Unit 3 - Neuro Conditions Flashcards
(119 cards)
1
Q
What is polioencephalomalacia?
A
Softening of the grey matter
2
Q
What is polioencephalomalacia due to (cellular level)?
A
Shifts in intracellular water due to impaired energy metabolism and/or ATP production and dysfunction of Na-K ATPase
3
Q
Polioencephalomalacia (PEM) is a histiological diagnosis that can be the end result of what disease processes?
A
Thiamine deficiency, sulfur toxicity, salt toxicity/water deprivation, and lead
4
Q
What clinical signs are associated with polio?
A
Central blindness, ataxia, proprioceptive deficits, opisthotonus, seizures, and altered mentation to the point of coma and death
Dorsomedial strabismus is reported
5
Q
How is polio diagnoised?
A
Clinical signs and history
Response to thiamine treatment
6
Q
What will CSF show in a patient with polio?
A
Mild to moderate increases in mononuclear cell count and protein concentration
7
Q
How is polio treated?
A
Parenteral thiamine
+/- Dexamethasone or mannitol
8
Q
What can cause thiamine deficiency?
A
Disruptions in the proper functioning of the rumen
Production of bacterial thiaminases under acidic conditions - grain overload
Ingestion of plants that contain thiaminases
Amprolium toxicity
9
Q
What is the prognosis of sulfur toxicity associated polio?
A
Poor
10
Q
What is water deprivation/salt toxicity commonly due to?
A
Water restriction or deprivation, followed by unrestricted water intake
11
Q
What is diagnosis of water deprivation/salt toxicity based on?
A
Serum biochemistry and CSF sodium concentrations
12
Q
How is water deprivation/salt toxicity treated?
A
Rehydration with hypertonic saline with slow reduction of sodium concentration through judicious fluid therapy
Thiamine
Anticonvulsants to control seizures
13
Q
What can cause lead toxicity?
A
Arsenical insecticides and herbicides, lead-acid batteries, leaded gasoline and motor oil, lubricants, linoleum, lead paint, etc
14
Q
What clinical signs are associated with lead toxicity?
A
Acute death without other signs Staggering Muscle tremors Chewing fits Salivation Bellowing Central blindness Frenzied/aggressive behavior Convulsions GI signs - anorexia, rumen atony, teeth grinding, and fetid diarrhea
15
Q
How is lead toxicity diagnosed?
A
Whole blood concentration determination
16
Q
How is lead toxicity treated?
A
Use of chelating agents - CaEDTA and thiamine
17
Q
What lesions does Vitamin A deficiency result in?
A
Thickening of the dura mater
Diminished CSF absorption
Narrowing/remodeling of foramen of the skull
Retinal degeneration and peripheral blindness
18
Q
What clinical signs are associated with vitamin A deficiency?
A
Anorexia, ill-thrift, blindness, diarrhea, and pneumonia
19
Q
How is Vitamin A deficiency diagnosed?
A
Clinical signs, plasma Vitamin A and carotene concentrations, as well as feedstuff/ration analysis
20
Q
How is Vitamin A deficiency treated?
A
Vitamin A
21
Q
What causes nervous coccidiosis?
A
Eimeria spp.
22
Q
What clinical signs are associated with nervous coccidiosis?
A
Depression, incoordination, twitching to seizure activity, opisthotonus, periodic tremors, nystagmus, bellwoing, and muscle fasciculations
23
Q
What differential diagnoses should be considered with nervous coccidiosis?
A
PEM, vitamin A deficiency, meningitis, and enterotoxemia
24
Q
How is nervous coccidiosis treated?
A
Coccidiosis tx - sulfadiamethoxine, amprolium
Thiamine
Supportive care
25
What is bovine bonkers also known as?
Ammonia toxicity
26
What clinical signs are associated with bovine bonkers?
```
Hyperesthesia
Ataxia
Sawhorse stance at rest but hyperactive
Circle propulsively
Appear blind
Abnormal vocalization
Dysphonia
Walking/running into objects
```
27
How is bovine bonkers treated?
There are no specific treatments described but thiamine and diazepam should be administered
28
What causes neonatal bacterial suppurative meningitis?
There is failure of passive transfer resulting in bacterial sepsis and the development of meningitis in neonatal calves
29
What is the most common pathogen isolated from neonatal bacterial suppurative meningitis?
E. coli
30
What are the potential routes of entry for neonatal bacterial suppurative meningitis?
Umbilicus, enteritis, and pneumonia
31
How do calves with neonatal bacteria suppurative meningitis present?
Depression and a poor suckle reflex to demonstrating opisthotonus, comatose, or develop seizure acitvity
32
How is neonatal bacterial suppurative meningitis diagnosed?
Abnormal CSF analysis - increased nucleated cells and protein concentration
33
How is neonatal bacterial suppurative meningitis treated?
Treatment is difficult - good supportive care is essential
34
What is histophilosis?
a disease complex with a diverse range of clinical manifestations of disease, including meningitis (infectious thromboembolic meningoencephalitis), pneumonia, arthritis, mastitis, urogenital infection, abortion, and myocarditis
35
The neurological manifestation of histophilosis is typically seen in what population?
Cattle on feed
36
What clinical signs are associated with TEME?
Can have sudden death OR
Profound depression, closed to semi-closed eyelids, recumbency, opisthotonus, convulsions, high fever, retinal hemorrhages
37
How is TEME presumptively diagnosed?
Based on history and PE
38
What does CSF analysis reflect in TEME patients?
Bacterial infection combined with hemorrhage
39
What does necropsy of a TEME fatality show?
Infarcts in the brain and spinal cord
40
What does histopath look like in a TEME patient?
Vasculitis, thrombosis, and neutriphil infiltrates
41
How is TEME treated?
Treatment is often unrewarding
| Parenteral oxytetracycline, NSAIDs
42
What can cause viral encephalitis?
Rabies, bovine herpesvirus encephalomyelitis, pseudorabies, malignant catarrhal fever, ovine/caprine lentiviral encephalitis, West Nile virus encephalomyelitis, Borna disease, and ovine encephalomyelitis
43
What are the wildlife reservoirs for rabies in the US?
Raccoon, skunk, fox, bat, and coyote
44
What is the incubation period for rabies?
30 - 90 days
45
Characterize paralytic rabies.
Progressive, ascending ataxia, paresis, and paralysis of extremities. Knuckling of fetlocks, swaying/unstable gait, and flaccid or deviated tail.
Drooling, yawning, tenesmus, and abnormal vocalization
46
Characterize furious rabies.
Altered mentation, hyperexcitability, and hyperesthesia.
| Loud, abnormal bellowing, and even nymphomania
47
How is rabies diagnosed post-mortem?
DFA or IFA testing
48
What is the infectious principal for transmissible spongiform encephalopathies?
Altered host protein and lacks nucleic acid - this abnormal prion protein induces structural change of the normal precursor protein
49
What are the clinical signs of scrapie?
```
Isolation from herd/flock
Aggression or loss of fear of humans
Severe weight loss
Poor appetite
Pruritis
Wool loss/break
Head bob
Muscle fasciculations
Uncoordinated movements
Other signs - nystagmus, depression, inability to swallow, dysphonia, and blindness
```
50
What are the clinical signs of BSE?
```
Apprehensiveness
Nervousness
Hyperesthesia
Reluctance to do normal things
Aggression towards humans and other animals
Manic kicking during milking
Over-reaction to noise and light stimuli
Low head carriage
Hypermetria
Tremors
Ataxia
Progressive weight loss
```
51
What diagnostic histological changes are associated with transmissible spongiform encephalopathies?
Accumulation of proteinaceous material and neuronal vacuolation
52
What is the most common disease of ruminants associated with cranial nerve and brainstem lesions?
Listeriosis
53
What is the most common form of listeriosis?
encephalitic form
54
Infection of Listeria monocytogenes is the result of what?
Entry of the bacteria through breaks in the oral mucosa and intra-axonal migration to the trigeminal ganglion and brainstem via the cranial nerves of the face
55
What clinical signs are associated with listeriosis?
CN deficits - trigeminal, facial, vestibulocochlear, or glossopharyngeal nerves can be affected
Depression, anorexia, fever, rumen atony, dehydration, and salivation
56
How is Listeriosis diagnosed?
Neurologic exam findings
57
What are the main differentials to consider with Listeriosis?
Otitis media/interna, brainstem abscess or tumor, pituitary abscess syndrome, and trauma
58
What is the most useful antemortem diagnostic test for Listeriosis?
CSF analysis - increased protein concentration and nucleated cell count
59
What histological findings are characteristic of Listeriosis?
Multifocal to coalescing areas of necrosis of the brainstem with infiltration of macrophages and neutrophils
60
How is Listeriosis treated?
Parenteral antibiotics, NSAIDs or steroids, fluids, B vitamins, and supportive care
61
What does otitis interna/media result in clinical signs of?
Unilateral facial nerve and/or vestibulocochlear nerve deficits
Otorrhea
62
What are the most common pathogens isolatated from otitis interna/media?
M. bovis, Pasteurella, M. hemolytica, H. somni, T. pyogenes, and Staphs and Streps
63
What is the most common risk factor for otitis interna/media?
Respiratory infection
Other factor: Feeding contaminated milk to dairy calves and kids/lambs
64
How is otitis interna/media treated?
Dependent on etiology
Abx for bacteria
Mites - ivermectin
65
What is the most often cultured bacteria from pituitary abscesses?
T. pyogenes
66
What clinical signs are associated with pituitary abscesses?
Depression, dysphagia, dropped jaw, blindness, and absence of pupillary light reflex
67
The presence of what pituitary abscess clinical sign is important to distinguish from listeriosis?
Blindness
68
What are the signs of cerebellar dysfunction?
Bilateral symmetric ataxia, hypermetria, and normal strength, with normal alert mentation
Base-wide stance and truncal sway when standing and walking
Mild head tremor is often present
Deficiency of menace response with diffuse disease
69
What causes cerebellar hypoplasia?
Intrauterine viral infection (BVDV between 75-150 days of gestation) or hereditary conditions
70
Calves born with cerebellar hypoplasia demonstrate what signs?
Symmetric signs of dysfunction without worsening clinical signs
Calves may be unable to rise, demonstrate opisthotonus and extensor rigidity in all limbs
Base-wide stance, ataxia, hypermetria, and head tremor
71
What is cerebellar abiotrophy?
An inherited disorder of cattle and sheep caused by the degeneration of neurons in the cerebellar cortex
72
What clinical signs are associated with cerebellar abiotrophy?
Development of ataxia, base-wide stance, intention tremors, and dysmetria
Calves are alert and strong, visual without a menace response
Neurologic signs may remain static or progress slowly over weeks and months
73
What is spastic paresis?
A genetic disorder which is progressive and involves the hind limbs
74
Spastic paresis is characterized by what?
Hypometria and hypertonia
Increased extensor tone of the gastrocnemius muscle that causes the extension of the hock
Hind limb is circumducted and advanced in a swinging motion with the toe off of the ground
75
How is spastic paresis treated?
Surgical treatments - tibial neurectomy and gastrocnemius tetony
76
What is spastic syndrome?
A progressive disorder of adult cattle characterized by episodic contractions of the lumbar muscles and extensor muscles of both rear limbs
77
What can cause grass staggers?
Perennial rye grass, Dallis grass, Bermuda grass, and Canary grass
78
What clinical signs can grass tetany animals have?
Hypersalivation and difficulty in prehension and swallowing
79
What is vertebral osteomyelitis and abscesses?
Bacterial infection of vertebrae is likely the result from intermittent bacteremia in young calves and yearling cattle stemming from pulmonary or umbilical infections
80
What etiologic agents are commonly isolated from vertebral osteomyelitis and abscesses?
T. pyogenes or F. necrophorum or mixed infections
81
How is vertebral osteomyelitis and abscesses diagnosed?
Based on history, clinical signs, and imaging
82
What is bloodwork of vertebral osteomyelitis and abscesses suggestive of?
Chronic infection - neutrophilia, increased globulin and fibrinogen concentrations
83
What type of treatment is indicated for vertebral osteomyelitis and abscesses?
Long term antibiotic therapy
84
What is enzootic ataxia in lambs due to?
Copper deficiency during the perinatal period
85
What lesion does enzootic ataxia cause?
Bilateral symmetric loss of myelin in the dorsolateral spinal tracts
86
What clinical signs do lambs with enzootic ataxia have?
Tetraparesis or progressive, ascending pelvic limb to tetra-ataxia w/in the first few months of age
87
How is enzootic ataxia treated?
Copper
88
What is the meningeal worm?
Paralaphostrongylus tenuis
89
When does onset of clinicial signs occur due to the meningeal worm?
4-8 weeks post infection
90
What clinical signs are associated with the meningeal worm?
Asymmetrical spinal cord lesions
Short-stride with toe dragging in the pelvic limbs
Progression to the thoracic limbs, with worsening ataxia, and circumduction of the pelvic limbs
Eventually stumbling and falling occurs
Posterior ataxia progresses and can lead to recumbency
91
How is meningeal worm definitively diagnosed?
Postmortem by demonstrating parasites in the spinal cord
92
How are meningeal worms treated/
Anthelminthics and anti-inflammatories
93
What are the clinical signs of peripheral nerve disease?
Muscle weakness, muscle atrophy, hyporeflexia, and reduced sensation if there is severe damage
94
What is a result of radial nerve injury?
Inability to extend the elbow, carpus, and fetlock
95
Is weight bearing possible if there was radial nerve injury?
When the limb is placed in extension, weight bearing is possible
96
What can cause sciatic nerve injury?
Inappropriate injection in the hind end, abscesses, and pelvic fractures
97
What does the sciatic nerve innervate?
The extensors of the hip and hock, flexors of the stifle, and flexors and extensors of the fetlock
98
If the sciatic nerve is damaged high, how will the animal present?
The hip, stifle, and hock are dropped and the fetlock is knuckled
The limb can support weight but drags when advanced
Atrophy of caudal thigh muscles
99
What does the tibial nerve innervate?
Flexors of the digit and extensors of the hock
100
What does injury to the tibial nerve cause?
Flexion of the hock and partial flexion of the fetlock
| Knucking is not as severe
101
What does injury to the peroneal nerve cause?
Extreme knuckling of the fetlock, as in walking on dorsum of fetlock because
102
What is femoral nerve injury common in?
Calves pulled with significant force with hip lock
103
What does injury to the femoral nerve result in?
Inability to extend the stifle and advance the limb, and the animal cannot support weight
Atrophy of the quadriceps can be dramatic and quick
104
What does injury to the obturator nerve result in?
The splayed leg appearance found in calving paralysis
| Weight bearing and can move limbs reasonably normally
105
How are peripheral nerve injuries treated?
```
Steroids unless preggers
Broad spectrum antibiotics
B vitamins
Supportive care
Opioids
```
106
Not on test: What causes tetanus?
Clostridium tetani
107
Not on test: What are the two important tetanus neurotoxins?
Tetanospasmin
| Tetanolysin
108
Not on test: Where is tetanolysin produced?
Locally in wounds
109
Not on test: What does tetanolysin do?
Causes necrosis of tissues, decreases oxygen tension, and facilitates proliferation and spread of the bacteria
110
Not on test: What does tetanospasmin do?
It gains entry into the neuron and travels retrograde up and crosses the synapse to become internalized into the interneurons. These interneurons regulate motor neuron activity particularly inhibition of inhibatory interneurons
111
Not on test: T/F: The binding of tetanospasmin is reversible.
False - it is irreversible
112
Not on test: What clinical signs are associated with tetanus?
```
Difficulty rising, ambulating
Sawhorse stance
Pump-handle tail
Loss of rumen motility
Lock-jaw, pharyngeal and tongue dysfunction
Erect ears and ardonic grin
Prolapse of 3rd eyelid
Death due to respiratory paralysis
```
113
Not on test: How is tetanus treated?
Elimination of infection and necrotic tissue, parenteral antibiotics, neutralization of free TeNT, relief of muscle spasms, and providing nursing care
114
Not on test: How is tetanus prevented?
Appropriate vaccination
| Preventative tetanus antitoxin
115
Not on test: What causes botulism?
Clostridium botulinum
116
Not on test: What clinical signs are associated with botulism?
Onset of 24-48 hours
Profound muscle weakness, slowly progressing to paralysis
Difficulty in prehension, chewing, and swallowing
Abnormally low head carriage and protrusion of the tongue from mouth and drooling
Recumbency
Death by respiratory paralyssi
117
Not on test: How is botulism daignosed?
Presence of BoNT
118
Not on test: How is botulism treated?
Supportive nursing care
Trivalent antitixoin - but will only bind to free toxin
Parenteral antibiotics
119
Not on test: How is botulism prevented?
Proper harvesting and ensiling of forages/feedstuffs
Vaccination for horses and minks in the US
Control of vermin
