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)
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
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
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
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
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
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
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
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
10
Q
Neoplasia of Spinal Cord
A
Typical Signalment: Any breed
Typical Age: Usually older
Localization: Anywhere depending on type
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
12
Q
Fracture-Lux
A
Type of Signalment:
Painful: Yes, IMMOBILIZE
13
Q
What does AMBULATORY mean?
A
at least 3 limbs are able to move/support the animal’s weight
14
Q
What is a myelopathy?
A
myelo - spinal cord/marrow
dz/disorder affecting the spinal cord:
-dura
-vertebrae
-epidural space
-neuro parenchyma
15
Q
What are the 3 different types of myelopathies, relative to the DURA?
A
Lecture 22, Slide 8
- Extradural
- Intradural, extramedullary
- Intramedullary
16
Q
What are the 2 types of myelopathies, relative to the SPINAL CORD?
A
Lecture 21, Slide 9
- intrinsic – affecting the neuro parenchyma
- extrinsic – everything else (outside of spinal cord parenchyma)
-also, in terms of dura, includes extradural and intradural, extrameduallary
17
Q
What are the 4 NAL classifications of myelopathies?
A
- C1-C5
- C6-T2
- T3-L3
- L4-caudal (S3)
18
Q
Findings are based on ______ and _______, NOT the underlying cause.
A
Findings are based on localization and severity, NOT The underlying cause.
19
Q
If there are LMN and UMN lesions, _____ always wins.
A
LMN always wins/LMN will mask UMN signs.
20
Q
Myelopathies have normal: (2)
A
- normal mentation
- CN function
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)
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
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
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
25
Severity levels from mild to severe (5)
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
26
Decerebellate posture:
-lesion affecting cerebellum
-extended TLs, +/- flexed PLs
-NE consistent with cerebellum lesion
-normal consciousness
27
What's the anatomy of a vertebral disc?
-nucleus pulposus in the center (jelly)
-annulus fibrosis around (dough)
28
IVDD Type I affects which types of dogs?
Chondrodysplastic! Short legs!
29
Which area of the spine does IVDD Type I mainly target?
any, BUT:
TL>cervical>LS
30
CS for IVDD Type I:
variable
-pain
-paresis
-ataxia
-hyperesthesia
-incontinence
-loss of pain sensation
-lameness
31
How would you diagnose IVDD Type I? (2)
-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
32
When would you conservatively manage IVDD Type I/Which GRADES would you consider CONSERVATIVE management?
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
33
What does CONSERVATIVE management of IVDD Type I entail? (3)
-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
34
When should SURGICAL management of IVDD Type I be considered?
-any grade can be surgical, esp grade 0-3
-rapid progression of IVDD should be considered for sx
-FAILED medical management
-severe pain
35
What are the BENEFITS of IVDD Type I surgery? (4)
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
36
What are the GOALS of surgical treatment of IVDD Type I? (3)
1. decompression
2. control hemorrhage
3. disc fenestration
Techniques:
1. hemilaminectomy
2. ventral slot
3. vacations of above
37
Post-Op management of IVDD Type I: (6)
Nursing Care
1. bladder management
2. recumbency care
3. pain management
Rehabilitation
1. maximize recovery
2. maintain muscle mass
3. maintain joint movement
38
How is Myelomalacia (MM) associated with IVDD Type I + any spinal cord injury?
-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
39
Progressive myelomalacia CS and Pathophysiology
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
40
What happens to the vertebral disc with IVDD Type II?
the annulus fibrosis hypertrophies!
-fibroid metaplasia/degeneration
-protrusion
-can happen with any dog
-results in spinal cord compression > meningeal/nerve root irritation
41
What is the most common location for IVDD Type II?
Common at L7-S1, BUT can occur anywhere
42
CS for IVDD Type II
-paraparesis/tetraparesis
-ataxia
-pain with palpation
-+/- lameness, incontinence
43
How would you diagnose IVDD Type II? (4)
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
44
When would CONSERVATIVE treatment be indicated for IVDD Type II? (4)
1. mild dz
2. very slowly progressive
3. non-painful
4. continent
PROGNOSIS: variable, exercise and physiotherapy effective
45
What is the treatment for CONSERVATIVE management of IVDD Type II? (3)
1. anti-inflammatories
2. physical rehab (some movement is good -- different than IVDD Type I)
3. supportive care
46
When is SURGICAL treatment indicated for IVDD Type II? (5)
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
47
What are the GOALS for SURGICAL treatment for IVDD Type II? (2)
1. decompression without destabilization
2. halt progression of dz
via hemilanimectomy vs pediculectomy
48
What does ANNPE stand for?
Acute Non-compressive Nucleus Pulposus Extrusion
aka Traumatic Disc Extrusion
49
ANNPE Pathophysiology?
high force/trauma -- tears annulus fibrosis and causes ASYMMETRICAL extrusion of NORMAL nucleus pulposus
-can cause compression, but very minimal
50
CS with ANNPE
-paresis/paralysis
-ataxia
-+/- LMN signs
-+/- hyperesthesia
51
How to diagnose ANNPE (1)
-MRI
52
What is the MEDICAL/supportive care treatment for ANNPE? (3)
1. crate rest
2. time
3. PT (once wound is healed)
53
When should SURGERY be indicated for ANNPE?
-if compressive
PROGNOSIS - good if intact nociception
54
Congenital spinal malformations are usually _______ findings.
Congenital malformations are usually INCIDENTAL findings.
55
Malformations of the vertebral body/vertebral disc are: (3)
-usually incidental findings
-mostly treatable
-neuro signs occur secondary to trauma or compression
56
Malformations of the vertebral arch/spinal cord are: (3)
-maybe incidental
-less treatable
-neuro signs from result of spinal cord malformation
57
What does AAI stand for?
Atlantoaxial instability
58
What is the definition of AAI?
instability of the C1-C1 joint -- leading to injury of the cranial cervical spinal cord and +/- caudal brainstem
can happen via malformation or trauma
59
What MALFORMATIONS can lead to AAI? (3)
1. malformation of C1 and C2
2. malformation of dens
3. ligament abnormalities
60
What TRAUMA can lead to AAI? (2)
1. dens fracture
2. ligamentous rupture
61
CS of AAI? (4)
1. cervical pain -- STIFF neck
2. tetraparesis/plegia
3. brainstem signs
4. seizure -like episodes
62
True/False: You must NOT FLEX the neck of a patient with AAI
TRUE -- you should NOT FLEX the neck -- this causes more compression of the spinal cord.
63
What kind of imaging is needed for AAI? (4)
IMMOBILIZE the patient before imaging
-rads (neutral, dynamic, ventrodorsal, oblique)
-CT
-myelography
-MRI
64
What does MEDICAL treatment of AAI entail?
INDICATIONS
-immature bones
-very small patient
-mild signs that are resolving
-cost concerns
TREATMENT
-splinting/bandaging (months)
-medication - NSAIDS
-cage confinement/rest
65
What does SURGICAL treatment of AAI entail?
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
66
What does CSM stand for?
Cervical SpondyloMyelopathy
aka Cervical Stenotic Myelopathy
67
Etiology of CSM (cervical spondylomyelopathy)
-genetic/congenital
-conformation
-nutritional - Ca?
-trauma (exercise)
68
What are the two types of CSM?
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
69
How to DIAGNOSE DA-CSM? (3)
-rads
-MRI
-myelography
70
When is MEDICAL treatment of DA-CSM indicated? (and OA)
-milder cases only
--pain only
--mild deficits
-cost constraints
-high risk patients (anesthetic and surgical risks)
71
When is SURGICAL treatment of DA-CSM indicated?
-controversial
-moderate/severe deficits
-acute deterioration
-focal lesion
-unresponsive to medical tx
72
What does MEDICAL treatment of DA-CSM entail? (4)
-rest
-analgesics (trama-gaba)
-anti-inflammatories (NSAIDs vs steroids)
-physical rehabilitation
PROGNOSIS: guarded
73
What does SURGICAL treatment of DA-CSM entail? (3)
-decompression - bc stenosis
--direct
--indirect with fusion
-motion preserving techniques
-also physical rehab
PROGNOSIS: Good
74
CS of CSM (6)
-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
75
What does OA-CSM stand for?
Osseous-associated cervical spondylomyelopathy
aka wobbler syndrome
think young giant breeds (and some large breeds) — GREAT DANE
76
Pathology of OA-CSM
-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)
77
OA-CSM Imaging
-rads (+/- myelogram)
-CT (+/- myelogram)
-MRI - GOLD STANDARD
--evaluates spinal cord parenchyma (increased intensity with spinal cord)
--guides treatment options
--identifies most severely affected sites
78
When is SURGICAL treatment for OA-CSM indicated?
-severe pain
-moderate/severe deficits
-focal lesion
-acute deterioration
79
Spinal Stenosis
-narrowed vertebral column
-congenital, developmental or acquired
-osseous and or soft tissues
80
Congenital Scoliosis
-lateral angulation of the spine
-congenital forms often progress
-causes:
--vertebral/ligamentous anomalies
--cystic spinal cord lesions
--abnormal muscular support
-neuro signs may occur
81
Spina Bifida
-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
82
Arachnoid Diverticulum
-fluid filled structures within the arachnoid
-congenital or acquired
-slowly progressive, non-painful myelopathy
-may be incidental
83
How would you DIAGNOSE GME (Granulomatous Meningoencephalomyelitis)?
-MRI
-CSF
--pleocytosis
--rule out infection
--mostly lymphocytes and macrophages
-definitive diagnosis: HISTOPATHOLOGY
84
What kind of dogs get GME?
-primarily small breeds -- toy breeds -- purse dogs
-but any breed can be affected
-usually young to middle aged
85
How do you treat GME?
-immune suppression
--steroids
--cyclosporine
--cytosine
-monitor CS
-recheck CSF
86
What's the prognosis for GME?
-if short term > good/fair
-if long term > guarded
87
What does SRMA stand for?
Steroid Responsive Meningitis Arteritis
88
CS for SRMA
-CERVICAL PAIN
-dullness/lethargy
-stiff gait
-febrile
-+/- IMPA (artery part of SRMA)
-NO NEURO DEFICITS
89
Which dogs get SRMA?
Any -- but think Boxers, Beagles, and Burmese Mt. Dogs
90
How do you DIAGNOSE SRMA?
-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
What is the TREATMENT for SRMA?
-immune suppression
--steroids
-monitor CS
-recheck CSF
92
What is the PROGNOSIS for SRMA?
Excellent -- most dogs can be tapered off meds completely
93
Infectious CNS dz can occur where?
1. spinal cord parenchyma
2. epidural space
3. vertebral column (disc, vertebrae)
94
CS of general Infectious CNS Dz
-acute/subacute onset (bacterial/diffuse dz)
-subacute to chronic (fungal)
-pain
-hyperesthesia
-spinal rigidity
-fever
-neuro deficits
95
How do you DIAGNOSE Infectious CNS Dz? (4)
-systemic evaluation
-culture!!!
-imaging (rads, advanced imaging)
-CSF analysis
96
3 Common forms of Infectious CNS Dz?
1. meningitis/myelitis
-focal
-multifocal
-diffuse
2. epidural empyema =extradural abscess
3. discospondylitis (secondary spread to spinal cord)
97
CS for Meningitis/Myelitis
-acute onset
-pain/hyperesthesia
-lethargy
-myelopathy w cranial signs
-60% neutrophilia on CBC
-50% febrile
98
How do you DIAGNOSE Meningitis/Myelitis? (3)
-MRI
-CSF
-Culture: blood, urine, CSF, tissue
99
What would CSF look like with Meningitis/Myelitis?
-neutrophilic pleocytosis
--increased production
--decreased glucose
--xanthochromia (yellow-ish CSF)
only 20% are culture positive!!!
100
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?
1. broad spectrum
2. bactericidal
3. B-lactamase
4. BBB cross function
101
More tx for Meningitis/Myelitis:
-Abx...
-anti-inflammatories
-NSAIDs
-Corticosteroids?
-supportive care
-monitoring
102
For meningitis/myelitis -- assume inflammation is immune-mediated if: (5)
-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
Discospondylitis definition:
infection involving the intervertebral disc and adjacent endplates
104
What is the pathogenesis of discospondylitis?
-primary dz
-foreign body migration
-hematogenous
-extension of disease
-penetrating wounds (trauma/surgery)
-immunosuppression
105
Most common site affected for discospondylitis?
L7-S1
BUT can occur anywhere
-mid thoracic vert.
-caudal cervical vert.
-lumbar vert.
can lead to multiple empyema
106
What are common organisms that cause discospondylitis?
-bacterial
--staphylococcus aureus/intermedius
--streoptococcus
--E. coli
-fungal
--aspergillus
107
What type of dogs usually get Discospondylitis?
-large/giant breeds (GSD - fungal, Aspergillus)
-purebred>mix
-males>females
-young to middle aged
-immunosuppressed dogs
-uncommon in cats
108
CS of Discospondylitis
-spinal pain (+/- myelopathy)
-30% have systemic signs
--inappetence
--fever
--weight loss
109
How would you DIAGNOSE Discospondylitis?
-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
Tx for Discospondylitis
-antibiotics (for bacterial infection)
--4 Bs
-exercise restriction
-analgesics
-anti-inflammatories (NSAIDs, corticosteroids?)
-surgery (to decompress and debride)
111
How long does Disco take to heal?
-weeks to years
-recheck rads 1-3mo, then q3-6mo to monitor
-fusion=healed
-recurrence is possible
112
What if the infection for Discospondylitis persists? (4)
1. recapture and repeat sensitivity
2.consider secondary infection
3. consider resistant organisms
4. consider non-infectious disease
113
What is the most common fungal organism that causes Disco in GSDs?
Aspergillus
-usually multiple discs
-guarded to poor prognosis
114
How do you treat fungal disco?
amphotericin B
azoles
culture and sensitivity
steroids or NSAIDs
generally seriously guarded prognosis
115
What does FCE stand for?
Fibrocartilaginous embolism
-infarction of the spinal cord
-obx of arterial supply via fibrocartilage
116
Which dogs get FCE?
ACTIVE Large breeds -- esp. Miniature Schnauzers, Min Pins and Shelties
117
What's the onset of FCE?
-Peracute, non-painful, often lateralized (similar to ANNPE)
118
How do you DIAGNOSE FCE?
-signalment, hx, NE
-MRI (intrinsic lesion -T2 hyper)
-CSF (mixed pleiocutosis +/- neutrophils)
-histopathology
119
How do you treat FCE?
-supportive care
-PT
variable time to recovery -- hours to months
120
What's the PROGNOSIS for FCE?
-depends on location and severity
--UMN lesion -- good prog
--LMN lesion -- guarded prog
--loss of nociception -- guarded prog
121
How to differentiate between FCE and ANNPE?
it's very hard!
-for ANNPE, usually lesion is right above disk space, unlike FCE
122
What is Degenerative Myelopathy?
-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
How do you DIAGNOSE DM?
-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
How do you TREAT DM?
-no known treatment
-SUPPORTIVE CARE
--physiotherapy
--regular exercise
--lean body weight
125
What is the PROGNOSIS for DM?
-poor to grave long term
126
What gene is associated with DM?
-SOD-1
if you're AA (affected) -- you're AT RISK for developing DM
-all dogs with DM have AA mutation
127
Non-neural (extradural) SPINAL CORD NEOPLASIAS:
-vertebral/osseous origin
-primary or metastatic
--sarcomas
--carcinomas
--myelomas
--osteochondroma/MCE
128
Lymphoma:
-can do anything
-anywhere
-any breed
-any age
129
What neoplasia can YOUNG (<2yo) dogs get?
-lymphoma
-SCTYD
-Osteochondroma
-PNST
-Meningioma
130
CS of Spinal Cord Neoplasia
-chronic onset
-pain
-weight loss, cachexia
-paraneoplastic, polyneuropathy
131
How to diagnose a Spinal Cord Neoplasia?
-exam
-systemic diagnostic work up
-imaging (rads, advanced)
-CSF
-biopsy
132
Do nervous system tumors cause bony changes seen on radiographs?
NO, they do not
133
What is the Cauda Equina?
bundle of nerve roots caudal to the conus meduallaris
conus meduallaris is the end of the spinal cord nerves
134
Where is the Cauda Equina in a dog/cat?
L7-caudal
135
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?
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
In the dog, the the spinal sacral cord segments are in which vertebral body?
L5
137
The sacral and caudal nerve roots all pass over the ________ disc space before exiting out of the foramen.
L7-S1
138
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?
-sciatic (L6-S2)
-pelvic (S1-S2)
-pudendal (S1-S3)
139
What is Cauda Equina Syndrome (CES)?
-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
CS of CES
-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
How do you DIAGNOSE CES?
-rule out myelopathy
-minimum database
-dynamic rads (flexed/extended)
-CSF
-MRI, CT
-culture
-biopsy
-surgical explore
-electrophysiology
-cytology
142
Lumbosacral Vertebral Canal Stenosis in Dogs
-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
How do you TREAT Lumbosacral Vertebral Canal Stenosis?
MEDICAL
-rest
-analgesics
-close vet supervision
-for dogs with mild signs
SURGERY
-dorsal laminectomy
144
What other differentials are there for Cadua Equina dz?
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
One motor unit innervates ONE/MANY myofibers.
One motor unit innervates MANY myofibers.
146
Type I Myofibers: What kind of metabolism and nickname?
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
Type II Myofibers: What kind of metabolism and nickname?
1. Glycolytic metabolism
2. fast twitch (generate force at a faster rate than type I)
better for short bursts of energy, easily fatigued
148
What 3 classes are there for Neuromuscular Dz?
1. neuropathies
2. juntionopathies
3. myopathies
149
CS of neuromuscular dz
-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
What is EMG?
Electromyography -- detects and characterizes electrical activity of patient's muscles
must be under general anesthesia
151
What does Normal Muscle do on EMG?
-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
There is NORMAL and ABNORMAL spontaneous activity on an EMG.
Why is there normal spontaneous activity?
-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
Why is there abnormal spontaneous activity on an EMG?
indicates MUSCLE MEMBRANE INSTABILITY
-secondary to denervation (denervation)
-primary muscle dz (myopathy)
154
What does abnormal spontaneous activity look like on an EMG? What does it SOUND like?
-fibrillation potentials & positive sharp waves (RAIN ON TIN ROOF)
-complex repetitive discharges (MOTORCYCLE IDLING)
-myotnic potentials (DIVE BOMBER - wax and waning)
155
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.
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
Open biopsies are usually done on SMALL/LARGE animals.
SMALL animals
157
Why must we be careful when choosing to do a nerve biopsy on an animal?
Because the nerve will NOT grow back -- morbidity. Must prepare owner and patient for deficits.
158
You can FIX or FREEZE nerve/muscle biopsies. Which is best for which tissue?
FIX nerves
FREEZE/FROZEN muscles
159
There are 3 categories of Neuropathies:
1. mononueropathies (single nerve affected)
2. multiple mononeuropathies (plexopathy) -- multiple nerves, but same anatomical site
3. polyneuropathy -- multiple nerves, different locations
160
Neuropathy - histological features
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
Neuropathy - histological features
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
Tetanus is a neuropathy at the level of the spinal cord.
Tetanus can be considered a toxico-infection. What's the pathophysiology of tetanus?
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
CS of Tetanus
-marked rigidity
-rinus sardonicus (weird face)
DIAGNOSE via history and CS
163
How do you TREAT tetanus? (4)
-antitoxin - deals with unbound toxin
-debridement
-antibiotics
-supportive care
164
Brachial plexus is a common place for MULTIPLE MONONEUROPATHIES. What can cause these multiple mononeuropathies?
1. Trauma - avulsion
2. neoplasia -MPNST
3. inflammatory (infection) - neuritis
165
What nerves are a part of the Brachial Plexus?
-musculocutaneous (c6,7,8) - biceps reflex
-radial (c7,8,t1) - weight bearing, triceps reflex
-median/ulnar
-lateral thoracic
-symapthetic
166
Lumbosacral Plexus is another common place for MULTIPLE MONONEUROPATHIES. Which nerves are from the LS Plexus?
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
Generalized neuromuscular disease usually entails what:
-LMN signs to all 4 limbs > general weakness
168
When a case is presented with PERACUTE FLACCID TETRAPARESIS/PARALYSIS what are your top 4 differentials?
1. Acute Polyradiculoneuritis (neuropathy)
2. Botulism
3. Tick paralysis
4. Fulminant (sudden)MG
169
Acute polyradiculoneuritis -- is a neuropathy
-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
How do you DIAGNOSE acute polyradiculoneuritis?
-CS
-Hx
-electrophysiology
EMG spontaneous activity 4-5 days
171
How do you TREAT acute polyradiculoneuritis?
-SUPPORTIVE care
-ventilation support
-plasmapharesis
RECOVERY
-time for remyelination and axonal regrowth
-weeks to months for full recovery
172
There are CHRONIC Polyneuropathies -- what could they be caused by?
-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
CS for Chronic Polyneuropathies
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
4. 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
Diabetic Polyneuropathy
Systemic issue causing polyneuropathy -- via chronic hypoglycemia
175
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?
Ca++ channels -- influx of Ca++
176
At the nerve terminal, Ca++ stimulates what to be released into the synapse?
Ach
177
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.
Na and K channels -- influx of Na and outflow K
178
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?
Voltage gated Na+ channels open, so more Na can come into the post-synaptic membrane causing depolarization for the muscle action potential
179
The addition influx of Na+ in the post-synaptic membrane causes what other voltage gates to open and in what location?
Opens voltage-gated Ca++ channels in T-tubules and Sarcoplasmic Reticulum -- leading to contraction of muscle
180
How is a neurotransmission stopped?
With ACETYLCHOLINESTERASE -- it rapidly hydrolyzes Ach in the synaptic cleft
181
How do you diagnose Juntionopathies?
Routine histopathology abnormalities are usually absent or non-specific.
Diagnose via:
-biochemical
-immunological
-toxicological
-electrodiagnostic testing
182
What classifications are there for Juntionopathies? (3)
1. pre-synaptic
2. synaptic
3. post-synaptic
183
What are PRE-SYNAPTIC DISORDERS for Junctionopathies?
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
Tick Paralysis is a Pre-synaptic Disorder! Which tick causes it?
Demacentor
185
Tick Paralysis -- a pre-synaptic disorder -- causes a reversible interference with Ca++ mediated Ach release - T/N
TRUE
186
How do you DIAGNOSE Tick Paralysis?
-find tick
-remove tick and see improvement
187
How do you TREAT Tick Paralysis?
-clip, tick hunt
-topical acaricide
-supportive care
-hyperimmune serum
188
Botulism is a Pre-synaptic disorder. How is it caused?
Ingestion of type C neurotoxin for C. Botulinum (from carrion/spoiled food)
189
Botulism causes an irreversible inhibition of Ach release from cholinergic nerve terminals. T/N
True
190
CS of Botulism
-fatal tetraplegia and areflexia (no tendon reflexes)
-mild weakness
-megaesophagus/aspiration pneumonia
191
How do you DIAGNOSE Botulism?
-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
How do you TREAT Botulism?
-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
Synaptic cleft disorders include:
1. cholinesterase inhibitors -- inhibit breakdown of Ach, prolong activity at receptors
-signs of toxicity: SLUD-E, salivation, lacrimation, urination, defecation, emesis
194
Post synaptic disorders include:
1. block binding of Ach to AchR
-competitive NM blockade
-think Myasthenia Gravis
195
Myasthenia Gravis
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
What age do dogs get Myasthenia Gravis?
Bimodal -- 2-4yo, 9-13yo
197
CS of Acquired MG
-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
How do you DIAGNOSE Acquired MG?
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
How do we TREAT Acquired MG?
-cholinesterase inhibitors
-elevated feeding
-plasmapharesis?
-immunosuppresion?
-spontaneous remission?
200
What's the PROGNOSIS of MG?
-guarded due to always being at risk of asp. pneumonia
201
What are the 2 classifications of myopathies?
1. inflammatory
2. non-inflammatory
202
X-linked muscular dystrophy is a myopathy. What deficiency does it cause?
Dystrophin -- cytoskeletal protein
203
Signalment and CS of X-linked Dystrophy
YOUNG WEAK ANIMALS
-goldens and other breeds
-onset 8-10 weeks
-progressive weakness, gait abnormalities, dysphagia
-muscle atrophy, some hypertrophy
204
How do you DIAGNOSE X-linked muscular dystrophy?
-elevated CK (100,000s)
-abnormal EMG
-muscle biopsy - multifocal necrosis, immunocytochemical staining
205
How do you TREAT muscular dystrophy?
THERE IS NO TREATMENT
-treat secondary complications - dysphagia, aspiration
206
What is Malignant Hyperthermia? (myopathy)
-triggered by anesthetic agents
-defect in Ca++ homeostasis -- opening Ca++ channels
-sustained increase in cytoplasmic Ca++
-continuous contraction
-mutation of RyR1 gene
207
What storage disorders are there? (myopathy)
1. glycogen
2. lipid
-increased lipid in type I myofibers
208
What is Myotonia Congenita?
-persistent muscle contraction
-chloride channelopathy
-congenital in dogs, goats, horses
-chow, min. schnauzer
209
CS of Myotonia Congenita
-stiff gait that improves with exercise
-muscle hypertrophy
-could progress or plateau
210
How do you DIAGNOSE Myotonia Congenita?
-percussion - dimple
-EMG - dive bomber -- myotonic potentials
-CK - normal to increased
-Muscle biopsy - non-specific abnormalities
211
Exertional rhabdomyolysis
-secondary to extreme exertion
212
How do you DIAGNOSE exertion rhabdomyolysis?
-hx
-PE - muscle pain
-BW - elevated CK
-urinalysis - myoglobinuria
213
How do you TREAT Myoglobinuria?
-supportive care
-diuresis for myoglobinuria
214
Masticatory Muscle Myopathy is an INFLAMMATORY Myopathy.
CS of Masticatory Muscle Myopathy
