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LA Clinical Medicine > Unit 3 - Neuro Conditions > Flashcards

Unit 3 - Neuro Conditions Flashcards

1
Q

What is polioencephalomalacia?

A

Softening of the grey matter

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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

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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

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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

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5
Q

How is polio diagnoised?

A

Clinical signs and history

Response to thiamine treatment

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6
Q

What will CSF show in a patient with polio?

A

Mild to moderate increases in mononuclear cell count and protein concentration

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7
Q

How is polio treated?

A

Parenteral thiamine

+/- Dexamethasone or mannitol

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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

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9
Q

What is the prognosis of sulfur toxicity associated polio?

A

Poor

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10
Q

What is water deprivation/salt toxicity commonly due to?

A

Water restriction or deprivation, followed by unrestricted water intake

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11
Q

What is diagnosis of water deprivation/salt toxicity based on?

A

Serum biochemistry and CSF sodium concentrations

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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

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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

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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
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15
Q

How is lead toxicity diagnosed?

A

Whole blood concentration determination

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16
Q

How is lead toxicity treated?

A

Use of chelating agents - CaEDTA and thiamine

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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

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18
Q

What clinical signs are associated with vitamin A deficiency?

A

Anorexia, ill-thrift, blindness, diarrhea, and pneumonia

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19
Q

How is Vitamin A deficiency diagnosed?

A

Clinical signs, plasma Vitamin A and carotene concentrations, as well as feedstuff/ration analysis

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20
Q

How is Vitamin A deficiency treated?

A

Vitamin A

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21
Q

What causes nervous coccidiosis?

A

Eimeria spp.

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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

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23
Q

What differential diagnoses should be considered with nervous coccidiosis?

A

PEM, vitamin A deficiency, meningitis, and enterotoxemia

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24
Q

How is nervous coccidiosis treated?

A

Coccidiosis tx - sulfadiamethoxine, amprolium
Thiamine
Supportive care

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25
Q

What is bovine bonkers also known as?

A

Ammonia toxicity

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26
Q

What clinical signs are associated with bovine bonkers?

A 
Hyperesthesia
Ataxia
Sawhorse stance at rest but hyperactive
Circle propulsively
Appear blind
Abnormal vocalization
Dysphonia
Walking/running into objects
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27
Q

How is bovine bonkers treated?

A

There are no specific treatments described but thiamine and diazepam should be administered

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28
Q

What causes neonatal bacterial suppurative meningitis?

A

There is failure of passive transfer resulting in bacterial sepsis and the development of meningitis in neonatal calves

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29
Q

What is the most common pathogen isolated from neonatal bacterial suppurative meningitis?

A

E. coli

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30
Q

What are the potential routes of entry for neonatal bacterial suppurative meningitis?

A

Umbilicus, enteritis, and pneumonia

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31
Q

How do calves with neonatal bacteria suppurative meningitis present?

A

Depression and a poor suckle reflex to demonstrating opisthotonus, comatose, or develop seizure acitvity

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32
Q

How is neonatal bacterial suppurative meningitis diagnosed?

A

Abnormal CSF analysis - increased nucleated cells and protein concentration

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33
Q

How is neonatal bacterial suppurative meningitis treated?

A

Treatment is difficult - good supportive care is essential

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34
Q

What is histophilosis?

A

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

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35
Q

The neurological manifestation of histophilosis is typically seen in what population?

A

Cattle on feed

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36
Q

What clinical signs are associated with TEME?

A

Can have sudden death OR
Profound depression, closed to semi-closed eyelids, recumbency, opisthotonus, convulsions, high fever, retinal hemorrhages

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37
Q

How is TEME presumptively diagnosed?

A

Based on history and PE

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38
Q

What does CSF analysis reflect in TEME patients?

A

Bacterial infection combined with hemorrhage

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39
Q

What does necropsy of a TEME fatality show?

A

Infarcts in the brain and spinal cord

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40
Q

What does histopath look like in a TEME patient?

A

Vasculitis, thrombosis, and neutriphil infiltrates

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41
Q

How is TEME treated?

A

Treatment is often unrewarding

Parenteral oxytetracycline, NSAIDs

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42
Q

What can cause viral encephalitis?

A

Rabies, bovine herpesvirus encephalomyelitis, pseudorabies, malignant catarrhal fever, ovine/caprine lentiviral encephalitis, West Nile virus encephalomyelitis, Borna disease, and ovine encephalomyelitis

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43
Q

What are the wildlife reservoirs for rabies in the US?

A

Raccoon, skunk, fox, bat, and coyote

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44
Q

What is the incubation period for rabies?

A

30 - 90 days

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45
Q

Characterize paralytic rabies.

A

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

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46
Q

Characterize furious rabies.

A

Altered mentation, hyperexcitability, and hyperesthesia.

Loud, abnormal bellowing, and even nymphomania

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47
Q

How is rabies diagnosed post-mortem?

A

DFA or IFA testing

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48
Q

What is the infectious principal for transmissible spongiform encephalopathies?

A

Altered host protein and lacks nucleic acid - this abnormal prion protein induces structural change of the normal precursor protein

49
Q

What are the clinical signs of scrapie?

A 
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
Q

What are the clinical signs of BSE?

A 
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
Q

What diagnostic histological changes are associated with transmissible spongiform encephalopathies?

A

Accumulation of proteinaceous material and neuronal vacuolation

52
Q

What is the most common disease of ruminants associated with cranial nerve and brainstem lesions?

A

Listeriosis

53
Q

What is the most common form of listeriosis?

A

encephalitic form

54
Q

Infection of Listeria monocytogenes is the result of what?

A

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
Q

What clinical signs are associated with listeriosis?

A

CN deficits - trigeminal, facial, vestibulocochlear, or glossopharyngeal nerves can be affected
Depression, anorexia, fever, rumen atony, dehydration, and salivation

56
Q

How is Listeriosis diagnosed?

A

Neurologic exam findings

57
Q

What are the main differentials to consider with Listeriosis?

A

Otitis media/interna, brainstem abscess or tumor, pituitary abscess syndrome, and trauma

58
Q

What is the most useful antemortem diagnostic test for Listeriosis?

A

CSF analysis - increased protein concentration and nucleated cell count

59
Q

What histological findings are characteristic of Listeriosis?

A

Multifocal to coalescing areas of necrosis of the brainstem with infiltration of macrophages and neutrophils

60
Q

How is Listeriosis treated?

A

Parenteral antibiotics, NSAIDs or steroids, fluids, B vitamins, and supportive care

61
Q

What does otitis interna/media result in clinical signs of?

A

Unilateral facial nerve and/or vestibulocochlear nerve deficits
Otorrhea

62
Q

What are the most common pathogens isolatated from otitis interna/media?

A

M. bovis, Pasteurella, M. hemolytica, H. somni, T. pyogenes, and Staphs and Streps

63
Q

What is the most common risk factor for otitis interna/media?

A

Respiratory infection

Other factor: Feeding contaminated milk to dairy calves and kids/lambs

64
Q

How is otitis interna/media treated?

A

Dependent on etiology
Abx for bacteria
Mites - ivermectin

65
Q

What is the most often cultured bacteria from pituitary abscesses?

A

T. pyogenes

66
Q

What clinical signs are associated with pituitary abscesses?

A

Depression, dysphagia, dropped jaw, blindness, and absence of pupillary light reflex

67
Q

The presence of what pituitary abscess clinical sign is important to distinguish from listeriosis?

A

Blindness

68
Q

What are the signs of cerebellar dysfunction?

A

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
Q

What causes cerebellar hypoplasia?

A

Intrauterine viral infection (BVDV between 75-150 days of gestation) or hereditary conditions

70
Q

Calves born with cerebellar hypoplasia demonstrate what signs?

A

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
Q

What is cerebellar abiotrophy?

A

An inherited disorder of cattle and sheep caused by the degeneration of neurons in the cerebellar cortex

72
Q

What clinical signs are associated with cerebellar abiotrophy?

A

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
Q

What is spastic paresis?

A

A genetic disorder which is progressive and involves the hind limbs

74
Q

Spastic paresis is characterized by what?

A

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
Q

How is spastic paresis treated?

A

Surgical treatments - tibial neurectomy and gastrocnemius tetony

76
Q

What is spastic syndrome?

A

A progressive disorder of adult cattle characterized by episodic contractions of the lumbar muscles and extensor muscles of both rear limbs

77
Q

What can cause grass staggers?

A

Perennial rye grass, Dallis grass, Bermuda grass, and Canary grass

78
Q

What clinical signs can grass tetany animals have?

A

Hypersalivation and difficulty in prehension and swallowing

79
Q

What is vertebral osteomyelitis and abscesses?

A

Bacterial infection of vertebrae is likely the result from intermittent bacteremia in young calves and yearling cattle stemming from pulmonary or umbilical infections

80
Q

What etiologic agents are commonly isolated from vertebral osteomyelitis and abscesses?

A

T. pyogenes or F. necrophorum or mixed infections

81
Q

How is vertebral osteomyelitis and abscesses diagnosed?

A

Based on history, clinical signs, and imaging

82
Q

What is bloodwork of vertebral osteomyelitis and abscesses suggestive of?

A

Chronic infection - neutrophilia, increased globulin and fibrinogen concentrations

83
Q

What type of treatment is indicated for vertebral osteomyelitis and abscesses?

A

Long term antibiotic therapy

84
Q

What is enzootic ataxia in lambs due to?

A

Copper deficiency during the perinatal period

85
Q

What lesion does enzootic ataxia cause?

A

Bilateral symmetric loss of myelin in the dorsolateral spinal tracts

86
Q

What clinical signs do lambs with enzootic ataxia have?

A

Tetraparesis or progressive, ascending pelvic limb to tetra-ataxia w/in the first few months of age

87
Q

How is enzootic ataxia treated?

A

Copper

88
Q

What is the meningeal worm?

A

Paralaphostrongylus tenuis

89
Q

When does onset of clinicial signs occur due to the meningeal worm?

A

4-8 weeks post infection

90
Q

What clinical signs are associated with the meningeal worm?

A

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
Q

How is meningeal worm definitively diagnosed?

A

Postmortem by demonstrating parasites in the spinal cord

92
Q

How are meningeal worms treated/

A

Anthelminthics and anti-inflammatories

93
Q

What are the clinical signs of peripheral nerve disease?

A

Muscle weakness, muscle atrophy, hyporeflexia, and reduced sensation if there is severe damage

94
Q

What is a result of radial nerve injury?

A

Inability to extend the elbow, carpus, and fetlock

95
Q

Is weight bearing possible if there was radial nerve injury?

A

When the limb is placed in extension, weight bearing is possible

96
Q

What can cause sciatic nerve injury?

A

Inappropriate injection in the hind end, abscesses, and pelvic fractures

97
Q

What does the sciatic nerve innervate?

A

The extensors of the hip and hock, flexors of the stifle, and flexors and extensors of the fetlock

98
Q

If the sciatic nerve is damaged high, how will the animal present?

A

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
Q

What does the tibial nerve innervate?

A

Flexors of the digit and extensors of the hock

100
Q

What does injury to the tibial nerve cause?

A

Flexion of the hock and partial flexion of the fetlock

Knucking is not as severe

101
Q

What does injury to the peroneal nerve cause?

A

Extreme knuckling of the fetlock, as in walking on dorsum of fetlock because

102
Q

What is femoral nerve injury common in?

A

Calves pulled with significant force with hip lock

103
Q

What does injury to the femoral nerve result in?

A

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
Q

What does injury to the obturator nerve result in?

A

The splayed leg appearance found in calving paralysis

Weight bearing and can move limbs reasonably normally

105
Q

How are peripheral nerve injuries treated?

A 
Steroids unless preggers
Broad spectrum antibiotics
B vitamins
Supportive care
Opioids
106
Q

Not on test: What causes tetanus?

A

Clostridium tetani

107
Q

Not on test: What are the two important tetanus neurotoxins?

A

Tetanospasmin

Tetanolysin

108
Q

Not on test: Where is tetanolysin produced?

A

Locally in wounds

109
Q

Not on test: What does tetanolysin do?

A

Causes necrosis of tissues, decreases oxygen tension, and facilitates proliferation and spread of the bacteria

110
Q

Not on test: What does tetanospasmin do?

A

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
Q

Not on test: T/F: The binding of tetanospasmin is reversible.

A

False - it is irreversible

112
Q

Not on test: What clinical signs are associated with tetanus?

A 
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
Q

Not on test: How is tetanus treated?

A

Elimination of infection and necrotic tissue, parenteral antibiotics, neutralization of free TeNT, relief of muscle spasms, and providing nursing care

114
Q

Not on test: How is tetanus prevented?

A

Appropriate vaccination

Preventative tetanus antitoxin

115
Q

Not on test: What causes botulism?

A

Clostridium botulinum

116
Q

Not on test: What clinical signs are associated with botulism?

A

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
Q

Not on test: How is botulism daignosed?

A

Presence of BoNT

118
Q

Not on test: How is botulism treated?

A

Supportive nursing care
Trivalent antitixoin - but will only bind to free toxin
Parenteral antibiotics

119
Q

Not on test: How is botulism prevented?

A

Proper harvesting and ensiling of forages/feedstuffs
Vaccination for horses and minks in the US
Control of vermin

LA Clinical Medicine (33 decks)

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