this from?
hemorrhage is the dominant lesion, from fracture of the basisphenoid bone from rearing over backward
46
what factor will determine the degree of spinal cord injury?
amount of space between spinal cord and vertebral canal is important
47
where is the extradural space the greatest?
cervical vertebral column, cranial thoracic and caudal lumbar region = spinal cord compression less likely intercapital ligaments (T2-T10): lower incidence of intervertebral disc extrusion in this region
48
major mechanisms of spinal cord injury
1. contusion: focal hemorrhage associated with fracture, luxation, subluxation or disc herniation 2. compression: extramedullary pressures (disc herniation, neoplasia, fracture, malformation
49
what are examples of compression of the spinal cord?
extramedullary pressures: disc herniation, vertebral and meningeal neoplasia, vertebral fracture/subluxation, vertebral malformation
50
microscopic lesions of spinal cord trauma
- hemorrhage (more prominent in grey matter) - axonal/myelin degeneration at site of compression - degeneration of axon and myelin sheath distal to site of injury (Wallerian degeneration)
51
acute spinal cord compression
- direct mechanical injury to spinal cord (contusion) - hypoxia: caused by injury to vessels, compression of vessels, release of NTs - ex: hansen type 1 intervertebral disc extrusion
52
hansen type 1 intervertebral disc extrusion is an example of what spinal cord injury?
acute spinal cord compression
53
what is an example of acute spinal cord compression?
hansen type 1 intervertebral disc extrusion
54
hansen type 1 disc extrusion
- acute extrusion of nucleus pulposus thru annulus fibrosus and into canal - usually associated with "chondroid" degeneration/metaplasia of nucleus pulposus" genetically programmed and starts early (6 mo) - chondrodystrophic breeds of dogs - lesions: degenerative, chalky white mineralization of nucleus pulposus
55
hansen type 1 disc extrusion is usually associated with
chondroid degeneration/metaplasia of nucleus pulposus: genetically programmed and starts early (6 mo)
56
in what breeds do we see hansen type 1 disc extrusion in?
chondrodystrophic breeds
57
chronic spinal cord compression
- direct but slowly developing injury to cord - low grade hypoxia due to compression of vessels: reduced perfusion, vascular stasis, increased hydrostatic pressure leads to edema ex: hansen type 2 intervertebral disc protrusion, cervical vertebral stenotic myelopathy (wobblers)
58
what are examples of chronic spinal cord progression?
1. hansen type 2 intervertebral disc protrusion 2. cervical vertebral stenotic myelopathy (wobblers)
59
1. hansen type 2 intervertebral disc protrusion 2. cervical vertebral stenotic myelopathy (wobblers) these are both examples of
chronic spinal cord compression
60
what is wobbler's syndrome and what does it lead to?
chronic spinal cord compression: cervical vertebral stenotic myelopathy. low grade hypoxia due to compression of vessels reduced perfusion, vascular stasis, increased hydrostatic pressure leading to edema
61
hansen type 2 disc protrusion
- bulging of disc material into vertebral canal - associated with "fibrous degeneration" of annlus (usually begins around 8-10 years of age) - more common in non-chondrodystrophic dogs
62
when does hansen type 2 disc protrusion begin?
8-10 years of age
63
a severe complication of spinal cord compression often leading to euthanasia is
ascending/descending hemorrhagic myelomalacia seen more with type 1 IVDD 12-24 hours after injury dog seems to be doing better and then crashes. get hemorrhage and necrosis that ascends up. unsure on pathogenesis
64
ascending/descending hemorrhagic myelomalacia
spinal cord compression consequence that is severe; acute and chronic lesions can result in these. more common with type 1 IVDD, 12-24 hours after injury
65
cervical vertebral stenotic myelopathy "wobblers syndrom"
- horses and large breed dogs - osseous: young adults: vertebral malformations often associated with degeneration of facet joints (osteochondrosis dissecans) - disc-associated: adult dogs born with congenital vertebral canal stenosis
66
what are the 2 types of wobblers syndrome?
- osseous: young adults: vertebral malformations often associated with degeneration of facet joints (osteochondrosis dissecans) - disc-associated: adult dogs born with congenital vertebral canal stenosis: prone to cord compression bc of smaller extradural space. C5-C6, C6-C7
67
what are the 2 characterizations of wobblers syndrome used in horses?
1. static: >1 year of age, compression regardless of neck position. C5-C6 and C6-C7 2. dynamic: usually 8-18 months of age. flexed neck: C3-C4, C4-C5
68
what is a necessary diagnostic for wobblers syndrome?
myelogram: actually see if you are getting compression