Block 2 #4 Flashcards
1
Q
What is an example of a spinal reflex?
A
patellar reflex
2
Q
What happens to spinal reflexes when LMN are involved?
A
Reduced or absent
3
Q
What does it mean if a patient is positive on a crossed extensor?
A
UMN involvement
4
Q
How is the neurological exam ordered?
A
Least offensive to most offensive
5
Q
What is an important finding that owners may not bring up in diffuse LMN diseases?
A
Voice change
6
Q
What lesion will cause LMN disease to both upper and lower limbs?
A
NONE!
7
Q
What is an elephant on a beach ball posture from?
A
diffuse LMN disease
8
Q
Do diffuse LMN patients have ataxia?
A
No
This is a CNS thing to have
9
Q
What are 4 common diffuse LMN diseases?
A
Acute canine polyradiculoneuritis (coonhound paralysis)
Botulism
Tick paralysis
Myasthenia gravis
10
Q
Do animals with diffuse LMN disease have patella reflex?
A
No
11
Q
What is the mechanism of acute canine polyradiculoneuritis?
A
Immune-mediated
12
Q
What is a time an animal can develop acute canine polyradiculoneuritis?
A
After rabies vaccine
13
Q
What is the pathogenesis of ACP?
A
Production of autoantibodies against axons and myelin
14
Q
What nerve roots are most affected?
A
Ventral - motor
15
Q
Which anatomic nerve roots are most affected?
A
Lumbar and sacral (rear end)
16
Q
What is a common symptom of ACP?
A
Change in bark (dysphonia)
17
Q
What causes botulism?
A
Ingestion of neurotoxins of clostridium botulinum
18
Q
Where do the neurotoxins come from?
A
Toxins in flesh (carrion) or spoiled food
19
Q
Where do toxins enter the nervous system?
A
At the nerve endings
20
Q
What is the molecular pathogenesis of botulism
A
Cleaves snap-25, VAMP, and syntaxin and prevent Act release from presynaptic terminal
21
Q
What type of muscles are affected by botulism?
A
Smooth and striated muscles (all? lol)
22
Q
What is the different between ACP and botulism on physical exam?
A
Megaesophagus common in botulism and not in ACP
Cranial nerves are affected in botulism but not in ACP
23
Q
Compare progression of botulism to ACP
A
Botulism is 1-3 week recovery, much shorter
24
Q
What is tick paralysis caused from?
A
tick paralysis
25
What is the pathogenesis of tick paralysis?
toxin interferes with function of Ca in the release of Ach
26
How long after tick attachment does it occur?
5-9 days
27
What is the difference between tick paralysis and the others?
Very rapid and death will occur if not removed fast enough
28
What is the most common diffuse LMN cause?
Myasthenia gravis
29
What are the 2 forms of myasthenia gravis?
Congenital vs acquired
30
What is the most common form of myasthenia gravis?
Acquired
31
What is the pathogenesis of myasthenia gravis?
Auto-antibody mediated destruction of Act receptors at the neuromuscular junction.
32
What are the 3 types of acquired myasthenia gravis?
Generalized (most common in vetted)
Focal
Fulminating (worse)
33
Where is the focal form limited to?
Esophagus
34
What is a differentiating thing about myasthenia gravis from the other diseases we've discussed?
Spinal reflexes are normally ok
35
What is the pathophysiology of myasenthia gravis?
Binding of autoantibodies to post-synaptic Ach receptor > compliment-mediated destruction of AchR
36
What is a very common symptom of dogs with myasthenia gravis?
Megaesophagus
37
How do you diagnose myasthenia gravis?
AchR autoantibody test
38
How is the congenital MG different?
No auto-immune component, just a defect in AchR
39
Why is swelling such a large problem in the brain?
Increases inter cranial pressure which reduces blood flow
40
What are the 4 mechanisms of edema in the brain?
Vasogenic
cytotoxic
intramyelinic
transependymal
41
What is vasogenic edema?
Leaky blood vessels
42
What is cytotoxic edema?
Rapid return to normal plasma osmolality where astrocytes cannot unload osmoses fast enough
43
What is the edema cycle?
A positive feedback loop between cytotoxic edema and vasogenic edema resulting in death
44
What is intramyelinic edema?
Splitting of myelin sheaths with fluid accumulation
45
What is transependymal edema?
Blockage of CSF flow, a slow loss of tissue
46
What is polioencephaloamalacia charactertized?
A morphological diagnoses
47
Where do ruminants need thiamine?
Cerebrocortical grey matter
48
When do ruminant get polio?
Ruminants can synthesize their own thiamine but when on high concentrate diets, this will lower rumen pH
49
How would a fat cat get thiamine polio?
Cats that go off food due to hepatic lipidosis (cats get thiamine in food)
50
What is chronic salt toxicity (bad name)
A morphological diagnosis of polio
Dehydrated animals are then given lots of fluid which changes the osmolality of the brain causing cytotoxic osmolality
51
What toxin-related polio can occur?
Large amounts of new feed stuffs are given
52
What are pigs especially susceptible to?
E coli
53
What are lambs especially susceptible to?
C. perfringens
54
What type of edema does salt toxicity trigger?
Cytotoxic
55
What type of edema does lead poisoning, endotoxins, and thiamine deficiency trigger?
Vasogenic edema
56
How does lead affect horses?
Much more sensitive than ruminants
Schwann cells, primary demyelination in PNS
57
What is infarction?
Tissue necrosis due to loss of blood flow
58
What is a septic emboli?
Embolism caused by bacteria that can get lodged in the brain
Thrombotic meningoencephalitis
59
What is the backup of blood supply to the grey matter of the spinal chord?
There isnt one!
It is an "end artery"
60
What happens if the end artery has an infarct?
malacia
61
What is pan necrosis?
Stoppage of all nutrient to the spot
62
What happens with a slow growing tumor?
Selective necrosis that doesn't trigger the edema cycle
63
Is there hemorrhage with a concussion?
NO!
64
What is a concussion?
Transient stretching of white matter tracts in the brainstem
65
What is another word for contusion?
Bruising
66
What is avulsion?
Stretching of vessels resulting in tearing
67
What may a hematoma trigger?
Edema cycle due to increased pressure
68
What is delayed onset arteriospasm?
constricting of vessels but may lead to an infarct
69
What are the factors mediating potency of arterioles?
Endothelial relaxation factor
Prostacyclin
70
What does subarachnoid hemorrhage release?
Oxyhemoglobin
71
What does the oxyhemoglobin cause an accumulation of?
Diacylglycerol
Endothelin-1
72
What can blood migrate through?
White matter
73
What is the migration of blood through white matter called?
Ascending-descending myelomalacia
74
What does ischemia mean?
Inadequate blood supply to a tissue
75
Where does the end artery for grey matter branch from?
Ventral spinal artery
76
What is the worst consequence of disc herniation?
Hemorrhage into the subarachnoid space causing ascending-descending myelomalacia
77
What is Wallerian degeneration?
An insult that happens cranial to an axon causing the axons caudal to die
78
What are the 3 organizations of the CNS?
Motor system
Sensory system
Vestibular system
79
Where are sensory neurons located?
Ganglia of the dorsal nerve root
80
What CN is the vestibulocochlear?
VIII
81
What is wobblers characterized by?
Stenosis of the spinal canal
82
What are the 2 manifestations of wobblers?
Cervicovertebral instability (CVI)
Cervicovertebral static stenosis (CSS)
83
What is another term for wobblers
Cervicovertebral stenotic myelopathy (CVSM)
84
What is cervicovertebral instability?
Dynamic, intermittent compression
85
What is cervicovertebral static stenosis?
Static, continuous compression
86
Why are clinical symptoms worse in the read for cervicovertebral stenotic myelopathy?
Spinal tracts to the rear are more superficial
87
When does wobblers arise?
Usually earlier in life
88
What are the causes of wobblers?
Environmental and genetic
89
What is the best diagnostic for wobblers?
Minimal sagittal diameter (MSD)
90
What is minimal sagittal diameter?
Ratio of spinal diameter to vertebral body diameter
91
What MSD would be wobbler positive?
<50%
92
What is the symmetry of EPM?
asymmetric disease!
93
What is the definitive host of EPM?
Opossum
94
What parts of the body does EPM affect?
Spinal cord, brain stem, and cerebrum
95
What is another term for Equine herpes virus?
Myeloencephalopathy
96
What does EHV cause?
Abortion in mares and neonatal disease
97
Does all EHV cause myeloencephalopathy?
No!
98
What is the relevant factor in EDM?
Vitamin E deficiency
99
What is EMND?
Equine motor neuron disease
100
What does EMND originate from?
Neurodegenerative oxidative stress
101
Is there ataxia with EMND?
NO!
102
Is CVM or CVI more common in young animals?
CVI
103
What type of horses are predisposed to wobblers?
Horses growing fast!
104
What protozoa causes EPM?
Sarcocystis neurona
105
What is the respiratory presentation of EHV?
Rhinopneumonitis
106
What is the neurological manifestation of EHV?
EHM (myeloencephalotpathy)
107
What is a defining clinical sign of EHV?
Urinary incontenence
Rear limb lameness
108
What is a positive diagnostic of EHV?
Xanthochromic CSF
109
What does xanthochromic CSF mean?
Increased protein (yellow)
110
What does EMND (equine motor neuron disease) affect?
Gray matter
111
What does EDM (equine degenerative myelopathy) affect?
White matter
112
Does EMND or EDM have muscle atrophy?
EMND
EDM does not!
113
What is a distinct sign of EMND?
No ataxia
114
Is there ataxia in EDM? Muscle atrophy?
No muscle atrophy! Yes ataxia
115
What is the most common cause of lameness is perfomance horses?
Navicular disease (palmar heel pain)
116
Where does navicular disease normally impact?
Bilateral forelimb
117
What is laminitis?
Inflammation of hoof lamina (velcro of hoof)
118
What are causes of laminitis?
Hormones (Cushings)
Sepsis
Supporting limb laminates
119
What is a type I P3 fracture?
Non-articular, palmar process
120
What is a type II P3 fracture?
Articular, palmar process
121
What is a type III P3 fracture?
Sagital, articular
122
What is a type IV P3 fracture?
Extensor process
123
