Smal animal SC disease Flashcards

1
Q

Typical age and breeds for FCEM?

A

most common in young adult dogs of the larger breeds of dogs:
miniature schnauzer, Labrador retriever,
boxer breeds

Dog: 2 months to 13 years and 5 months, with a median of 4–6 years in the majority of studies

Cats: DSH
from 6 months to 17 years (median, 10 years)

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2
Q

Why are some animals very painful at the onset of FCEM?

A

Central neurogenic pain refers to spontaneous pain associated with CNS parenchymal lesions that do not involve the meninges. Acute spinal cord injury or ischemia may be related to spontaneous pain in addition to some loss of sensory function caudal to the lesion. The extreme discomfort exhibited by some dogs at the onset of spinal cord ischemia associated with fibrocartilaginous embolism may well be an example of spontaneous central neurogenic pain. The pathophysiology of this form of pain is poorly understood, but disinhibition of dorsal gray column neuronal cell bodies that project into the spinothalamic pathway or a disturbance of the lateral spinothalamic tract, the ventral spinothalamic tract, or both, which results in spontaneous discharge, are possible explanations.

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3
Q

4 hypothesis of embolus entering the vasculature in FCEM

A

1) Direct penetration of nucleus pulposus fragments into spinal cord or vertebral vessels

2) Chronic inflammatory neovascularization (arterial and venous) of the degenerated
intervertebral disc

3) Presence of embryonic remnant vessels within the nucleus pulposus (which is normally
avascular in adults)

4) Mechanical herniation of nucleus pulposus into the vertebral bone marrow sinusoidal venous channels, with subsequent retrograde entrance into the basivertebral vein
and internal vertebral venous plexus. (Schmorl’s node)

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4
Q

What is a Schmorl node?

A

intervertebral disc material in the marrow of the vertebral bodies (one of proposed mechanisms for FCEM, common in humans, rare finding in dogs)

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5
Q

Where does nephroblastoma usually occur in the dog, and what is the typical signalment?

A

T 10-L 2 SCS
Intradural-extraparenchimal

Dogs younger than 2,5 years old

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6
Q

Why does a nephroblastoma usually always involve SCS T10-L2)

A

correlates with the site of embryonic renal development from intermediate mesoderm and the embryonic mesonephros.

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7
Q

Most common cause of infectious myelitis in dogs?

A

Canine distemper virus. Other infectious diseases are caused by protozoal agents (Toxoplasma gondii, Neospora caninum), Rickettsia species, and fungal agents.

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8
Q

Most common isolates from dogs with discospondylitis?

A

Staphylococcus pseudintermedius is the most common isolate. Streptococcus species and Escherichia coli have also been isolated in this lesion. Be aware that, particularly in intact male and female dogs, Brucella canis has been identified in these infections and that it is contagious to humans.
Aspergillus spp.- German Shepherd Dogs

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9
Q

MST for dogs with nephroblastoma?

A

70 days (one study) - 374 (another)

BrewerD.M,Cerda-GonzalezS,DeweyC.W,et al.Spinal cord nephroblastoma in dogs: 11 cases (1985-2007).J Am Vet Med Assoc.2011;238:618–624.

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10
Q

Where do 80% of IVD extrusion occur in the dog? Why?

A

T10 and L3 vertebrae

This may relate to the increased motion of the vertebral column at this level compared with the more stable thoracic area. In addition, between the first 10 thoracic vertebrae, an intercapital ligament courses transversely across the dorsal surface of the intervertebral disc to connect the heads of the ribs where they articulate with both adjacent vertebrae. This is an added support to the articulation of the vertebral bodies and may help to prevent intervertebral disc herniation or protrusion between thoracic vertebrae cranial to T10.

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11
Q

In which domestic species is lymhoma the most common vertebral neoplasia?

A

Cats and cattle

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12
Q

Most common region for lymphoma in the spinal cord?

A

Thoracolumbar, usually restricted to 1-3 foramina

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13
Q

Typical dog breeds for deg. Myelopathy?

A

German shepherd dog
boxer,
Cavalier King Charles spaniel,
Pembroke Welsh corgi,
kuvasz,
Bernese mountain dog.

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14
Q

4 stages of DM based on clinical signs?

A
  1. Ambulatory pelvic limb UMN paresis and GP ataxia
  2. Nonambulatory paraparesis and GP ataxia to paraplegia with areflexia in the pelvic limbs, mild muscle atrophy, and some incontinence
  3. LMN paraplegia with thoracic limb paresis and ataxia
  4. LMN tetraplegia, severe atrophy, dysphagia, and tongue paresis
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15
Q

Typical breeds and signs of SAD

A

Pug dogs and french bulldogs

GP ataxia and UMN paresis, affected dogs often have fecal incontinence and have a low tail carriage

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16
Q

Wat is shown in the image? Multiple Afghan hounds from the litter are recumbant, with a spastic paraparesis and GP ataxia of the pelvic limbs. They are 8 MO

A

A microscopic section of the C8 spinal cord segment from a young Afghan hound with myelinolysis. Note the sparing of the fasciculus proprius and the nerve roots.

Afghan hound myelinolytic encephalomyelopathy is inherited as an autosomal recessive gene disorder. It is a unique primary demyelination that causes necrosis of myelin but spares the axons. It appears to start in the myelin in the midthoracic spinal cord segments and to progress cranially and caudally. The clinical signs begin with mild pelvic limb spastic paresis and ataxia and loss of control of the trunk muscles by 7 to 10 days. They are followed by thoracic limb spastic paresis and ataxia and then recumbency by about 14 to 21 days. The initial onset of clinical signs ranges between 3 and 13 months of age. The myelinolytic lesion is bilaterally symmetric in all the funiculi but spares the fasciculus proprius. The “naked” demyelinated axons float unsupported in their funiculi among a plethora of lipid-filled macrophages. One of the earliest publications on this disorder erroneously explained this lesion as a vascular compromise. Primary demyelination with axonal sparing cannot be caused by any known vascular disorder. The unique distribution of this lesion is unexplained. Most of these dogs also have the same primary demyelination of the axons that surround the dorsal nucleus of the trapezoid body. No clinical signs have been associated with the lesion in the trapezoid body. This inherited myelinolytic disorder was confirmed at autopsy in the dogs in this litter. MRI studies of these dogs have not been described.

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17
Q

Which vertebral body has a high chance of fracture and why?

A

Cranial aspect of the body of C2 (axis)

This may be the result of the physical stress that is placed there, where the dens articulates with the atlas. The latter acts as a fulcrum when flexion of the head and neck is forced. In addition, the presence of two growth plates in the cranial portion of the body of the axis may be a risk factor for a fracture there.

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18
Q

Name the ossification centres of the axis

A
  • Center 1 - cranial articular surface of the axis body and the dens.
  • Intercentrum 1 - for the ventral arch (body) of the atlas.
  • Centrum of proatlas: small apex of the dens.
  • Intercentrum 2: narrow ossification center between the ossification centers of centrum 1 and centrum 2.
  • Centrum 2: central region of the body of the axis.
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19
Q

Which ligaments participate in the normal alignment between atlas and axis?

A

1) transverse ligament of the atlas - attached on both sides of the ventral arch of the atlas and passes dorsal to the dens
2) dorsal longitudinal atlantoaxial ligament - dorsal arch of the atlas and the spine of the axis
3) apical and two lateral (alar) ligaments - attach the apex of the dens to the basioccipital bone cranially

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20
Q

Where are the pathological lesions with “inherited encephalomyelopathy and polineuropathy” of rotweilers located?

A

The spinal cord lesion consists of a bilateral symmetric axonopathy with secondary demyelination and astrogliosis, which is most pronounced in the lateral and ventral funiculi. This lesion is not limited to the spinocerebellar tracts. Many tracts are affected, including the UMN tracts, which is why the gait disorder is typical for a dysfunction of the GP and UMN systems. The thoracolumbar segments are most affected, which possibly suggests where the degenerative lesion first develops and explains why the clinical signs are first observed in the pelvic limbs. Vacuolation of neuronal cell bodies is scattered through the spinal cord and brain, with no other evidence of any microscopic abnormality of these neurons. The brains of these dogs test negative for prion protein. A neuropathy is prominent in the recurrent laryngeal nerves and scattered in other long nerves. Denervation atrophy of all the intrinsic laryngeal muscles except for the cricothyroideus is significant

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21
Q

Neuro signs in “inherited encephalomyelopathy and polineuropathy” of rotweilers

A

The clinical signs begin at about 6 to 8 weeks of age and may start with either inspiratory dyspnea or paraparesis and pelvic limb ataxia. Some of the dogs that first exhibited the signs of laryngeal paralysis had laryngeal tie-back surgery to improve their breathing before the clinical signs were first observed in the pelvic limbs. It is paramount that the veterinary surgeon be aware of this disorder and counsels the owner appropriately before surgery. All dogs progress in a few weeks to tetraparesis and ataxia in all four limbs. Some dogs develop megaesophagus and regurgitate, and some dogs have bilateral microphthalmia. These small eyes appear to be sunken into the orbits, and therefore the third eyelids become prominent. Horner syndrome does not occur in these dogs. A few dogs have been reported to exhibit clinical signs of dysfunction of the cerebellum or the vestibular system

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22
Q

Name the inherited neurodegenerative disorders of the Rottweiler breed

A

1) inherited encephalomyelopathy and polineuropathy
2) neuroaxonal dystrophy
3) leukoencephalomyelopathy
4) motor neuron disease
5) polyneuropathy (axonopathy)
6) distal neuropathy
7) dystrophynopathy (Duchane type of muscular dystrrophy)

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23
Q

Which nerves innervate the lateral scapular muscles (eg. Atrophy of lateral scapular muscles seen in dogs with disk associated spondlomyelopatyhy)

A

C6-7 SCS - suprascapular nerve (supraspinatus and infraspinatus m.) and subscapular nerve (subscapular muscle)

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24
Q

Which storage disease is most common in West highland white terriers and Cairn terriers?

A

Globoid cell leukodystrophy (Krabbes disease)

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25
Q

Which enzyme is deficient in Globoid cell leukodystrophy?

A

Galactosylceraminase-1 (Beta galactocerebrosidase)

Accumulation of galactosylsphingosine (psychosine)

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26
Q

What is the most likey DD? (See image)

2 month old Cairn terrier with signs of a progressive gait disorder that initially affected the pelvic limbs and progressed to tetraparesis with sublte cerebellar signs

A

Globoid cell leukodystrophy (Krabbes disease)

Galactosylceramidase 1 deficiency (accumulation of galactosylsphingosine)

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27
Q

Expression of which retrogene is associated with premature/accelerated IVD degeneration in dogs?

A

fibroblast growth factor 4 (FGF4) retrogene on chromosome 12 in chondrodystrophic breeds

*
This process, called Hansen type I intervertebral disc extrusion (IVDE), also occurs in non-chondrodystrophic breeds at a much lower frequency, and unassociated with the FGF4 retrogene.

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28
Q

Sensitivity of MRI for IVDD diagnosis?

A

> 98.5%

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29
Q

Benefits of MRI for IVDD diagnosis?

A
  • enhanced diagnostic performance over CT in dogs with peracute signs,
  • differentiating disc extrusion from protrusion.
  • Residual compression after surgery also can be detected
  • prognostication.
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30
Q

MRI prognostic factors for worse locomotor outcome and development of progressive myelomalacia (PMM).

A
  • Presence and extent of intramedullary T2 hyperintensity,
  • T2 hypointensity,
  • attenuation of the cerebrospinal fluid (CSF) signal on HASTE/T2* sequences
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31
Q

Minimal sequences to be obtained for IVDD disease MRI?

A

A minimum of T2W sagittal and transverse images should be acquired.

HASTE and short Tau inversion recovery (STIR), T1-weighted (T1W) and T1W post-contrast sequences might be considered but do not serve as replacements for standard T2W imaging sequences.
Supported by moderate-level evidence.

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32
Q

Benefits of CT over MRI in IVDD?

A
  • rapid acquisition
  • lower cost
  • better at distinguishing acute from chronic extrusions
  • sensitivity 81-100%
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33
Q

Effect of age and size of dogs on CT accuracy for diagnosis of IVDD?

A

less accurate in:
older (>5 years) and
smaller dogs (<7 kg).

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34
Q

In which canine patients could we reccommend CT as a first line advanced dx imaging modality?

A

young to middle-aged adult, chondrodystrophic dogs when acute TL-IVDE is suspected –> low likelihood we will miss a lesion, but lower cost/faster acquisition

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35
Q

Reccurence rate for medically vs. surgically treated dogs with IVDD?

A

15% to 66% compared with much lower rates for dogs managed by both hemilaminectomy and fenestration

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36
Q

Outcomes of dog treated medically vs surgically for IVDD based on severity of presenting signs?

A
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37
Q

Minimal suggested period of restricted activity in dogs with IVDD treated conservatively?

A

at least 4 weeks to promote healing of the annulus fibrosus

This period should include confinement to a restricted area (crate ideally, or a small room without furniture) except for when performing rehabilitation exercises or outdoor toileting. There should be no off-leash walking, no jumping on or off furniture and no access to stairs during this time. Supported by low-level evidence.

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38
Q

Effect of durotomy on outcome and PMM in dogs with IVDD?

A

for dogs with severe neurologic signs may improve outcome and lessen risk of PMM

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39
Q

Fenestration of the herniated disc space at the time of surgical decompression is recommended or not? to minimize risk of recurrence at the site of herniation.

A

it is reccomended

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40
Q

Rate of reccurence of IVDD for dogs undergoing decompressive surgery?

A

up to 19%

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41
Q
A
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42
Q

Which percentage of recurrences of IVDD develop within 1-2 disc spaces of the original extruded disc?

A

87.5%

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43
Q

Rate of recurrence od IVDD is higher in which breeds of dogs?

A

dachshunds (25%) and
French bulldogs (44%)

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44
Q

In which dog breeds does the Consensus recommend fenestration even if the discs are not mineralized?

A

in breeds predisposed to IVDE such as dachshunds and French bulldogs

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45
Q

Reported risks/complications of fenestration?

A
  • extrusion of additional disc into the vertebral canal at the site of extrusion,
  • the potential to induce vertebral instability,
  • increased morbidity when performed at L5-6 & L6-7,
  • pneumothorax
  • hemothorax (chemonucleolysis),
  • neuromuscular complications secondary to trauma to the peripheral nerve or nerve root,
  • hemorrhage from the sinus or vertebral artery,
  • development of spondylosis deformans
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46
Q

Overall reported complication rate associated with various fenestration techniques?

A

low at 0.01%

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47
Q

Fenestration is not recommended for which sites in the dog?

A

routine fenestration of L4-5 and more caudal sites is not recommended

Caudal to L3-4, fenestration carries increased risk

Fenestration at T10-11 and above usually is not recommended due to the low rate of disc extrusion at these sites.

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48
Q

How long does it take for the void in the annulus fibrosus to heal after fenestration?

A

4-16 weeks by invasion of fibrocartilage

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49
Q

Percutaneous laser disc ablation (PLDA) is considered a safe and useful method in limiting recurrent disc extrusion, true or false?

A

true (low - moderate level of evidence ina large number of dogs)

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50
Q

Use of dexamethasone in IVDD in dogs?

A

Increased risk of urinary tract infection and gastrointestinal disease.

Reduced quality of life in dogs managed medically for IVDE.

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51
Q

Use of dimethyl sulfoxide (DMSO) in dogs with IVDD?

A

dogs treated with the matrix metalloproteinase (MMP) inhibitor GM6001 with a dimethyl sulfoxide (DMSO) carrier or DMSO alone showed significantly improved locomotor outcome compared to those treated with a saline control.

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52
Q

Which percentage of dogs had persistently increased mechanical sensory thresholds (MST) suggesting neuropathic pain after TL-IVDE?

A

15%

normally the values stabilise by 6 weeks after hemilaminectomy

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53
Q

Epidural application of morphine or morphine & dexmedetomidine & hydromorphone is associated with better postoperative (48 h) pain control in dogs with IVDD, true or false?

A

true

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54
Q

Erector spinae block is associated with better postoperative (24 h) pain control in dogs with IVDD, true or false?

A

true

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55
Q

Fentanyl patch can be considered as a good means of pain control in dogs with IVDD, true or false?

A

Plasma levels therapeutic, pain control adequate (72 h)

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56
Q

Adjunctive Pregabalin 4 mg/kg q8h post op was associated with better pain control for 5 days post-op in dogs with IVDD, true or false?

A

true,

1) pregabalin - Better pain control for 5-d postop
2) gabapentin - No benefit over placebo for 5-d postop

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57
Q

Both pre- and postoperative electroacupuncture are associated with reduced pain in dogs undergoing surgery for IVDD?

A

False

Preoperative acupuncture reduced intraoperative need for fentanyl, reduced pain on recovery from anesthesia.

Postoperative electroacupuncture No benefit for 3-d postop.

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58
Q

Pulsed electromagnetic fields are associated with reduced postop pain in dogs with IVDD?

A

true, up to 6 weeks

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59
Q

Use of harmonic blade for surgery in dogs with IVDD was associated with reduced postoperative pain?

A

true, up to 30 days

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60
Q

Minimally invasive surgery was associated with reduced need for opioids and postoperative pain in dogs with IVDD?

A

true

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61
Q

Analgesia recommended post-op IVDD by the ACVIM consensus?

A
  • opioids IV or SC for 24 to 48 hours postoperatively (longer if needed)
  • fentanyl patch for 3 to 5 days postoperatively
  • NSAIDs for 7 days postoperatively in addition to or instead of a fentanyl patch
  • +/- pregabalin q 8 h
  • pre- and intraoperative interventions such as erector spinae block, epidural morphine as well as postoperative pulsed electromagnetic field therapy (PEMF) have been proven to decrease intra- and postoperative pain and their use can be considered
62
Q

Adverse effects for dogs treated alone or in combination with NSAID and corticosteroids for IVDD?

A

Diarrhea, gastritis, GI ulceration, regurgitation and pancreatitis.

They occur at comparable rates in dogs treated with NSAIDs or corticosteroids alone, but at higher rates if these drug classes are combined.

Fatal colonic perforations have been described in dogs treated with high doses of dexamethasone, and dogs treated with dexamethasone are more likely to develop urinary tract infections (UTIs) and diarrhea than those treated with other or no glucocorticoids

63
Q

Risk associated with use of opioids in therapy of IVDD in dogs?

A

can increase the risk of gastro-esophageal reflux and regurgitation, as can medications that cause sedation such as gabapentin and pregabalin.

64
Q

Which percentage of dogs treated surgically for IVDD develop aspiration pneumonia?

A

up to 6.8%

Vomiting and regurgitation are risk factors for aspiration pneumonia (therefore, careful with using opioids and drugs that cause sedation)

65
Q

Dogs with severe injury, even if they recover pain perception and motor function, might have suboptimal continence, true or false?

A

true

66
Q

The method of of bladder evacuation used does not influence the frequency of UTI, true or false?

A

true

but

prolonged placement of indwelling catheters might delay recovery of voluntary urination and increase the risk of UTI

67
Q

Frequency of UTI ranges in dogs with IVDD in the postoperative period?

A

0% to 42% in the first postoperative week,
17% to 36% in the first 6 weeks and
15% at 3 months

68
Q

Most common bacterial isolate, frequently is associated with antibiotic resistance in dogs with IVDD?

A

E.coli

69
Q

Risk factors for UTI in dogs with IVDD include:

A
  • severity of neurologic deficits,
  • duration of retention incontinence and
  • duration of indwelling catheterization
70
Q

Cranberry extract decreases the risk of UTI, true or false?

A

false

71
Q

Rehabilitation impacts the rate of recovery of walking, walking coordination, proprioceptive placing or muscle mass in dogs with incomplete injuries from IVDD?

A

false

72
Q

In dogs with incomplete injuries, rehabilitation performed postoperatively is safe but fails to demonstrate benefit on the rate or extent of recovery of walking compared to dogs receiving only basic exercises (e.g., PROM, assisted walking). True or false?

A

true

these findings suggest that more intensive, tailored rehabilitation protocols are not needed for all dogs with incomplete injuries to achieve a successful outcome (i.e., independent, coordinated ambulation)

73
Q

Early initiation of hydrotherapy or underwater treadmill (UWTM) therapy (at approximately 1 vs 3 weeks) might improve the likelihood of recovery of ambulation among persistently paraplegic DPN dogs, true or false?

A

true

74
Q

The IVDD consensus statements recommends initiation of physical therapy at what time? How long should it be continued?

A

initiation within a 24-hour to 14-day window postoperatively and continuing for at least 2 to 6 weeks

75
Q

Duration of confinement and activity restriction post-op in dogs with IVDD?

A

at least 4 weeks

76
Q

Clinical signs of PMM in dogs with TL-IVDD include (8)?

A
  • loss of pelvic limb reflexes,
  • loss of pelvic limb, trunk, and abdominal muscle tone (difficulty retaining sternal recumbency)
  • cranial progression of the cutaneous trunci reflex (CTR) caudal border;
  • Horner syndrome,
  • diffuse pain,
  • thermodysregulation,
  • malaise
  • ultimately thoracic limb involvement and ventilatory failure
77
Q

usual time-window when PMM develops in dogs after TL-IVDD?

A

24 hours up to 14 days

usually within days

78
Q

Prevalence of PMM in deep-pain negative dogs?

A

10-33%

79
Q

Sensitivity/specificity of serum GFAP for detection of PMM

A

97.7% specific but only 75% sensitive

80
Q

Serum phosphorylated neurofilament heavy protein (pNfH) shows significant elevation in dogs with PMM at 24 hours, but not at presentation, true or false?

A

true

81
Q

Myelography finding associated with PMM in dogs?

A

Presence of contrast within the cord parenchyma (identified in both focal or progressive myelomalacia)

82
Q

Risk factors for development of PMM?

A
  • injury severity (deep-pain negative dogs at highest risk)
  • lesion location (lumbar intumescence highest risk)
  • French bulldog breed (maybe due to also highest prevalence of lumbar IVDE)
83
Q

Corticosteroids might lower the risk for PMM in dogs?

A

true,

but
only one retrospective cohort, so low level of evidence to support use of corticosteroids as means of protection against PMM

84
Q

Currently, there is no association between timing of surgery and development of PMM?

A

true

85
Q

Durotomy after decompression may lower the risk of developing PMM in deep-pain negative dogs?

A

true

The rate of PMM was 21.5% for hemilaminectomy alone compared to 0% for hemilaminectomy plus durotomy

86
Q

There is a negative association between prolonged anesthetic time and neurologic outcome in paraplegic DPN dogs, true or false?

A

true

87
Q

In which cases does the Consensus for IVDD suugest to consider extensive hemilaminectomy with durotomy?

A

dogs with imaging and clinical risk or suspicion of PMM

88
Q

4 regions of the IVD?

A

the nucleus pulposus,
the transitional zone,
the annulus fibrosus and the
cartilaginous endplates

89
Q

The nucleusu pulposus is derived from which cells? Which cells are they replaced by as the animal ages?

A

derived from the notochord

physaliferous notochordal cells can be seen within the ground substance in the young animal and are gradually replaced by chondrocyte like cells with age

90
Q

Which molecules are produced by the notochord cells?

A

type 2 collagen and proteoglycans

The proteoglycans consist of a protein backbone onto which are attached glycosaminoglycans. The most common glycosaminoglycan side chains include chondroitin-6-sulfate and keratan sulfate.

91
Q

Which cells can be seen in the transitional zone of the IVD?

A

Chondrocyte like cells can be seen as well as increasing numbers of fibrocyte like cells moving peripherally away from the nucleus pulposus.

These cells lie within a fibrous matrix that appears distinct from the more basophilic matrix of the nucleus pulposus.

As the transitional zone blends into the annulus fibrosus the fibrous matrix becomes organized into a lamellar orientation.

92
Q

How is the annulus fibrosus built?

A

Inner and outer regions.
Concdentric fibrocartilage lamellae (fibrocytes in well-organised bundles of collagen)

  • inner annulus fibrosus –> anchored to the cartilaginous endplates
  • outer annulus fibrosus –> anchored to the epiphyseal bone of the adjacent vertebrae by Sharpey’s fibers
93
Q

What are Sharpey’s fibers?

A

fibers which connect the outer layer of the annnulus fibrosus to the epiphyseal bone

94
Q

Vascularisation/innervation of the IVD

A

The nucleus pulposus, annulus fibrosus and transitional zone have no blood supply

Only the outer layer of the annulus fibrosus of the layer is lightly innervated

95
Q

How are the IVD structures supplied by nutrients?

A

Thru the cartilaginous endplates via osmosis/diffusion.
For large molecules, the central concave regions of the endplates have channels that allow passage of nutrients via bulk flow in response to loading of the disc.

The cartilaginous endplates lie immediately adjacent to a rich vascular network from the epiphyseal arterial supply from which nutrients gain access to the IVD.

96
Q

Explain the process of IVD degeneration

A

Chobdroid metaplasia: notochord cells are replaced by chondrocyes; loss of proteoglycans (particulary chondroitin sulfate) and dehydration; collagen content increases and type II is preplaced by type I&raquo_space; biomechanical failure&raquo_space; fissuring of the annulus fibrosus&raquo_space; sclerosis of the endplates&raquo_space; calcification of the IVD

97
Q

The fibroblast growth factor 4 (FGF4) retrogene associated with chondrodystrophy and early IVD degeneration is located on which loci?

A

Chrhromosome 12

also chromosome 18 for Dachshunds

98
Q

Which IVD spaces have an increased risk of extrusion?

A

T11-12 and L2-3 IVDs

99
Q

Radiographic evidence supportive for IVD extrusion?

A
  • narrowing of the disc space,
  • narrowing of the articular facets,
  • narrowing and/or increased opacity of the intervertebral foramen,
  • presence of mineralized disc material within the vertebral canal
  • vacuum phenomenon
100
Q

Studies have shown that disc calcification at ____ years of age was a significant predictor of disc herniation later in life and also a risk factor for recurrent herniation following surgery.

A

2 years

101
Q

Which blood vessel damage occurs in Acute Intervertebral Disc Extrusion With Extensive Epidural Hemorrhage?

A

internal venous plexus

102
Q

Where in the spinal column is the Acute Intervertebral Disc Extrusion With Extensive Epidural Hemorrhage reported?

A

Only TL spine (not in the cervical)

103
Q

Dog breeds with reported Acute Intervertebral Disc Extrusion With Extensive Epidural Hemorrhage? Why?

A

more common in medium to large breed dogs (pit bull terrier, American Staffordshire terrier, Labrador retriever, German Shepherd dog and Rottweiler) than small chondrodystrophic breeds,

leading to speculation that epidural volume is larger in these breeds and thus the vertebral venous plexus is not compressed enough by the extruded material to stop hemorrhage when lacerated.

104
Q

Main disease process affecting the IVD in Hansen type 2 IVDD?

A

Fibroid metaplasia

The notochordal cells are slowly replaced by fibrocytes, collagen content increases,

BUT!!!***
Histopathological comparisons between the IVD of chondrodystrophic and non chondrodystrophic dog breeds have found features of chondroid metaplasia (chondrification and replacement of notochordal cells by chondrocytes within the nucleus pulposus) in both groups of dogs. Investigators have been careful to point out that Hansen’s original descriptions had referred to overall degree of fibrosis of the disc, not fibroid metaplasia of the nucleus pulposus specifically, which perhaps had been somewhat misunderstood for many years

105
Q

Typical signalment for Hansen type 2 IVDD?

A

non-chondrodystrophic dog breeds over 7 years of age

106
Q

Most common spinal column location of HNPE?

A

Cervical vert. column

107
Q

MRI criteria for diagnosing HNPE?

A
  • Ventral, midline extradural material (T2-weighted hyperintense, T1-weighted hypointense) overlying an IVD
  • Associated spinal cord compression, with or without intramedullary T2-weighted hyperintensity
  • Characteristic bi-lobed “seagull” shaped appearance to the extradural material
  • Reduced volume of T2-weighted hyperintense nucleus pulposus signal in the affected IVD.
108
Q

Criteria for CT diagnosis of HNPE?

A

Using contrast-enhancxed-CT, HNPE
was visualised as a hypodense extradural compressive lesion with rim enhancement immediately dorsal
to the intervertebral disc space, with a sensitivity of 91% and a specificity of 100%.

109
Q

Which percentage of dogs with ANPE show lateralised neuro signs?

A

90%

(in cats more symmetrical than dogs)

110
Q

Most common cause of ANPE in cats?

A

up to 75% of cats with ANNPE present following external trauma

111
Q

Most common spinal column location of ANPE?

A

thoracolumbar junction

likely reflecting the increased biomechanical forces at the junction between two stable vertebral segments

112
Q

MRI criteria for diagnosing ANPE

A
  • Focal intramedullary T2-weighted hyperintensity of the spinal cord
  • Spinal cord lesion located overlying an IVD
  • Reduced volume of T2-weighted hyperintense nucleus pulposus signal in the affected IVD
  • Mild narrowing of the affected IVD in mid-sagittal view
  • Small volume extradural material (T2-weighted hyperintense, T1-weighted hypointense) dorsal to the IVD with minimal to no spinal cord compression.
113
Q

MRI characteristics of Intradural/Intramedullary Intervertebral Disc Extrusion (IIVDE)?

A
  • areas of intramedullary hypointensity on T2-weighted, T1-weighted and gradient echo (T2*) sequences overlying an IVD
  • reduced nucleus pulposus volume,
  • a linear tract running from the associated IVD to the spinal cord parenchyma
114
Q

Percentage of dogs with a reduced volume of nucleus pulposus in an adjacent IVD in FCEM?

A

23.6% - usually the IVD caudal to the intramedullary hyperintensity

115
Q

Theories how the fobrocartilaginous material gets into the circulation to cause FCEM?

A

1) Schmorl’s nodes like in humans - herniation of nucleus pulposus into the endplate (but rare in dogs) - lest likely theory

2) directly into the internal vertebral venous plexus or spinal arterial vasculature

3) via new blood vessels forming in annulus fibrosus undergoing age related degenerative changes

4) 2+3

5) Presence of embryonic remnant vessels within the nucleus pulposus (which is normally
avascular in adults)

116
Q

Percentage of animals where external trauma or exercise is reported prior to FCEM?

A

30%

117
Q

Percentage of small breed dogs out of all dogs with FCEM?

A

24% (1/4)

118
Q

Most common small-breed dog with reported FCEM?

A

Miniature Schnauzer (60% of all small breeds)

119
Q

Breed of dog with very early onset of FCEM (puppy paralysis)?

A

Irish wolfshound puppies

120
Q

MRI criteria for FCEM?

A
  • Focal intramedullary T2 hyperintensity, focused on the gray matter and frequently lateralized.
  • Spinal cord lesion overlying vertebral body, not IVD.
  • No evidence of extradural material in the region of the lesion.
  • Subtle reduction in volume of T2-weighted hyperintense nucleus pulposus signal in the disc caudal to the spinal cord lesion.
121
Q

Percentage of dogs with IVDD presenting to the veterinary hospitals?

A

2.3–3.7% of admissions

122
Q

dogs receiving >1 h of daily exercise were less likely to have IVDE compared to dogs receiving <30 min of daily exercise and not allowed to jump on and off furniture, true or false?

A

True

123
Q

4 goals of medical tx of IVDE?

A

(i) to avoid further disc herniation to minimize additional damage to the spinal cord;
(ii) provide pain relief;
(iii) allow the extruded disc material to gradually dissipate by phagocytosis over time;
(iv) and leave the ruptured disc annulus to seal by fibrosis over time.

124
Q

Classification of SAD?

A
  • Type 1 is extradural without involvement of the nerve,
  • Type II is extradural with involvement of the nerve roots,
  • Type III is intradural
125
Q

Most accepted theory of SAD formation?

A
  • the theory of a 1-way valve formed by arachnoid proliferation in which cerebrospinal fluid (CSF) is allowed to flow into the region with pressure changes but cannot flow out
  • this supports a congenital etiology despite the range of ages over which clinical signs become apparent as it allows for progressive expansion and therefore, progressive compression of the spinal cord.
126
Q

Most represented breeds for SAD?

A

pugs, rottweilers, and French bulldogs,
- Pugs make up 28% (92/324),
- Rottweilers 19% (62/324), and
- French bulldogs 13% (43/324)

127
Q

Diseases (most commonly) associated/concurrent with SAD in dogs?

A
  • in pugs, caudal articular process dysplasia
  • in a recent study in pugs with thoracolumbar SAD, 58% had intervertebral disc disease at the same or adjacent sites
128
Q

Sex predisposition for SAD?

A

male sex (ca. 80% of all dogs) (unknown why)

129
Q

Mean age for developing SAD?

A
  • In a study of 122 dogs, the overall median age of onset of signs was 36 mo and did not vary with diverticulum location.
  • However, in a smaller study, SAD dogs in a cervical location were younger with a mean age of 31 mo compared to a mean age of 6.2 y in those with thoracolumbar diverticula.
130
Q

Incidence for cervical vs. thoracolumbar SAD?

A
  • cervical 41% to 71%
  • thoracolumbar 29% to 58%
    (depending on the study)
131
Q

Breed predisposition for different locations of SAD in dogs?

A
  • Pugs, mostly thoracolumbar localization
  • French mostly thoracolumbar localization
  • Rottweilers cervically located lesions
  • In general, dogs with cervical diverticula were significantly larger and dogs with thoracolumbar lesions were more likely to be small breeds
132
Q

Most common location for a thoracolumbar SAD?

A

T9–T13

133
Q

Most SAD lesions are located in the dorsal midline subarachnoid space (XX%-XX%) but they can also occur ventrally, laterally, or in a combination of these surrounding the spinal cord.

A

83% to 90%

134
Q

In 1 study of SAD, dogs with bilobed or multilobed lesions were all Rottweilers, and in another study of 10 Rottweilers, all bilobed lesions occurred in a caudal cervical locationm, true or false?

A

true

135
Q

Most common neuro sign in dogs with SAD?

A
  • slowly progressive/waxing-waning proprioceptive ataxia was the most common clinical sign in 1 study, present in 92.6% of cases, and
  • hypermetria was present in 21.3%.
  • Paresis, was much less common, and 50% of the dogs with paresis had concurrent neurologic disease that could have accounted for this finding.
136
Q

Urinary and fecal incontinence in dogs with SAD are typically attributed to which localisation?

A

thoracolumbar

137
Q

Why do some dogs with SAD develop urinary/fecal incontinence?

A

As lesions are usually located dorsally, fecal incontinence typically occurs secondary to compression of the dorsally located ascending sensory pathways.
Disruption of these pathways interrupts relay of sensory information to the sensory cortex, via the thalamic nuclei, for conscious recognition of rectal distension and defecation.

138
Q

Incidence of urinary and fecal incontinence in dogs with SAD?

A

3.3% - 4.1%

139
Q

Incidence of pain in dogs with SAD?

A
  • variable with 18.9% of dogs showing discomfort.
  • however, only 10% were specified to be painful on palpation
  • Given that some dogs have concurrent disease, as well as leptomeningeal adhesions, this may play a role in the detection of spinal discomfort.
140
Q

Magnetic resonance imaging in dogs with SAD is ideal for evaluating the spinal cord parenchyma to find concurrent lesions such as ___________ and _____________.

A

edema or syringomyelia
and
adhesions

141
Q

Which MRI sequence, besides sagittal T1W and T2W, can help in the diagnosis of SAD in dogs?

A
  • half-Fourier acquisition single-shot turbo spin-echo pulse sequence (HASTE) in sagittal plane
  • it increases the signal intensity of cerebrospinal fluid, while fat has little or no signal so it helps visualize the subarachnoid space and has a relatively short acquisition time
  • In a study comparing diagnosis of SAD with T2W imaging alone and HASTE, the sensitivity of T2W alone was 25% compared with the sensitivity of T2W and HASTE at 52.8%. Though not perfect, false negatives were reduced from 75% to 47.2% after the addition of HASTE
142
Q

Typical CSF findings in dogs with SAD?

A
  • usually normal
  • ca. 20% will show non-specific elevations in total protein and 9.2% to 10% have evidence of a mild mononuclear pleocytosis
143
Q

Role of prednisolone in the treatment of SAD in dogs?

A
  • 26% show improvement on pred
  • questionable efficacy prior to surgery

The only study assessing medical management and its outcome as it compares to surgical management is a study of 96 dogs in which 52% of dogs were treated medically, with the treatment of choice being variable courses of prednisone in 44/50 dogs.
Based on recheck visits and owner assessments, over a median follow-up of 24 mo, only 26% showed improvement on prednisone. Anecdotally, corticosteroids are often recommended before surgery, but in a recent study 5 cases in which steroids were used for 2 mo or longer in the perioperative period, showed no association with a better outcome. Whether or not it helps in removing the secondary intramedullary changes observed in the cord (edema, pre-syrinx, syrinx/syringomyelia) is also unknown.

144
Q

Surgical management has been described with various procedures and approaches including hemilaminectomy, dorsal laminectomy, and ventral slot, based on the location of the diverticulum, combined with some variation of durotomy, durectomy, diverticulum fenestration, dural marsupialization, and vertebral stabilization.
To date, no one procedure is superior and follow-up times are widely variable making assessment of success with each separate procedure difficult to determine. True or false?

A

true

*but:
Although not statistically significant, 1 study did find a trend towards a better outcome when marsupialization of the dura was performed

145
Q

Findings showing a trend towards a positive outcome after surgery in dogs with SAD?

A
  • patients younger than 3 y old
  • duration of clinical signs less than 4 mo.
146
Q

A recent study evaluating short- and long-term outcomes following surgery in pugs found that though 82% had a successful short-term post-operative outcome (6 mo), in the long term (12 mo or longer) 86% of pugs showed deterioration with 50% of those undergoing repeat MRI that showed a recurrent SAD or new SAD, true or false?

A

true

147
Q

Caudal articular process dysplasia, are present in _______________ % of pugs, and can be found in clinically normal or abnormal dogs.

A

91.2% to 97%

148
Q

Which SAD conformation (cranially or caudally thetherd) possibly has a better short-term outcome?

A

thoracolumbar caudal tethered SAD

149
Q

Which surgical technique in dogs with SAD can result in mild post-operative deterioration?

A

closure of the durotomy incision

150
Q
A