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VET433A > Week 4 - Neuro > Flashcards

Week 4 - Neuro Flashcards

1
Q

IVDD Type I

A

nucleus pulposus extrusion
chondroid metaplasia/degeneration with nuclear mineralization
TL>cervical>LS
–less in thoracic region due to intercapital ligament (adds more structure to vertebrae)

Typical Signalment: Chondrodystrophic (short legged) dogs only + Frenchies
Typical Age: Young adults (1-6yo)
Typical Onset/Presentation: Acute
Progressive: Both, potentially progressive
Painful: Yes
Pathophysiology: disc degerantes, nucleus pulposus loses water content and becomes dry, is extruded
Comments: Could be symmetric/asymmetric
Surgical referral: anytime when they are non-ambulatory (Grade 3) or more (ex. Grade 2,1,0)

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2
Q

IVDD Type II

A

Typical Signalment: LARGER breed dogs
Typical Age: Middle age to older (5-12yo)
Type of onset/presentation: Chronic (>2 weeks)
Progressive: Yes, slowly
Painful: Yes, but usually bigger dogs that can hide pain better (less pain expression)
Pathology: Annulus fibrosis protrusion due to fibroid metaplasia/degernation

-common at L7-S1

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3
Q

ANNPE (Acute Non-compressive Nucleus Pulposus Extrusion)

A

Typical Signalment: any breed
Typical Age: Young enough to still have healthy discs
Type of Onset/Presentation: Acute/peracute, inability to walk
Progressive? Both, depends on if animal continues to extrude disc (most of the time if it is just the one episode)
Painful? Can be both – acuteness will be less pain…?
Pathophysiology: High traumatic force to a normal hydrated disc (different from IVDD Type I/Type II) - extrusion of NORMAL nucleus pulposus

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4
Q

AAI (Atlantoaxial Instability)

A

Typical Signalment: Small toy breeds (YORKIE, Pomeranian, Chihuahua, Miniature Poodle)
Typical Age: Juvenile to young, hx of neck pain
Type of Onset/Presentation: Acute via some sort of event (tripping, playing frisbee, etc)
Progressive: Usually progressive/recurring
Painful: Yes
Pathology: Instability of the C1-C2 joint -> leads to brain injury of cranial cervical spinal cord (ex. ligament issues), can be traumatic event

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5
Q

DA-CSM (Disc-Associated Cervical Spondylomyelopathy)

A

Typical Signalment: Large dogs (Dobermans), Large/Giant breeds
Typical Age: Middle-aged
Type of Onset/Presentation: Chronic, takes time
Progressive: Yes
Painful: Yes
Pathology: congenital
Comments:
-Localization – C5-C6-C7
-mostly ventral compression
-symmetrical/asymmetrical signs

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6
Q

FCE (Fibrocartilaginous embolism)

A

Typical Signalment: ACTIVE large breed breeds (but can be Miniature Schnauzer, Min. Pin., Sheltie)
Typical Age: Young to middle aged (any age)
Type of Onset/Presentation: Peracute onset, during exercise (dog was playing then freezes then falls)
Progressive: No
Painful: No
Pathology:
Comments: Similar to ANNPE, hard to discern the two, usually asymmetric (lateralized)
Localization: can happen anywhere where there is vessels and discs

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7
Q

DM (Degenerative Myelopathy)

A

Typical Signalment: GSD, Corgi, Boxer
Typical Age: Older (esp. for corgis)
Type of Onset/Presentation: Chronic, slowly progressive
Progressive: Yes, slowly
Painful: No
Pathology:
Location: ALWAYS starts with T3-L3 localization, could be asymmetric, Gene - SOD-1 (homozygous mutated SOD-1 = at risk, but doesn’t mean they have it at that time)
Diagnosis: Exam, definitely usually post-mortem

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8
Q

GME (Granulomatous meningo-encephalitis/myelitis

A

Typical Signalment: small breeds (purse dogs)
Typical Age: 1-8 years old… young to middle aged
Type of Onset: Acute
Progressive: Yes without treatments
Painful: Yes
Diagnosis: Definitive dx = pathology
-MRI
-CSF: pleocytosis, increased macs and lymphocytes (mononuclear cells)
Localization: Anywhere - can affect brain and spinal cord, most commonly encephalitis

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9
Q

SRMA (Steroid Responsive Meningitis Arteritis)

A

Inflammatory dz

Typical Signalment: Beagles, Burmese Mt. Dogs, Boxers
Typical Age: Younger than GME dogs (1-2 years old), rarely >2yo
Localization:
Type of Onset: Acute, waxing and waning
Progressive: Yes, without treatment
Painful: Yes, cervical pain
Comment: No neuro deficits
CSF: Neutrophilic pleocytosis - dilemma is if it’s bacterial infxn

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10
Q

Neoplasia of Spinal Cord

A

Typical Signalment: Any breed
Typical Age: Usually older
Localization: Anywhere depending on type

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11
Q

Discospondylitis

A

Infectious dz

Signalment: GSD (fungal), bacterial – any, large/giant dog breeds
Type of Onset: Usually chronic, but can be acute if fracture/lux
Painful: Yes, extremely
Localization: L7 - S1, but can be seen anywhere
Tx: if you can’t get confirmation of bacterial agent – use the 4Bs with abx – 1. crosses BBB, 2. bactericidal, 3. beta-lactams, 4. broad spectrum

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12
Q

Fracture-Lux

A

Type of Signalment:
Painful: Yes, IMMOBILIZE

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13
Q

What does AMBULATORY mean?

A

at least 3 limbs are able to move/support the animal’s weight

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14
Q

What is a myelopathy?

A

myelo - spinal cord/marrow

dz/disorder affecting the spinal cord:
-dura
-vertebrae
-epidural space
-neuro parenchyma

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15
Q

What are the 3 different types of myelopathies, relative to the DURA?

A

Lecture 22, Slide 8

  1. Extradural
  2. Intradural, extramedullary
  3. Intramedullary
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16
Q

What are the 2 types of myelopathies, relative to the SPINAL CORD?

A

Lecture 21, Slide 9

  1. intrinsic – affecting the neuro parenchyma
  2. extrinsic – everything else (outside of spinal cord parenchyma)
    -also, in terms of dura, includes extradural and intradural, extrameduallary
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17
Q

What are the 4 NAL classifications of myelopathies?

A
  1. C1-C5
  2. C6-T2
  3. T3-L3
  4. L4-caudal (S3)
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18
Q

Findings are based on ______ and _______, NOT the underlying cause.

A

Findings are based on localization and severity, NOT The underlying cause.

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19
Q

If there are LMN and UMN lesions, _____ always wins.

A

LMN always wins/LMN will mask UMN signs.

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20
Q

Myelopathies have normal: (2)

A
  1. normal mentation
  2. CN function
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21
Q

Describe UMN vs LMN

A

UMN
1. the boss - “supervises”
2. cell bodies in brain
3. generally “inhibits” LMNs

LMN
1. the worker – “effector”
2. cell bodies in spinal cord and brainstem
3. LMN pools for limbs in intumescences
-TLs - cervical (C6-T2)
-PLs - lumbar (L4-S3)

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22
Q

Describe UMN vs LMN SIGNS/DEFICITS

A

UMN signs:
-normal to HYPER - reflexes and tonicity
-disuse atrophy (slow, minimal)
-paresis/paralysis

LMN signs:
-normal to HYPO - reflexes and tonicity
-neurogenic atrophy (rapid and severe)
-paresis/paralysis

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23
Q

What are the nerves involved with the Cutaneous Trunci/Panniculus reflex?

A

-afferent: dermatomes (L6 to rostral)
-efferent: lateral thoracic nerve (C8-T1)

T3-L3 myelopathy – loss of reflex about 2 spinal cord segments caudal to lesion
C6-T2 – loss of reflex regardless of site of stimulation

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24
Q

Schiff-Sherrington (T3-L3) characteristics: (3)

A

-extension of TLs (+/- neck)
-severe T3-L3 myelopathy
-normal postural reflexes

-NE will be normal – aside from extension of the TLs
-no brain/CN deficits

-thoracic limbs are normal during exam, only postural abnormality (not “postural reflex” abnormality

-lesion of border cells – loss of inhibition

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25
Q

Severity levels from mild to severe (5)

A
  1. painfulness
  2. conscious proprioception
  3. voluntary movement
  4. superficial pain sensation
  5. deep pain perception/sensation
    -loss of DPP = loss of the most protected nerve fibers

ex. if you LOSE deep pain sensation, most severe sign/neuro deficit

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26
Q

Decerebellate posture:

A

-lesion affecting cerebellum
-extended TLs, +/- flexed PLs
-NE consistent with cerebellum lesion
-normal consciousness

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27
Q

What’s the anatomy of a vertebral disc?

A

-nucleus pulposus in the center (jelly)
-annulus fibrosis around (dough)

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28
Q

IVDD Type I affects which types of dogs?

A

Chondrodysplastic! Short legs!

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29
Q

Which area of the spine does IVDD Type I mainly target?

A

any, BUT:
TL>cervical>LS

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30
Q

CS for IVDD Type I:

A

variable

-pain
-paresis
-ataxia
-hyperesthesia
-incontinence
-loss of pain sensation
-lameness

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31
Q

How would you diagnose IVDD Type I? (2)

A

-radiographs (in situ mineralization)

-MRI (T2W - fluid and fat hyperintense)
–loss of disc hydration (dark discs)
–deviation of spinal cord
–loss of CSF/epidural fat

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32
Q

When would you conservatively manage IVDD Type I/Which GRADES would you consider CONSERVATIVE management?

A

conservative management ONLY with milder signs of IVDD Type I
-pain only (grade 5)
-ambulatory (grade 4)
-nonambulatory with good voluntary motor function (grade 3) – MAYBEEEEeeee conservative management

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33
Q

What does CONSERVATIVE management of IVDD Type I entail? (3)

A

-CAGE REST
–no walks, jumping, playing
–2-4 weeks (4-6 weeks)

-analgesia
–NSAID, Trama-gaba
–not more than 7 days)

-anti-inflammatory
–NSAID
–not more than 7 days

PROGNOSIS: reoccurrence is common, may progressively decline

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34
Q

When should SURGICAL management of IVDD Type I be considered?

A

-any grade can be surgical, esp grade 0-3
-rapid progression of IVDD should be considered for sx
-FAILED medical management
-severe pain

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35
Q

What are the BENEFITS of IVDD Type I surgery? (4)

A
  1. greater outcome with intact deep pain perception
  2. lower recurrence rate (esp if fenestrations are done)
  3. faster resolution of pain
  4. usually faster recovery
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36
Q

What are the GOALS of surgical treatment of IVDD Type I? (3)

A
  1. decompression
  2. control hemorrhage
  3. disc fenestration

Techniques:
1. hemilaminectomy
2. ventral slot
3. vacations of above

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37
Q

Post-Op management of IVDD Type I: (6)

A

Nursing Care
1. bladder management
2. recumbency care
3. pain management

Rehabilitation
1. maximize recovery
2. maintain muscle mass
3. maintain joint movement

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38
Q

How is Myelomalacia (MM) associated with IVDD Type I + any spinal cord injury?

A

-spinal cord become toothpaste (spinal cord necrosis)
-mostly seen in PARAPLEGIA, DPP negative

-dogs with negative DPP
-can have a peracute decline
-loss of DPP >48hr poorer prognosis
–lack of improvement by 2 weeks = poor prognosis for recovery

-10-15% risk of ascending/descending myelomalacia = FATAL!!!
–spinal cord necrosis secondary to ischemia
–will affect ventilation as MM will necrose the nerves that innervate the muscles that help breathe -> so can lead to respiratory arrest

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39
Q

Progressive myelomalacia CS and Pathophysiology

A

CS - systemically ill:
-fever
-pain
-inappetence

NE:
-acute onset, transverse myelopathy
-diffuse progressive myelopathy signs

SOMETIMES imaging

Pathophysiology:
-will affect ventilation as MM will necrose the nerves that innervate the muscles that help breathe -> so can lead to respiratory arrest > then will reach cervical area and damage phrenic nerve (which innervates diaphragm) – will breathe more to try and create negative pressure

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40
Q

What happens to the vertebral disc with IVDD Type II?

A

the annulus fibrosis hypertrophies!

-fibroid metaplasia/degeneration
-protrusion
-can happen with any dog

-results in spinal cord compression > meningeal/nerve root irritation

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41
Q

What is the most common location for IVDD Type II?

A

Common at L7-S1, BUT can occur anywhere

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42
Q

CS for IVDD Type II

A

-paraparesis/tetraparesis
-ataxia
-pain with palpation
-+/- lameness, incontinence

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43
Q

How would you diagnose IVDD Type II? (4)

A
  1. radiography
    -narrowed disc space
    -end-plate sclerosis
    -osteophyte production
    -spondylosis
  2. myelography
  3. CT
  4. MRI - GOLD STANDARD – see picture Lecture 24, Slide 12
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44
Q

When would CONSERVATIVE treatment be indicated for IVDD Type II? (4)

A
  1. mild dz
  2. very slowly progressive
  3. non-painful
  4. continent

PROGNOSIS: variable, exercise and physiotherapy effective

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45
Q

What is the treatment for CONSERVATIVE management of IVDD Type II? (3)

A
  1. anti-inflammatories
  2. physical rehab (some movement is good – different than IVDD Type I)
  3. supportive care
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46
Q

When is SURGICAL treatment indicated for IVDD Type II? (5)

A
  1. moderate to severe myelopathy
  2. short hx or ACUTE onset
  3. incontinence
  4. deteriorating
  5. chronic pain

PROGNOSIS:

GUARDED
-prolonged hx
-multiple discs
-possible other underlying dz
-LMN signs present
-owner expectation

GOOD
-short hx - weeks to months
-focal lesion - 1 compression
-pain is a significant finding
-no other underlying dz
-owner expectation

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47
Q

What are the GOALS for SURGICAL treatment for IVDD Type II? (2)

A
  1. decompression without destabilization
  2. halt progression of dz

via hemilanimectomy vs pediculectomy

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48
Q

What does ANNPE stand for?

A

Acute Non-compressive Nucleus Pulposus Extrusion

aka Traumatic Disc Extrusion

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49
Q

ANNPE Pathophysiology?

A

high force/trauma – tears annulus fibrosis and causes ASYMMETRICAL extrusion of NORMAL nucleus pulposus

-can cause compression, but very minimal

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50
Q

CS with ANNPE

A

-paresis/paralysis
-ataxia
-+/- LMN signs
-+/- hyperesthesia

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51
Q

How to diagnose ANNPE (1)

A

-MRI

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52
Q

What is the MEDICAL/supportive care treatment for ANNPE? (3)

A
  1. crate rest
  2. time
  3. PT (once wound is healed)
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53
Q

When should SURGERY be indicated for ANNPE?

A

-if compressive

PROGNOSIS - good if intact nociception

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54
Q

Congenital spinal malformations are usually _______ findings.

A

Congenital malformations are usually INCIDENTAL findings.

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55
Q

Malformations of the vertebral body/vertebral disc are: (3)

A

-usually incidental findings
-mostly treatable
-neuro signs occur secondary to trauma or compression

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56
Q

Malformations of the vertebral arch/spinal cord are: (3)

A

-maybe incidental
-less treatable
-neuro signs from result of spinal cord malformation

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57
Q

What does AAI stand for?

A

Atlantoaxial instability

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58
Q

What is the definition of AAI?

A

instability of the C1-C1 joint – leading to injury of the cranial cervical spinal cord and +/- caudal brainstem

can happen via malformation or trauma

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59
Q

What MALFORMATIONS can lead to AAI? (3)

A
  1. malformation of C1 and C2
  2. malformation of dens
  3. ligament abnormalities
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60
Q

What TRAUMA can lead to AAI? (2)

A
  1. dens fracture
  2. ligamentous rupture
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61
Q

CS of AAI? (4)

A
  1. cervical pain – STIFF neck
  2. tetraparesis/plegia
  3. brainstem signs
  4. seizure -like episodes
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62
Q

True/False: You must NOT FLEX the neck of a patient with AAI

A

TRUE – you should NOT FLEX the neck – this causes more compression of the spinal cord.

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63
Q

What kind of imaging is needed for AAI? (4)

A

IMMOBILIZE the patient before imaging

-rads (neutral, dynamic, ventrodorsal, oblique)
-CT
-myelography
-MRI

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64
Q

What does MEDICAL treatment of AAI entail?

A

INDICATIONS
-immature bones
-very small patient
-mild signs that are resolving
-cost concerns

TREATMENT
-splinting/bandaging (months)
-medication - NSAIDS
-cage confinement/rest

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65
Q

What does SURGICAL treatment of AAI entail?

A

INDICATIONS (usually indicated)
-moderate to severe neuro deficits/pain
-recurrent episodes of cervical pain
-unresponsive to medical treatment
-angulation of dens

METHODS
-dorsal – BUT DO VENTRAL

PROGNOSIS for sx
-good

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66
Q

What does CSM stand for?

A

Cervical SpondyloMyelopathy

aka Cervical Stenotic Myelopathy

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67
Q

Etiology of CSM (cervical spondylomyelopathy)

A

-genetic/congenital
-conformation
-nutritional - Ca?
-trauma (exercise)

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68
Q

What are the two types of CSM?

A
  1. DA-CSM - disc-associated CSM (think doberman)
  2. OA-CSM - osseous-associated CSM (think great dane)

ALL CSM dogs have stenosis (absolute vs. relative) - static and/or dynamic compression

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69
Q

How to DIAGNOSE DA-CSM? (3)

A

-rads
-MRI
-myelography

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70
Q

When is MEDICAL treatment of DA-CSM indicated? (and OA)

A

-milder cases only
–pain only
–mild deficits

-cost constraints
-high risk patients (anesthetic and surgical risks)

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71
Q

When is SURGICAL treatment of DA-CSM indicated?

A

-controversial

-moderate/severe deficits
-acute deterioration
-focal lesion
-unresponsive to medical tx

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72
Q

What does MEDICAL treatment of DA-CSM entail? (4)

A

-rest
-analgesics (trama-gaba)
-anti-inflammatories (NSAIDs vs steroids)
-physical rehabilitation

PROGNOSIS: guarded

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73
Q

What does SURGICAL treatment of DA-CSM entail? (3)

A

-decompression - bc stenosis
–direct
–indirect with fusion

-motion preserving techniques
-also physical rehab

PROGNOSIS: Good

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74
Q

CS of CSM (6)

A

-difficulty walking (tetraparesis)
-ataxia
-neck pain

-hypermetria
-CP deficits
-reflex deficits

-if DA-CSM > due to C5-6-7 favored localization, TLs can present LMN and PLs as UMN
-OA-CSM – PLs often worse than TLs

OA
-chronic progressive cervical myelopathy
-PLs signs seen first
-often acute decline

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75
Q

What does OA-CSM stand for?

A

Osseous-associated cervical spondylomyelopathy

aka wobbler syndrome

think young giant breeds (and some large breeds) — GREAT DANE

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76
Q

Pathology of OA-CSM

A

-hypertrophy of bony structure, NOT disc related like DA-CSM – hypertrophy causes stenosis/compression of spinal cord

-bony proliferation of vertebrae around articulations (typically dorsolateral compression)

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77
Q

OA-CSM Imaging

A

-rads (+/- myelogram)
-CT (+/- myelogram)

-MRI - GOLD STANDARD
–evaluates spinal cord parenchyma (increased intensity with spinal cord)
–guides treatment options
–identifies most severely affected sites

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78
Q

When is SURGICAL treatment for OA-CSM indicated?

A

-severe pain
-moderate/severe deficits
-focal lesion
-acute deterioration

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79
Q

Spinal Stenosis

A

-narrowed vertebral column
-congenital, developmental or acquired
-osseous and or soft tissues

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80
Q

Congenital Scoliosis

A

-lateral angulation of the spine
-congenital forms often progress

-causes:
–vertebral/ligamentous anomalies
–cystic spinal cord lesions
–abnormal muscular support

-neuro signs may occur

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81
Q

Spina Bifida

A

-presence of midline cleft due to failure of vertebral arch fusion
-size of cleft related to amount of spina cord anomaly present
-one or multiple vertebrae affected

-diagnose - rads, MRI
–bulldogs, manx cats - heritable

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82
Q

Arachnoid Diverticulum

A

-fluid filled structures within the arachnoid
-congenital or acquired
-slowly progressive, non-painful myelopathy
-may be incidental

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83
Q

How would you DIAGNOSE GME (Granulomatous Meningoencephalomyelitis)?

A

-MRI

-CSF
–pleocytosis
–rule out infection
–mostly lymphocytes and macrophages

-definitive diagnosis: HISTOPATHOLOGY

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84
Q

What kind of dogs get GME?

A

-primarily small breeds – toy breeds – purse dogs
-but any breed can be affected

-usually young to middle aged

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85
Q

How do you treat GME?

A

-immune suppression
–steroids
–cyclosporine
–cytosine

-monitor CS
-recheck CSF

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86
Q

What’s the prognosis for GME?

A

-if short term > good/fair
-if long term > guarded

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87
Q

What does SRMA stand for?

A

Steroid Responsive Meningitis Arteritis

88
Q

CS for SRMA

A

-CERVICAL PAIN
-dullness/lethargy
-stiff gait
-febrile
-+/- IMPA (artery part of SRMA)
-NO NEURO DEFICITS

89
Q

Which dogs get SRMA?

A

Any – but think Boxers, Beagles, and Burmese Mt. Dogs

90
Q

How do you DIAGNOSE SRMA?

A

-diagnosis of exclusion
-rule out other dz with minimum database (CBC/chem/thoracic rads/abdominal US)
-MRI

-CSF
–neutrophilic pleocytosis – but this could also just mean bacterial infection (so must differentiate with MRI)
–elevated protein

91
Q

What is the TREATMENT for SRMA?

A

-immune suppression
–steroids

-monitor CS
-recheck CSF

92
Q

What is the PROGNOSIS for SRMA?

A

Excellent – most dogs can be tapered off meds completely

93
Q

Infectious CNS dz can occur where?

A
  1. spinal cord parenchyma
  2. epidural space
  3. vertebral column (disc, vertebrae)
94
Q

CS of general Infectious CNS Dz

A

-acute/subacute onset (bacterial/diffuse dz)
-subacute to chronic (fungal)
-pain
-hyperesthesia
-spinal rigidity
-fever
-neuro deficits

95
Q

How do you DIAGNOSE Infectious CNS Dz? (4)

A

-systemic evaluation
-culture!!!
-imaging (rads, advanced imaging)
-CSF analysis

96
Q

3 Common forms of Infectious CNS Dz?

A
  1. meningitis/myelitis
    -focal
    -multifocal
    -diffuse
  2. epidural empyema =extradural abscess
  3. discospondylitis (secondary spread to spinal cord)
97
Q

CS for Meningitis/Myelitis

A

-acute onset
-pain/hyperesthesia
-lethargy
-myelopathy w cranial signs
-60% neutrophilia on CBC
-50% febrile

98
Q

How do you DIAGNOSE Meningitis/Myelitis? (3)

A

-MRI
-CSF
-Culture: blood, urine, CSF, tissue

99
Q

What would CSF look like with Meningitis/Myelitis?

A

-neutrophilic pleocytosis
–increased production
–decreased glucose
–xanthochromia (yellow-ish CSF)

only 20% are culture positive!!!

100
Q

Tx for Meningitis = Abx

When choosing an antibiotic and you don’t have sensitive testing/when no culture is positive, be aware of the 4 Bs – what are the 4Bs?

A
  1. broad spectrum
  2. bactericidal
  3. B-lactamase
  4. BBB cross function
101
Q

More tx for Meningitis/Myelitis:

A

-Abx…
-anti-inflammatories
-NSAIDs
-Corticosteroids?
-supportive care
-monitoring

102
Q

For meningitis/myelitis – assume inflammation is immune-mediated if: (5)

A

-culture negative
-no organisms seen
-no other site of infection
-minimal contrast enhancement on MRI
-appropriate signalment and hx

ALL inflammation will respond to steroid initially, so must monitor

103
Q

Discospondylitis definition:

A

infection involving the intervertebral disc and adjacent endplates

104
Q

What is the pathogenesis of discospondylitis?

A

-primary dz
-foreign body migration
-hematogenous
-extension of disease
-penetrating wounds (trauma/surgery)
-immunosuppression

105
Q

Most common site affected for discospondylitis?

A

L7-S1

BUT can occur anywhere
-mid thoracic vert.
-caudal cervical vert.
-lumbar vert.

can lead to multiple empyema

106
Q

What are common organisms that cause discospondylitis?

A

-bacterial
–staphylococcus aureus/intermedius
–streoptococcus
–E. coli

-fungal
–aspergillus

107
Q

What type of dogs usually get Discospondylitis?

A

-large/giant breeds (GSD - fungal, Aspergillus)
-purebred>mix
-males>females
-young to middle aged
-immunosuppressed dogs
-uncommon in cats

108
Q

CS of Discospondylitis

A

-spinal pain (+/- myelopathy)

-30% have systemic signs
–inappetence
–fever
–weight loss

109
Q

How would you DIAGNOSE Discospondylitis?

A

-imaging
–rads (+/- myelography) - under anesthesia, complete vertebral column
–CT - gold standard for bone
–MRI - gold standard for soft tissue

-culture
–aspirates of lesion/disc
–surgical site
–blood
–urine
–CSF

-cytology
-serology (for Brucella)

110
Q

Tx for Discospondylitis

A

-antibiotics (for bacterial infection)
–4 Bs

-exercise restriction
-analgesics
-anti-inflammatories (NSAIDs, corticosteroids?)

-surgery (to decompress and debride)

111
Q

How long does Disco take to heal?

A

-weeks to years

-recheck rads 1-3mo, then q3-6mo to monitor

-fusion=healed

-recurrence is possible

112
Q

What if the infection for Discospondylitis persists? (4)

A
  1. recapture and repeat sensitivity
    2.consider secondary infection
  2. consider resistant organisms
  3. consider non-infectious disease
113
Q

What is the most common fungal organism that causes Disco in GSDs?

A

Aspergillus

-usually multiple discs
-guarded to poor prognosis

114
Q

How do you treat fungal disco?

A

amphotericin B
azoles
culture and sensitivity
steroids or NSAIDs

generally seriously guarded prognosis

115
Q

What does FCE stand for?

A

Fibrocartilaginous embolism

-infarction of the spinal cord
-obx of arterial supply via fibrocartilage

116
Q

Which dogs get FCE?

A

ACTIVE Large breeds – esp. Miniature Schnauzers, Min Pins and Shelties

117
Q

What’s the onset of FCE?

A

-Peracute, non-painful, often lateralized (similar to ANNPE)

118
Q

How do you DIAGNOSE FCE?

A

-signalment, hx, NE
-MRI (intrinsic lesion -T2 hyper)
-CSF (mixed pleiocutosis +/- neutrophils)
-histopathology

119
Q

How do you treat FCE?

A

-supportive care
-PT

variable time to recovery – hours to months

120
Q

What’s the PROGNOSIS for FCE?

A

-depends on location and severity
–UMN lesion – good prog
–LMN lesion – guarded prog
–loss of nociception – guarded prog

121
Q

How to differentiate between FCE and ANNPE?

A

it’s very hard!

-for ANNPE, usually lesion is right above disk space, unlike FCE

122
Q

What is Degenerative Myelopathy?

A

-slowly progressive degeneration of specific spinal cord tracts and nerve roots in the TL region
-starts as a T3-L3 myelopathy
-chronic
-NON-PAINFUL
-asymmetrical at first

123
Q

How do you DIAGNOSE DM?

A

-diagnosis of exclusion (RULE OUT IVDD TYPE II)

-MRI – WNL most of the time
-CSF – increased protein + normal cell count
-genetic testing – SOD-1 gene

definitive diagnosis - histopathology

124
Q

How do you TREAT DM?

A

-no known treatment

-SUPPORTIVE CARE
–physiotherapy
–regular exercise
–lean body weight

125
Q

What is the PROGNOSIS for DM?

A

-poor to grave long term

126
Q

What gene is associated with DM?

A

-SOD-1

if you’re AA (affected) – you’re AT RISK for developing DM

-all dogs with DM have AA mutation

127
Q

Non-neural (extradural) SPINAL CORD NEOPLASIAS:

A

-vertebral/osseous origin
-primary or metastatic

–sarcomas
–carcinomas
–myelomas
–osteochondroma/MCE

128
Q

Lymphoma:

A

-can do anything
-anywhere
-any breed
-any age

129
Q

What neoplasia can YOUNG (<2yo) dogs get?

A

-lymphoma
-SCTYD
-Osteochondroma
-PNST
-Meningioma

130
Q

CS of Spinal Cord Neoplasia

A

-chronic onset
-pain
-weight loss, cachexia
-paraneoplastic, polyneuropathy

131
Q

How to diagnose a Spinal Cord Neoplasia?

A

-exam
-systemic diagnostic work up
-imaging (rads, advanced)
-CSF
-biopsy

132
Q

Do nervous system tumors cause bony changes seen on radiographs?

A

NO, they do not

133
Q

What is the Cauda Equina?

A

bundle of nerve roots caudal to the conus meduallaris

conus meduallaris is the end of the spinal cord nerves

134
Q

Where is the Cauda Equina in a dog/cat?

A

L7-caudal

135
Q
  1. At birth the spinal cord and vertebral canal are the SAME or DIFFERENT lengths?
  2. As one matures, the spinal cord is SHORTER/LONGER/THE SAME LENGTH than vertebral column?
A
  1. same lengths
  2. spinal cord is shorter than vertebral canal/column

this is significant bc spinal cord segment may not really line up with the same vertebrae. they mostly line up from T1-L2.

136
Q

In the dog, the the spinal sacral cord segments are in which vertebral body?

A

L5

137
Q

The sacral and caudal nerve roots all pass over the ________ disc space before exiting out of the foramen.

A

L7-S1

138
Q

Nerve roots –> Spinal nerves (exit foramen) –> spinal nerves fuse to form peripheral nerves.

What are the most important peripheral nerves that come from the Cauda Equina?

A

-sciatic (L6-S2)
-pelvic (S1-S2)
-pudendal (S1-S3)

139
Q

What is Cauda Equina Syndrome (CES)?

A

-group of neuro signs cause by a lesion affecting the cauda equina

-CANNOT distinguish CES clinically from LMN spinal cord signs (like a L7-cd myelopathy), so MUST rule out myelopathy first

140
Q

CS of CES

A

-Motor - LMN signs to all or some - tail, anus, pelvic limbs
–tail (Cd1 - 5+) - reduced carriage, reduced wag, flaccid
–anus (S1-S3) - reduced/absent perineal reflex, incontinent
–pelvic (L7-S1) -reduced withdrawal and gastroc reflex, neuro muscle atrophy, unilateral PL lameness

PARAPARESIS, not plegia

-bladder (dribbling, incontinence)
-sensory abnormalities (reduced CP, altered body sensation (hyperesthesia, hypo, anesthesia)
-patellar pseudo-exaggeration (lazy – prolonged extension phase, loss of antagonism of femoral nerve muscles)
-apparent spinal pain

141
Q

How do you DIAGNOSE CES?

A

-rule out myelopathy
-minimum database
-dynamic rads (flexed/extended)
-CSF
-MRI, CT
-culture
-biopsy
-surgical explore
-electrophysiology
-cytology

142
Q

Lumbosacral Vertebral Canal Stenosis in Dogs

A

-acquired, large breeds (GSDs)
-males>females
-slowly progressive
-NE: no deficits, pain, LMN signs
-may be asymmetric
-stenosis secondary to:
–type II disc protrusion
–hypertrophy/hyperplasia of ligaments

DIAGNOSE:
-ortho exam
-spinal rads
–dynamic views (instability)
-CSF
-CT
-MRI
-electrophysiology

PROGNOSIS:
-varies
-mild signs – good
-incontinence – poor even with surgery

143
Q

How do you TREAT Lumbosacral Vertebral Canal Stenosis?

A

MEDICAL
-rest
-analgesics
-close vet supervision
-for dogs with mild signs

SURGERY
-dorsal laminectomy

144
Q

What other differentials are there for Cadua Equina dz?

A

ANOMALOUS
-congenital issues – spina bifida, sacrocaudal dysgensis

INFECTIOUS
-discospondylitis
–bacterial good prog
–fungal poor prog
–no neuro deficits
–CBC - leukocytosis, left shift
–rads lags, may need CT/MRI for current display of issue

TRAUMA
-common
-great prognosis bc so robust
-surgery is best, esp for cauda equina compression/instability

145
Q

One motor unit innervates ONE/MANY myofibers.

A

One motor unit innervates MANY myofibers.

146
Q

Type I Myofibers: What kind of metabolism and nickname?

A
  1. oxidative metabolism
  2. slow twitch (slow twitch as they generate force at a slower rate comparably with type II)

better for longer exercises, doesn’t fatigue as easily

147
Q

Type II Myofibers: What kind of metabolism and nickname?

A
  1. Glycolytic metabolism
  2. fast twitch (generate force at a faster rate than type I)

better for short bursts of energy, easily fatigued

148
Q

What 3 classes are there for Neuromuscular Dz?

A
  1. neuropathies
  2. juntionopathies
  3. myopathies
149
Q

CS of neuromuscular dz

A

-focal or generalized weakness
-gait abnormalities
-paresis/paralysis
-exercise-induced weakness
-decreases/absent reflexes
-postural alterations
-dyspnea (difficult breathing)
-dysphonia (altered voice)
-dysphagia (difficult swallowing)
-regurge

-muscle atrophy
-muscle hypertrophy
-skeletal deformities

-CERVICAL VENTROFLEXION
–classic fo weakness in cats
–pathognomonic of neuromuscular dz, but could be any classification

-megaesophagus

150
Q

What is EMG?

A

Electromyography – detects and characterizes electrical activity of patient’s muscles

must be under general anesthesia

151
Q

What does Normal Muscle do on EMG?

A

-when needle is not moving, there are no waves

-INSERTIONAL ACTIVITY - normal bc disruption of muscle membrane
–normal short burst but stops when needle stops
–decreased size in wave = suggest decreased muscle mass
–increased size = hyper excitable muscle membrane

-then ELECTRICAL SILENCE when needle is not moving

152
Q

There is NORMAL and ABNORMAL spontaneous activity on an EMG.

Why is there normal spontaneous activity?

A

-when the needles is close to a neuromuscular junction

-MEPPs – miniature end plate potentials (end plate noise)
-release of ACh from NM junction

-SEASHORE sound

153
Q

Why is there abnormal spontaneous activity on an EMG?

A

indicates MUSCLE MEMBRANE INSTABILITY
-secondary to denervation (denervation)
-primary muscle dz (myopathy)

154
Q

What does abnormal spontaneous activity look like on an EMG? What does it SOUND like?

A

-fibrillation potentials & positive sharp waves (RAIN ON TIN ROOF)
-complex repetitive discharges (MOTORCYCLE IDLING)
-myotnic potentials (DIVE BOMBER - wax and waning)

155
Q

Another form of Electrodiagnostic testing (in addition to EMG) is NERVE CONDUCTION VELOCITY.

  1. If there is normal nerve conduction velocity, then it suggests abnormalities are from a NEUROPATHY/MYOPATHY.
  2. If there is abnormal nerve conduction velocity, then it suggest abnormalities are from a NEUROPATHY/MYOPATHY.
A
  1. If there is normal nerve conduction velocity, then it suggests abnormalities are from a MYOPATHY.
  2. If there is normal nerve conduction velocity, then it suggests abnormalities are from a NEUROPATHY.
156
Q

Open biopsies are usually done on SMALL/LARGE animals.

A

SMALL animals

157
Q

Why must we be careful when choosing to do a nerve biopsy on an animal?

A

Because the nerve will NOT grow back – morbidity. Must prepare owner and patient for deficits.

158
Q

You can FIX or FREEZE nerve/muscle biopsies. Which is best for which tissue?

A

FIX nerves
FREEZE/FROZEN muscles

159
Q

There are 3 categories of Neuropathies:

A
  1. mononueropathies (single nerve affected)
  2. multiple mononeuropathies (plexopathy) – multiple nerves, but same anatomical site
  3. polyneuropathy – multiple nerves, different locations
160
Q

Neuropathy - histological features

A
  1. angular atrophy of Type I and Type II (caused by denervation)
  2. pyknotic nuclear clumps - end stage denervation
  3. denervation and reinnervation (on history, looks like one type of muscle - not a mix of both type 1 and 2)
160
Q

Neuropathy - histological features

A
  1. angular atrophy of Type I and Type II (caused by denervation)
  2. pyknotic nuclear clumps - end stage denervation
  3. denervation and reinnervation (on history, looks like one type of muscle - not a mix of both type 1 and 2)
    –this process leads to a bunch of myofibers being innervated by a few/one axon, which can then lead to (changes myofibers to one type as well)
  4. group atrophy (if the few/one axon is damaged)
    –grouped atrophy means chronicity
161
Q

Tetanus is a neuropathy at the level of the spinal cord.

Tetanus can be considered a toxico-infection. What’s the pathophysiology of tetanus?

A

In anaerobic condition, C. tetani infects body. Produced toxin in body. Toxin enters nerve and ascends cord. Destroys inhibitory neuron (Renshaw cell) synapse to a-LMN. Results in “disinhibition” of LMN = tetany

irreversible – so takes weeks to heal

162
Q

CS of Tetanus

A

-marked rigidity
-rinus sardonicus (weird face)

DIAGNOSE via history and CS

163
Q

How do you TREAT tetanus? (4)

A

-antitoxin - deals with unbound toxin
-debridement
-antibiotics
-supportive care

164
Q

Brachial plexus is a common place for MULTIPLE MONONEUROPATHIES. What can cause these multiple mononeuropathies?

A
  1. Trauma - avulsion
  2. neoplasia -MPNST
  3. inflammatory (infection) - neuritis
165
Q

What nerves are a part of the Brachial Plexus?

A

-musculocutaneous (c6,7,8) - biceps reflex
-radial (c7,8,t1) - weight bearing, triceps reflex
-median/ulnar
-lateral thoracic
-symapthetic

166
Q

Lumbosacral Plexus is another common place for MULTIPLE MONONEUROPATHIES. Which nerves are from the LS Plexus?

A
  1. femoral (L4,5,6) - weight bearing, PATELLAR reflex
  2. sciatic (l6,7,s1) - withdrawal/flexion and GASTROC reflex
  3. pudendal (s1,2,3)
  4. pelvic (s1,2,3)
167
Q

Generalized neuromuscular disease usually entails what:

A

-LMN signs to all 4 limbs > general weakness

168
Q

When a case is presented with PERACUTE FLACCID TETRAPARESIS/PARALYSIS what are your top 4 differentials?

A
  1. Acute Polyradiculoneuritis (neuropathy)
  2. Botulism
  3. Tick paralysis
  4. Fulminant (sudden)MG
169
Q

Acute polyradiculoneuritis – is a neuropathy

A

-rapid onset (acute) - <48hr flaccid tetraparesis/plegia
-LMN signs in all 4 limbs
-often history of bite or antigenic stimulus in past 2 weeks

PATHOPHYSIOLOGY
-immune-mediated attack of the ventral root predominantly (motor)
-so motor function lost,SENSORYremains

170
Q

How do you DIAGNOSE acute polyradiculoneuritis?

A

-CS
-Hx
-electrophysiology

EMG spontaneous activity 4-5 days

171
Q

How do you TREAT acute polyradiculoneuritis?

A

-SUPPORTIVE care
-ventilation support
-plasmapharesis

RECOVERY
-time for remyelination and axonal regrowth
-weeks to months for full recovery

172
Q

There are CHRONIC Polyneuropathies – what could they be caused by?

A

-metabolic (endocrine dz)
-toxins - drugs
-infectious (protozoal)
-neoplastic (lymphoma)
-paraneoplastic
-congenital
-degenerative/unknown cause - doesn’t have a lot of great tx for it
–MOST COMMON
–do everything/test – ex. blood test to see if they have any abnormality to treat

173
Q

CS for Chronic Polyneuropathies

A
  1. PLs more affected
  2. generalized weakness/LMN signs, but not as severe as acute polyneuropathy
    3.distal muscles are weaker, so plantigrade/palmigrade stance
  3. laryngeal paralysis/stridor seen in dogs
    –recurrent laryngeal is the longest nerve in the body, so one of the first nerves to be affected
174
Q

Diabetic Polyneuropathy

A

Systemic issue causing polyneuropathy – via chronic hypoglycemia

175
Q

An action potential will reach a nerve terminal. There will be a decrease in membrane potential (shoots up on action potential) – this causes which channels to open, thus causing an influx of which ion?

A

Ca++ channels – influx of Ca++

176
Q

At the nerve terminal, Ca++ stimulates what to be released into the synapse?

A

Ach

177
Q

Ach binds on the post-synaptic membrane, causing what cation channels to open, thus causing the flow of what? Remember, this is the start of the action potential in muscle.

A

Na and K channels – influx of Na and outflow K

178
Q

After Ach bins on the postsynaptic membrane – causing an influx of Na+ and outflux of K+, what other voltage gate channel opens to cause an influx of?

A

Voltage gated Na+ channels open, so more Na can come into the post-synaptic membrane causing depolarization for the muscle action potential

179
Q

The addition influx of Na+ in the post-synaptic membrane causes what other voltage gates to open and in what location?

A

Opens voltage-gated Ca++ channels in T-tubules and Sarcoplasmic Reticulum – leading to contraction of muscle

180
Q

How is a neurotransmission stopped?

A

With ACETYLCHOLINESTERASE – it rapidly hydrolyzes Ach in the synaptic cleft

181
Q

How do you diagnose Juntionopathies?

A

Routine histopathology abnormalities are usually absent or non-specific.

Diagnose via:
-biochemical
-immunological
-toxicological
-electrodiagnostic testing

182
Q

What classifications are there for Juntionopathies? (3)

A
  1. pre-synaptic
  2. synaptic
  3. post-synaptic
183
Q

What are PRE-SYNAPTIC DISORDERS for Junctionopathies?

A
  1. decreased Ach release > causes weakness
    –hypoglycemia
    –hypermagnesemia
    –botulism
    –tick paralysis
    –aminoglycosides
  2. increased Ach release > causes weakness
    -caused by continued depolarization of post synaptic membrane and depletion of pre-synaptic vesicles
    –hypomagnesemia
    -envenomation
184
Q

Tick Paralysis is a Pre-synaptic Disorder! Which tick causes it?

A

Demacentor

185
Q

Tick Paralysis – a pre-synaptic disorder – causes a reversible interference with Ca++ mediated Ach release - T/N

A

TRUE

186
Q

How do you DIAGNOSE Tick Paralysis?

A

-find tick
-remove tick and see improvement

187
Q

How do you TREAT Tick Paralysis?

A

-clip, tick hunt
-topical acaricide
-supportive care
-hyperimmune serum

188
Q

Botulism is a Pre-synaptic disorder. How is it caused?

A

Ingestion of type C neurotoxin for C. Botulinum (from carrion/spoiled food)

189
Q

Botulism causes an irreversible inhibition of Ach release from cholinergic nerve terminals. T/N

A

True

190
Q

CS of Botulism

A

-fatal tetraplegia and areflexia (no tendon reflexes)
-mild weakness
-megaesophagus/aspiration pneumonia

191
Q

How do you DIAGNOSE Botulism?

A

-detection of organism or toxin in ingesta, vomit, feces, serum
-neutralization test in mice
-in vitro antigenicity testing

-dogs - type C reported
-cats - no natural cases reported

192
Q

How do you TREAT Botulism?

A

-supportive care
-ventilation support
-C. botulinum antitoxin (for A, B, and E – but not C)
–only affects unbound toxin, not bound toxin at NM junction

RECOVERY - 1-3 weeks, risk for aspiration pneumonia

193
Q

Synaptic cleft disorders include:

A
  1. cholinesterase inhibitors – inhibit breakdown of Ach, prolong activity at receptors
    -signs of toxicity: SLUD-E, salivation, lacrimation, urination, defecation, emesis
194
Q

Post synaptic disorders include:

A
  1. block binding of Ach to AchR
    -competitive NM blockade
    -think Myasthenia Gravis
195
Q

Myasthenia Gravis

A

Congenital
-deficiency or functional disorder of nicotinic AchR – uncommon in dogs/cats

Acquired
-autoimmune attack against AchR resulting in depletion of receptors – uncommon in cats, common in dogs
-what also can happen is phagocytose of receptors with complement, damage to post synaptic membrane, widening of the cleft, etc.

196
Q

What age do dogs get Myasthenia Gravis?

A

Bimodal – 2-4yo, 9-13yo

197
Q

CS of Acquired MG

A

-esophageal, pharyngeal, facial weakness
-generalized weakness
–lameness or down in PL
-exercise intolerance
-regurge, megaesophagus
-aspiration pneumonia
-mediastinal mass (thymoma) – do rads to see so we can try and treat and see resolve of CS
-acute tetraplegia - uncommon

198
Q

How do you DIAGNOSE Acquired MG?

A
  1. immunological testing - GOLD standard
    -measure AchR antibodies in serum
    -stain muscle for IgG on endplates
  2. Pharmalogical testing
    -short acting Actylcholinesterase inhibitor
    -not specific for MG, other NM dz can responsd
  3. Electrodiagnostic testing
    -repetitive stimulation
    -decremental response
199
Q

How do we TREAT Acquired MG?

A

-cholinesterase inhibitors
-elevated feeding

-plasmapharesis?
-immunosuppresion?
-spontaneous remission?

200
Q

What’s the PROGNOSIS of MG?

A

-guarded due to always being at risk of asp. pneumonia

201
Q

What are the 2 classifications of myopathies?

A
  1. inflammatory
  2. non-inflammatory
202
Q

X-linked muscular dystrophy is a myopathy. What deficiency does it cause?

A

Dystrophin – cytoskeletal protein

203
Q

Signalment and CS of X-linked Dystrophy

A

YOUNG WEAK ANIMALS

-goldens and other breeds
-onset 8-10 weeks

-progressive weakness, gait abnormalities, dysphagia
-muscle atrophy, some hypertrophy

204
Q

How do you DIAGNOSE X-linked muscular dystrophy?

A

-elevated CK (100,000s)
-abnormal EMG
-muscle biopsy - multifocal necrosis, immunocytochemical staining

205
Q

How do you TREAT muscular dystrophy?

A

THERE IS NO TREATMENT

-treat secondary complications - dysphagia, aspiration

206
Q

What is Malignant Hyperthermia? (myopathy)

A

-triggered by anesthetic agents
-defect in Ca++ homeostasis – opening Ca++ channels
-sustained increase in cytoplasmic Ca++
-continuous contraction
-mutation of RyR1 gene

207
Q

What storage disorders are there? (myopathy)

A
  1. glycogen
  2. lipid
    -increased lipid in type I myofibers
208
Q

What is Myotonia Congenita?

A

-persistent muscle contraction
-chloride channelopathy
-congenital in dogs, goats, horses

-chow, min. schnauzer

209
Q

CS of Myotonia Congenita

A

-stiff gait that improves with exercise
-muscle hypertrophy

-could progress or plateau

210
Q

How do you DIAGNOSE Myotonia Congenita?

A

-percussion - dimple
-EMG - dive bomber – myotonic potentials
-CK - normal to increased
-Muscle biopsy - non-specific abnormalities

211
Q

Exertional rhabdomyolysis

A

-secondary to extreme exertion

212
Q

How do you DIAGNOSE exertion rhabdomyolysis?

A

-hx
-PE - muscle pain
-BW - elevated CK
-urinalysis - myoglobinuria

213
Q

How do you TREAT Myoglobinuria?

A

-supportive care
-diuresis for myoglobinuria

214
Q

Masticatory Muscle Myopathy is an INFLAMMATORY Myopathy.

A

CS of Masticatory Muscle Myopathy

VET433A (8 decks)

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