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SA DX & TX I > Exam 2 - Spinal Cord Disease > Flashcards

Exam 2 - Spinal Cord Disease Flashcards

1
Q

if there is a lesion in the spinal cord at C1-C6, what would you expect to see in the animals gait?

A

long-strided gaits in all 4 limbs

-overextension
-UMN paresis

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2
Q

if there is a lesion in the spinal cord at C6-T2, what would you expect to see in the animals gait?

A

two engine gait

thoracic - short stride, LMN paresis
pelvic - long stride, UMN paresis

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3
Q

if there is a lesion in the spinal cord at T3-L3, what would you expect to see in the animals gait?

A

pelvic limb - long strided & harder to advance legs

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4
Q

if there is a lesion in the spinal cord at L4-Cd5, what would you expect to see in the animals gait?

A

normal thoracic limbs

pelvic limbs - short strided

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5
Q

what spinal cord lesions will have deficits in all 4 legs with postural reactions?

A

C1-C6 & C6-T2

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6
Q

what spinal cord lesions will have deficits in the pelvic limbs with postural reactions?

A

T3-L3 & L4-Cd5

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7
Q

T/F: mentation is normal in spinal cord disease as well as cranial nerve assessment

A

true

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8
Q

T/F: animals with cervical spinal cord disease often are more so ataxic/paretic in the pelvic limbs than the thoracic

A

true

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9
Q

what is schiff-sherrington syndrome?

A

extensor rigidity in the thoracic limbs without
thoracic limb paresis or ataxia occurs due to loss of the fasciculus proprius, which normally exerts an inhibitory effect on C6-T2 alpha
motor neurons

spinal shock may be present

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10
Q

what is spinal shock?

A

severe, acute T3-L3 myelopathy pelvic limb hyporeflexia that occurs because of the loss of facilitory input to LMNs at the lumbosacral intumescence

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11
Q

when & why is the panniculus reflex used?

A

assesses the cutaneous trunci & efferent output through the lateral thoracic nerve (C8-T1 nerve roots)

severe lesions in the T3-L3 spinal cord or loss of C8-T1 alpha motor neurons or associated nerve roots

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12
Q

with spinal cord injury, function is classically lost in what order?

A
  1. proprioception
  2. motor/urinary voiding
  3. superficial nociception
  4. deep nociception
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13
Q

if you do a CSF analysis & have a normal cell count & protein, what can you rule out?

A

meningitis & meningomyelitis

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14
Q

T/F: CSF abnormalities are not often specific to one etiology, so it is best used in combination with vertebral column imaging

A

true

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15
Q

radiographs are highly specific for what?

A

fractures

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16
Q

what are radiographs good for in spinal disease?

A

bone tumors & vertebral fractions

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17
Q

what are radiographs not great for in spinal disease?

A

disk herniation

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18
Q

how are lesions classified in myelograms?

A
  1. extradural
  2. intradural-extramedullary
  3. intramedullary
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19
Q

what are some reasonable uses for myelograms in spinal cord disease?

A

disk herniation & instability

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20
Q

what are the disadvantages in using myelograms in spinal cord disease?

A

artifacts, not a multi-planar technique, lesion misclassification

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21
Q

what are the adverse effects associated with myelograms?

A

seizures, hypotension, & death

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22
Q

what imaging modality is the standard of care for diagnosing vertebral fractures & luxation?

A

computed tomography

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23
Q

what are the potential disadvantages in using CT for spinal cord disease?

A

potential for missing soft tissue lesions & non-mineralized disks

if no lesions seen - consider IV contrast

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24
Q

T/F: CT is great for diagnosing lesions in the CNS

A

false

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25
Q

what is the imaging modality of choice for spinal cord/vertebral column pathology especially parenchymal lesions?

A

MRI

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26
Q

other than spinal cord/vertebral column pathology/parenchymal lesions, what else is MRI useful for?

A

lesions in the brain & vestibular system

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27
Q

what are the advantages of using MRI for diagnosing spinal cord disease?

A

more detailed location of the pathology, better evaluation of prognosis, & different weightings

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28
Q

the better soft tissue detail provided in MRI scans is better why?

A

better ability to:
-detect soft tissue masses
-detect subtle disk protrusion
-detect spinal cord edema & hemorrhage

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29
Q

in T1 weightings, ____ is hypointense (dark) & ____ is hyperintense (bright)

(fat/fluid)

A

fluid

fat

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30
Q

in T2 weightings, ____, ____, ___, & _____ may show up hyperintense (bright)

A

fluid, CSF necrosis, edema, & hemorrhage

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31
Q

MRI is the only imaging modality that can be used to diagnose what?

A

FCE & syringohydromyelia

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32
Q

in acute spinal cord injury, what is the primary injury?

A

initial mechanical insult the spinal cord suffers

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33
Q

what are the 2 generally most important sub-forms of primary injury?

A

compression & contussions

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34
Q

in spinal cord disease, what is secondary injury?

A

biochemical cascade that results because of the primary injury

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35
Q

what are the sub-classifications of secondary injuries?

A
  1. oxidative
  2. vascular
  3. immunological
  4. excitotoxicity
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36
Q

why should steroids not be used in treatment of any acute & severe traumatic spinal cord injuries?

A

they increase the risk of adverse effects, such as:

UTI development, gi ulcers, & diarrhea

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37
Q

if your treatment in an acute spinal cord injury is aiming to address the primary injury, what can that include?

A

laminectomy and/or stabilization

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38
Q

if your treatment in an acute spinal cord injury is aiming to address the secondary injury, what can that include?

A

fluid therapy & analgesia - OPIODS, NSAIDS, muscle relaxers, etc

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39
Q

what is the most important component of aftercare? why? what should it include?

A

nursing!!!

patients often will have significant disability

rotate the patient, ensure access to food & water, & evaluate bladder emptying because management may be necessary

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40
Q

how can you look to see if urinary function is normal in an animal with spinal cord injury/disease?

A

observe them, post-voiding ultrasound, post-voiding catheterization

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41
Q

what lesion location is associated with upper motor neuron bladder?

A

lesion cranial to S1 spinal cord

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42
Q

what injury severity is associated with upper motor neuron bladder?

A

usually animal is non-ambulatory

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43
Q

what is the pathogenesis of UMN bladder?

A

pons can’t sense when the bladder is full & signaling to the bladder is lost - sensory & UMN pathways are disrupted

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44
Q

what are the clinical signs & features of UMN bladder?

A

LMN pelvic signs, increased tone to the internal urethral sphincter, firm bladder because increased tone to the detrussor muscle, external urethral sphincter remains closed, & reflex dysynergia

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45
Q

what are the clinical signs & features of LMN bladder?

A

flaccid bladder, constant leaking of urine due to loss of innervation of pelvic & pudendal nerves, intact pathways to internal urethral sphincter, & loss of detrussor muscle function & LMNs to external urethral sphincter

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46
Q

what injury severity is associated with lower motor neuron bladder?

A

non-ambulatory patient

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47
Q

what lesion location is associated with lower motor neuron bladder?

A

lesion in S1-S3

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48
Q

what is the basic bladder treatment plan in spinal cord injuries?

A

eliminate over-distension with bladder expression or catheterization

UTIs - treating only when voluntarily voiding & preventing ascending infection/sepsis

pharmacotherapy

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49
Q

what is the first line of drugs used for UMN bladder?

A

alpha-antagonists to relieve internal sphincter spasticity

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50
Q

what 2 drugs are the most common alpha-antagonists used in UMN bladder?

A

phenoxybenzamine & prazosin

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51
Q

how does bethanecol work for UMN bladder treatment?

A

increases detrussor contractility & may also increase internal sphincter tone

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52
Q

why should you wait to use bethanecol until after the patient is on alpha-antagonists?

A

the bethanecol may increase internal sphincter tone which would add to your problems

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53
Q

what is your first choice of drug for LMN bladder?

A

bethanecol

can add alpha blockers if it’s ineffective

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54
Q

which of the following is true in an UMN bladder?

a. tone to the external urethral sphincter is reduced
b. alpha agonists are the best treatment
c. bethanecol is the best treatment
d. muscarinic tone is preserved

A

d. muscarinic tone is preserved

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55
Q

T/F: in an UMN bladder, the lack of parasympathetic ability to inhibit sympathetic control is what causes clinical signs

A

true

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56
Q

what are very important components to recovery in animals with spinal cord injuries?

A

physical therapy - active weight bearing, prevent disuse atrophy, passive range of motion, & can shorten recovery time

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57
Q

T/F: in some animals with spinal cord injury, cage restriction is required

A

true

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58
Q

why is cage restriction required in FCE recovery? what about post-surgical candidates & vertical column instability?

A

FCE - prevent self-inflicted trauma secondary to paresis or ataxia

post surgery/instability - extremely important for healing of surgical incisions, closure disk-associated annular tears, & will enable fusion in animals with vertebral column instability

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59
Q

why do you want to not overdo cage rest?

A

can lead to disuse atrophy

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60
Q

what type of IVD does this represent? what is it?

A

type II - slow process where the annulus fibrosis thickens up

PROTRUSION

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61
Q

what type of IVD does this represent? what is it?

A

type I - acute injury

EXTRUSION

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62
Q

what fibers make up the annulus fibrosis?

A

tough type II collagen fibers

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63
Q

when should conservative treatment be used for cervical disk herniation patients?

A

acute, single episode of neck pain & mild paresis or a client unwilling to consider surgery

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64
Q

what is the conservative treatment plan used for cervical disk herniation?

A

blood work + rads, ‘don’t know’ speech

cage rest, anti-inflammatories (NSAIDS), & analgesia

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65
Q

when should surgical treatment be used for cervical disk herniation patients?

A

multiple episodes or acute significant ataxia

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66
Q

what is the percentage of recovery in an animal with cervical disk herniation that is hyperesthetic only or has minimal ataxia?

A

prognosis >90% recovery

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67
Q

what is the percentage of recovery in an animal with cervical disk herniation that is non-ambulatory tetraparetic or tetraplegic?

A

prognosis 70-75%

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68
Q

what surgeries are performed to correct herniated cervical disks?

A

ventral slots & dorsal laminectomies

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69
Q

what is the agent that causes non-infectious inflammatory steroid-responsive meningitis?

A

unknown - likely auto-immune

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70
Q

what is the pathogenesis of non-infectious inflammatory steroid-responsive meningitis?

A

immune-mediated vasculitis of the leptomeningeal arteries with meningitis

infiltration of the CNS parenchyma sometimes present

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71
Q

what animals are typically affected by non-infectious inflammatory steroid-responsive meningitis?

A

6 month -2 year old large breed dogs & beagles

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72
Q

what are the clinical signs seen with non-infectious inflammatory steroid-responsive meningitis?

A

severe neck pain, +/- cervical myelopathy, may be febrile & have peripheral neutrophilia, negative culture, unremarkable imaging, & abnormal CSF fluid

73
Q

what is characteristic of the CSF fluid in non-infectious inflammatory steroid-responsive meningitis?

A

significant neutrophilic pleocytosis with elevated proteins!!

74
Q

what is the treatment used for non-infectious inflammatory steroid-responsive meningitis?

A

immunosuppressive doses of corticosteroids, can add antibiotic while waiting for titer, & analgesia

75
Q

what is the prognosis for non-infectious inflammatory steroid-responsive meningitis?

A

often good

76
Q

what are some examples of viruses that can be a cause of infectious/inflammatory spinal cord disease?

A

FIV, FeLV, & distemper

77
Q

what are some examples of rickettsials that can be a cause of infectious/inflammatory spinal cord disease?

A

ehrlichia, RMSF

78
Q

what are some examples of funguses that can be a cause of infectious/inflammatory spinal cord disease?

A

cryptococcosis, histo, blasto, & coccidiomycosis

79
Q

what are some examples of protozoas that can be a cause of infectious/inflammatory spinal cord disease?

A

toxoplasmosis in both dogs & cats

neosporosis in dogs

80
Q

what animals are more commonly affected by lymphoma causing spinal cord disease?

A

middle aged cats

81
Q

what animals are more commonly affected by meningioma causing spinal cord disease?

A

older dogs with chronic issues - usually cranial cervical region

82
Q

what are some examples of metastatic neoplasia that can cause spinal cord disease?

A

prostatic adenocarcinoma, melanoma, hemangiosarcoma, & lymphoma

83
Q

what does FCEM stand for?

A

fibrocartilaginous embolic myelopathy

84
Q

what is the pathogenesis of FCEM?

A

fibrocartilage obstructs a spinal artery or vein resulting in spinal cord ischemia/infarction

85
Q

what part of the CNS is more susceptible to FCEM?

A

gray matter

86
Q

what animals are typically affected by FCEM?

A

adult, large breed dogs with signs that develop after exercise

87
Q

what are the clinical signs associated with FCEM?

A

develops after exercise

can worsen neurologically for 24 hours, initially yelp, or appear uncomfortable

88
Q

what is seen on the neuro exam that is supportive of FCEM?

A

asymmetric myelopathy without paraspinal hyperesthesia

89
Q

what lesion location is more common in FCEM?

A

T3-L3 or L4-S3 more common than cervical

90
Q

what is the definitive diagnostic used for FCEM?

A

necropsy

91
Q

how is FCEM diagnosed?

A

diagnosis of exclusion - neuro exam & history consistent with the disorder, with a frequently normal CSF

92
Q

what is the best ante-mortem diagnostic test for FCEM?

A

MRI shows T2 weighted hyperintensity

93
Q

T/F: in FCEM, the myelogram & CT are usually normal but you may have spinal cord swelling which is non-specific

A

true

94
Q

what is a poor prognostic indicator for FCEM?

A

no deep pain

95
Q

T/F: in FCEM, LMN or bilateral signs may have a slower recovery than lateralized UMN paresis

A

true

96
Q

what is the treatment for FCEM?

A

fluid therapy & supportive care

97
Q

what are the 2 overlapping causes associated with cervical spondylomyelopathy?

A
  1. malformation & malarticulation in the young giant breed - static form
  2. instability & malarticulation in older, large breed dogs - dynamic form
98
Q

what is the pathogenesis of cervical spondylomyelopathy?

A

compression caused by a combination of vertebral malformation, malarticulation, & instability

99
Q

what dog breed is most commonly affected by the static form of cervical spondylomyelopathy?

A

great danes

100
Q

what is the pathogenesis of the static form of cervical spondylomyelopathy?

A

vertebral body tipping & stenotic canals, secondary articular process osteophytosis, ligamentous hypertrophy, & synovial cysts

usually gradual spinal cord compression - predominantly dorsal to dorsolateral

101
Q

what may be seen on a VD myelogram on a patient with the static form of cervical spondylomyelopathy?

A

hourglass shape

102
Q

what dog breed is most commonly affected by the dynamic form of cervical spondylomyelopathy?

A

doberman pinscher

103
Q

what is the pathogenesis of the dynamic form of cervical spondylomyelopathy?

A

vertebral instability may lead to disk degeneration & herniation, hypertrophy of the ligamentum flavum/DLL, articular process osteophytosis & synovial cysts, & vertebral body tipping

compression usually ventral & dorsal & often dynamic

104
Q

what are the clinical signs of cervical spondylomyelopathy?

A

slowly progressive, chronic, painful myelopathy - some animals may have an apparently acute onset of signs

signs may wax & wane

105
Q

what is the common lesion location of cervical spondylomyelopathy in great danes?

A

lesions in the mid-cervical region

106
Q

what is the common lesion location of cervical spondylomyelopathy in older dogs with instability?

A

lesions in the caudal cervical region

107
Q

how is cervical spondylomyelopathy diagnosed using radiographs & CT?

A

rads - hypertrophy of the articular processes, disk space collapse, vertebral body tipping, & canal stenosis

CT - use to confirm diagnosis

108
Q

what is the treatment for cervical spondylomyelopathy?

A

mildly affected animals may be managed medically, but surgery is the definitive therapy

109
Q

what is the surgical treatment for giant breeds with cervical spondylomyelopathy?

A

dorsal decompression

110
Q

what is the surgical treatment of cervical spondylomyelopathy in breeds with instability?

A

distraction/fusion

111
Q

what is the prognosis for non-ambulatory animals with cervical spondylomyelopathy?

A

guarded

112
Q

what is the recurrence of cervical spondylomyelopathy?

A

20-30%

113
Q

what is the pathogenesis of atlantoaxial subluxation?

A

hypoplasia or aplasia of the dens, loss of ligamentous support, the dens becomes malpositioned dorsally, a-a ligament failure, & then subluxation/luxation

114
Q

what animals are most commonly affected by atlantoaxial subluxation?

A

young toy breed dogs

115
Q

what are the clinical signs associated with atlantoaxial subluxation?

A

acute or chronic C1-C6 signs, usually symmetrical, occasionally caudal brainstem involvement, & paraspinal hyperesthesia

116
Q

how is atlantoaxial subluxation diagnosed?

A

sedated or anesthetized radiographs

117
Q

what is the best recommendation concerning FCEM?

a. medical management with steroids
b. icy hot
c. myelogram is the best way to visualize the lesion
d. MRI to diagnose & physical rehabilitation
e. MRI to diagnose & euthanasia if there is a T2W hyperintensity

A

d. MRI to diagnose & physical rehabilitation

118
Q

what is the treatment used for atlantoaxial subluxation?

A

surgery - vertebral stabilization

neck braces

prognosis is better for ambulatory patients

119
Q

fractures & subluxation in the spine is most commonly where?

A

thoracolumbar vertebral column

120
Q

what is the most commonly fractured cervical vertebrae?

A

C2

121
Q

what are the clinical signs of trauma causing spinal cord disease?

A

myelopathy, paraspinal hyperesthesia, & other body systems affected

122
Q

how is spinal cord disease from trauma diagnosed?

A

most commonly by radiographs - 75% sensitive for fractures & luxations & 95% specific

123
Q

when is surgery indicated in trauma causing spinal cord disease?

A

multiple compartments are involved or there is obvious instability

124
Q

what is the best predictor of outcome in regards to trauma causing spinal cord disease?

A

neurological function

125
Q

what is the treatment for spinal cord disease caused by trauma?

A

conservative management is possible & sometimes surgery

126
Q

what are poor prognostic factors of spinal cord disease caused by trauma?

A

no motor function & no deep nociception

127
Q

what is a positive prognostic indicator for spinal cord disease caused by trauma?

A

non-ambulatory animal but has motor function will do well if appropriately treated

128
Q

what is the pathogenesis of brachial plexus injury?

A

traction or abduction on the limb, nerve roots are more vulnerable because they lack perineurium

injury may lead to:
-neuropraxia, axonotomesis, neurotomesis

129
Q

what is the pathogenesis of ascending/descending myelomalacia?

A

typically a disk in the thoracolumbar area - necrosis of the spinal cord radiating from an injury that is an acute presentation within 1 week of disk injury

130
Q

what are the clinical signs associated with ascending/descending myelomalacia?

A

animals with UMN paraplegia may develop LMN signs, LMN paresis of thoracic limbs, cutaneous trunci reflex migrates cranially, soft LMN abdomen showing decreased tone

131
Q

what is the prognosis of ascending/descending myelomalacia?

A

poor - extreme pain & death due to ventilatory failure

132
Q

what is the usual etiology of diskospondylitis?

A

usually bacterial but can be fungal

133
Q

what agents are usually involved in diskospondylitis?

A

staph, strep, e. coli, & brucella

134
Q

what are some examples of chronic bacteremia that can lead to diskospondylitis?

A

UTI, dental disease, bacterial endocarditis, & pyoderma

135
Q

what is the pathogenesis of diskospondylitis?

A

sluggish capillary flow at vertebral endplates - bacteria becomes easily stuck

136
Q

what is the common lesion location of diskospondylitis?

A

lumbosacral region

137
Q

what are the clinical signs associated with diskospondylitis?

A

large breed older dogs with a gradual onset of paraspinal hyperesthesia, fever, loss of lean body mass, & paresis/ataxia

138
Q

how is diskospondylitis diagnosed?

A

spinal rads are often sufficient - look for end plate lysis, sclerosis, & disk space collapse

139
Q

T/F: there is a 2-4 week lag time of imaging in regards to clinical signs of diskospondylitis

A

true

140
Q

what diagnostics are run in a suspected case of diskospondylitis to identify the causative organism?

A

bloodwork, UA, culture, echo, dental exam, blood culture, & brucella testing

141
Q

what is the treatment for diskospondylitis?

A

1st generation cephalosporins - usually a response in 1st week of treatment, but continue treatment for 2-3 months

analgesia & reimaging are both important

142
Q

what is the common cause of L4-S3 acute myelopathy?

A

aortic thromboembolism

143
Q

what is the pathogenesis of an aortic thromboembolism?

A

paraplegic animal due to infarction

144
Q

what are the clinical signs associated with aortic thromboembolism?

A

acute paraplegia that is bilateral in the pelvic limbs, severe myalgia, cold distal extremities, & limb cyanosis

145
Q

how is an aortic thromboembolism diagnosed?

A

ultrasound aortic bifurcation, clinical signs, CK usually very high, & can use doppler on the affected limbs

146
Q

what is the treatment for an aortic thromboembolism causing spinal cord disease?

A

address the underlying cardiac disease & dehydration - reperfusion injury is a concern

147
Q

what is the pathogenesis of lumbosacral disease?

A

more than just a disk herniation!

degenerative/malformative conditions leading to the compression of cauda equina at L7-S1 disk space

can be from instability, malformation, canal stenosis, or disk herniation - often see disk protrusion, hypertrophy of ligamentum flavum, & nerve root compression

148
Q

what animals are often affected by lumbosacral disease?

A

middle aged to older large breed dogs - german shepherds

149
Q

what are the clinical signs associated with lumbosacral disease?

A

may present with lumbosacral pain, LMN paresis, & LMN bladder dysfunction

150
Q

how is lumbosacral disease diagnosed?

A

spinal rads, EMG/nerve conduction tests, & CT/MRI is best for imaging combined with electrophysiology

151
Q

what is the treatment for lumbosacral disease?

A

decompressive surgery with or without stabilization

152
Q

what are positive prognostic indicators for animals with lumbosacral disease?

A

animals with minimal ataxia & weakness

153
Q

what are poor prognostic indicators for animals with lumbosacral disease?

A

urinary incontinence, very active dogs, & dogs with significant neurological defects

154
Q

what is the causative agent of tetanus?

A

clostridium tetani

155
Q

what is the pathogenesis of tetanus?

A

tetanospasmin - toxin blocks the release of neurotransmitters causing rigidity, spasticity, & seizures

lack of glycine & gaba = rigidity, spasticity, & seizures

156
Q

what are the clinical signs of glycine inhibition in tetanus?

A

extensor rigidity, opisthotonus, trismus, globe retraction with 3rd eyelid elevation, sardonic grin, restrictive breathing

157
Q

what are the clinical signs of GABA inhibition in tetanus?

A

seizures & tremors

158
Q

non-spasmogenic toxins in tetanus lead to what?

A

storms of tachycardia & bradycardia

159
Q

how is tetanus diagnosed?

A

clinical signs, history, presence of wound

160
Q

what is the treatment used for eliminating the toxin or infection in tetanus cases?

A

debride & lavage wound, treat with penicillin or metronidazole, & consider tetanus antitoxin

161
Q

what is the symptomatic treatment for tetanus?

A

muscle relaxants, treat the seizures, short acting beta blocker if autonomic storm, fluids, oxygen, & magnesium CRI

162
Q

what are poor prognostic indicators in tetanus patients?

A

younger dogs & dogs with severe signs

163
Q

T/F: in a brachial plexus injury, chronic paresthesia/lack of function can require amputation

A

true

164
Q

what animals are more commonly affected by nerve sheath tumors?

A

older large breed dogs - more so thoracic limb

165
Q

what are the clinical signs associated with nerve sheath tumors?

A

history of progressive muscle atrophy, occasional axillary pain, & potentially have other limb involvement if the tumor invades the spinal cord parenchyma

166
Q

how are nerve sheath tumors diagnosed?

A

radiographs & electrophysiology to confirm for neurogenic atrophy & localize the nerve involved

167
Q

what is the best imaging modality to use for diagnosing a nerve sheath tumor?

A

MRI

168
Q

why is myelogram not great when looking for a nerve sheath tumor?

A

may just appear as an intradural-extramedullary mass

169
Q

if the dura is breached in a nerve sheath tumor, what may be seen in the CSF?

A

increased proteins

170
Q

what are poor prognostic indicators of nerve sheath tumors?

A

proximally located tumors, spinal cord involvement

171
Q

what treatment is available for nerve sheath tumors?

A

amputation with laminectomy or chemo (doxorubicin) for high mitotic index tumors

172
Q

what animals are typically affected by IVDD?

A

2-6 year old chondrodystrophoid dogs, male > female

lesions at the thoracolumbar junction

173
Q

what imaging modality is ideal for diagnosing IVDD?

A

MRI - rads may miss stuff

CT is reasonable

174
Q

conservative therapy for IVDD is best for what patients?

A

patients with mild neurological deficits & without history of repeated episodes

175
Q

what are the 2 treatment options for IVDD?

A

conservative treatment or surgery

176
Q

conservative therapy for IVDD doesn’t work well for what patients?

A

chronically affected patients, larger/older dogs, animals with multiple episodes, & severely affected animals

177
Q

T/F: in dogs with IVDD, severely ataxia or non-ambulatory animals will be better treated with surgery

A

true

178
Q

epidermal empyema seen on MRI is common in what disease?

A

diskospondylitis

179
Q

what is the treatment used for degenerative myelopathy?

A

physical rehabilitation slows the progression

SA DX & TX I (59 decks)

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