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Neuro Flashcards

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1
Q

What are the main goals of a neurological examination?

A

Detect the presence of neurological disease, determine the location of the lesion

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2
Q

What aspects of a neurological exam must be performed in ruminants

A

Mentation/level of consciousness
Cranial nerve function
Posture
Gait and placing in ambulatory animals
Spinal reflexes in recumbent animals
Rectum, bladder, anus, and tail function

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3
Q

What is the brain functionally divided into for a neuro exam?

A

Forebrain, cerebellum, brain stem

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4
Q

Generalized lower motor neuron signs are due to disease of what

A

Peripheral nerve, neuromuscular junction, or muscle

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5
Q

What are the components of the forebrain?

A

Telencephalon (cerebrum) and diencephalon (thalamus and associated structures)

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6
Q

What signs are typical of a forebrain lesion?

A

Altered mentation, seizures, postural reaction deficits, facial hypoexthesia, loss of vision, compulsive pacing, circling, dorsomedial strabismus, dysphagia, alterations in behavior (head pressing, yawning, biting)

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7
Q

With lateralizing forebrain disease, where do clinical signs occur relative to the lesion? What is the exception to this rule?

A

Contralateral to the lesion; exception is circling- towards the lesion

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8
Q

What are differentials for forebrain disease?

A

Polioencephalomalacia, lead toxicity, salt/water intoxication, nonprotein nitrogen poisoning, vitamin A deficiency, bacterial, viral, protozoal infection, trauma, metabolic, congenital (hydrocephalus) etc.

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9
Q

Which disorders can cause polioencephalomalacia?

A

Thiamine deficiency, sulfur toxicity, lead toxicity, salt/water intoxication

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10
Q

What are causes of disturbed thiamine metabolism?

A

Increased rumen bacterial thiaminase activity, production or ingestion of inactive thiamin analogs (amprolium), impaired absorption, ingestion of thiaminases, increased excretion

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11
Q

What are sources of sulfur in ruminant diets?

A

Molasses, beet, corn, cruciferous crops, high protein forage, alfalfa

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12
Q

What group of animals are most likely to develop polioencephalomalacia?

A

Calves and lambs <18 months and kids 2-6 months

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13
Q

Which herds are more likely to develop a polioencephalomalacia outbreak?

A

Those on feedlots with high carb, low roughage diets

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14
Q

How does high sulfur lead to polioencephalomalacia?

A

Depletes ATP leading to symmetrical laminar cortical necrosis

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15
Q

What clinical signs are associated with polioencephalomalacia?

A

Central blindness (normal PLR), staggering gait, wandering, opisthotonus and dorsomedial strabismus
Can develop brain stem dysfunction with advanced disease

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16
Q

How is polioencephalomalacia diagnosed?

A

History, clinical signs, dietary sulfur level, CSF analysis with mononuclear pleocytosis, moderate protein elevation, and xanthochromia, response to thiamine supplementation

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17
Q

How is polioencephalomalacia treated?

A

Parenteral thiamine, removal of dietary sulfur source, supportive care

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18
Q

What is the prognosis of polioencephalomalacia?

A

Good if animal isn’t recumbent yet
Severely affected animals can recover but still have signs

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19
Q

How is polioencephalomalacia prevented?

A

Dietary management, adaptation to high-concentrate rations, analysis of sulfur levels in feed and water

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20
Q

Which animals is lead toxicity most common in?

A

2-6 month old beef cows

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21
Q

What diet promotes the absorption of lead?

A

Milk based diets

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22
Q

How does lead cause polioencephalomalacia?

A

Crosses the BBB and concentrates in the brain, causes microvascular damage, cell death, cerebral edema, neurotransmitter dysfunction, and decreased glucose uptake

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23
Q

What clinical signs are associated with lead toxicity polioencephalomalacia?

A

Forebrain dysfunction with GI signs

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24
Q

How is lead poisoning diagnosed?

A

CBC with nucleated RBCs and basophilic stippling, whole blood lead levels can be used for acute disease, urinary lead levels following chelation therapy can be used for chronic disease

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25
How is lead toxicity treated?
Removal of sources of lead, administer calcium disodium EDTA, supportive care, thiamine administration
26
What is the prognosis for lead toxicity?
Fair providing aggressive treatment is initiated early
27
What group of animals most commonly gets salt/water intoxication?
Range cattle, feeder calves, and lambs
28
What are potential causes of salt/water intoxication?
Overeating with oral electrolytes, ingestion of brackish or contaminated water, restricted access to water, hot weather
29
What are the characteristic lesions of salt/water toxicity?
Laminar cerebrocortical necrosis and edema
30
What clinical signs are associated with salt/water toxicity?
Forebrain disease, colic, fluid filled rumen, diarrhea, IV hemolysis and hemoglobinuria
31
How is salt/water toxicity diagnosed?
History, ratio of CSF sodium to serum sodium >1 is suggestive, CSF sodium concentration >200meq/L is suggestive
32
How do you replace a water deficit in ruminants without causing water toxicity?
Use sodium containing fluids (no dextrose!), provide small amounts of fresh water frequently, replace fluids slowly over 1-2 days
33
What is the prognosis for salt/water intoxication?
Fair if treated early
34
Which animals are predisposed to vitamin A deficiency?
Growing ruminants on drylot or feedlot
35
Which feeds are naturally low in vitamin A?
Cereal grain, beet pulp and cottonseed hulls
36
How are vitamin A levels in feed affected by prolonged storage?
They decline over time
37
How does vitamin A deficiency damage the brain?
Causes thickening of dura mater resulting in diminished CSF absorption and hydrocephalus
38
What kind of blindness does vitamin A deficiency cause?
Night blindness, PLRs will be absent Vitamin A is necessary for retina function, deficiency can also lead to bony remodeling and stenosis of optic foramen
39
What clinical signs are associated with vitamin A deficiency?
Forebrain disease, blindness, anorexia, ill-thrift, diarrhea, pneumonia
40
How is vitamin A deficiency diagnosed?
Assay of vitamin A and carotene in plasma and feed
41
How is vitamin A deficiency treated?
With vitamin A supplementation
42
Describe the transmission and progression of rabies
Inoculation from bite -> incubation for 3w-6m -> virus travels up peripheral nerves to CNS -> rapidly progressive neuro signs and death
43
What are the clinical forms of rabies?
Cerebral (furious), brain stem (dumb), spinal cord (paralytic)
44
What are common clinical signs of rabies?
Excessive salivation, behavioral changes (aggressiveness), hyperesthesia, pharyngeal paresis/paralysis, flaccid limb paresis/paralysis
45
How is rabies diagnosed?
No antemortem test; fluorescent antibody testing on fresh brain tissue
46
How is rabies prevented?
Inactivated vaccine for ruminants, vaccinate/eradicate wildlife
47
Which animals are prone to bacterial meningoencephalitis/brain abscess?
Neonatal and weanling cattle, sheep, and goats
48
What is the typical history of an animal with bacterial meningoencephalitis?
Inadequate or failure of passive transfer, concurrent illness (enteritis, polyarthritis, omphalophlebitis)
49
What are the causative agents of bacterial meningoencephalitis?
E. coli, Strep spp., Pasteurella spp., Salmonella spp., Staph spp., Mycoplasma in kids
50
What are clinical signs of meningoencephalitis?
Diffuse or multifocal brain disease, fever, cervical pain, sepsis
51
How is meningoencephalitis diagnosed?
CSF with neutrophilic pleocytosis and culture with bacterial growth
52
What are potential causes of brain abscesses?
Head trauma, dehorning, otitis media/interna, bacterial infection elsewhere in the body
53
What are causative organisms of brain abscesses?
Trueperella pyogenes, Corynebacterium, Bacteroides, Actinomyces, Fusobacterium spp.
54
What diagnostic tests can be performed for a brain abscess?
CSF analysis (neutrophilic to mononuclear inflammation), advanced imaging
55
How are brain abscesses treated?
Surgical drainage and long term antibiotic therapy, poor prognosis
56
What is the primary function of the cerebellum?
Coordination of movement- rate and range of movement (but not initiation)
57
What clinical signs to cerebellar lesions cause?
Incoordination without paresis; dysmetric gait (usually hypermetric), intention tremor of the head, ataxia, wide based stance, occasionally pendulous nystagmus, absent menace response, vestibular signs
58
What side to signs of cerebellar disease appear relative to the lesion?
The ipsilateral (same) side
59
What are differentials for cerebellar disease?
Cerebellar malformation due to BVD, cerebellar abiotrophy/degeneration, metabolic storage disorders, Scrapie, thromboembolic meningoencephalitis, rabies, toxins, trauma, neoplasia, verminous encephalomyelitis, bacterial meningoencephalomyelitis
60
What type of virus causes bovine viral diarrhea?
A togavirus
61
Describe the pathogenesis of BVD leading to cerebellar malformation
Fetus is exposed during second trimester (vaccine or infection) -> virus destroys germinal layer of cells and Purkinje cells of cerebellum -> cerebellar hypoplasia and atrophy -> hydranencephaly
62
What clinical signs are seen in animals with cerebellar malformation due to BVD?
Mild- hypermetric gait, intention tremor of the head Severe- recumbent with opisthotonus and extensor rigidity of the limbs
63
How do you diagnose cerebellar malformation due to BVD?
Positive pre-suckle BVD titer
64
How is cerebellar malformation due to BVD prevented/treated?
No treatment; prevented by vaccination of dams
65
What are the parts of the brainstem?
Mesencephalon (midbrain), pons, myelencephalon (medulla oblongata)
66
What systems does the brainstem control?
UMN nuclei for voluntary movement, control of consciousness, cranial nerves III-XII
67
What are clinical signs of brainstem lesions?
UMN signs- tetraparesis or hemiparesis, postural reaction deficits, altered levels of consciousness, cranial nerve deficits (most commonly vestibular)
68
Which side do brain stem disease symptoms occur relative to the lesion?
Ipsilateral (same) side
69
What are clinical signs of vestibular disease?
Ataxia with falling, rolling, or circling, head tilt, strabismus (positional), nystagmus
70
Describe peripheral vestibular disease
Involves peripheral vestibular sensing apparatus in inner ear, other signs of brain stem disease aren't seen, nystagmus is either horizontal or rotary, facial nerve may be involved
71
Describe central vestibular disease
Involves vestibular nuclei in medulla oblongota, may see other brainstem signs, may see cranial nerve V and VII signs, vertical and positional nystagmus
72
Describe paradoxical vestibular disease
Can be seen with lesions in specific areas of the cerebellum, head tilt and nystagmus are directed away from the side of the lesion, other signs of central vestibular disease are still ipsilateral to the lesion
73
What are differential diagnoses for vestibular disease?
Listeriosis, thromboembolic meningoencephalomyelitis, bacterial meningoencephalomyelitis, rabies, verminous encephalomyelitis, trauma, otitis media/interna, trauma
74
Which animals are most likely to get otitis media/interna?
Feedlot cattle and sheep
75
How is otitis media/interna usually acquired? What historic clinical signs might the animals have?
Hematogenous spread or ascending infection from respiratory tract, may also have pharyngitis or rhinitis
76
What are common isolates from otitis media/interna?
Pasteurella, Corynebacterium, Histophilus, Mannheimia, Mycoplasma
77
What clinical signs are associated with otitis media/interna?
Ipsilateral ataxia, circling, positional ventral nystagmus, horizontal or rotary nystagmus, facial nerve paralysis
78
How is vestibular disease from otitis media/interna diagnosed?
Radiographs of tympanic bulla, aural or pharyngeal endoscopy, cytology and culture of fluid from myringotomy
79
How is vestibular disease from otitis media/interna treated?
Long term (4 week) antibiotic therapy based on culture and sensitivity (combo of tulathromycin and oxytetracycline if no culture)
80
What is the prognosis for vestibular disease caused by otitis media/interna?
Good if treatment is started early, but residual deficits may remain
81
What is the most common disease associated with cranial nerve deficits in ruminants?
Listeriosis
82
Describe the causative agent of Listeriosis
Listeria monocytogenes- facultative intracellular gram + rod found in soil, silage, and feces
83
What weather conditions is listeriosis associated with?
Cold wet conditions and poor quality silage (pH>5.5)
84
Describe the pathophysiology of listeriosis
Organism travels up cranial nerves (V, VII) via buccal mucosa, enters brain stem and forms microabscesses; can also spread hematogenously
85
What clinical signs are associated with listeriosis?
Ataxia and/or paresis, depression, involvement of CN V, VII, VIII, IX, X, and/or XII
86
How is listeriosis diagnosed?
History and clinical findings, CSF analysis showing moderate mononuclear to mixed pleocytosis and increased protein concentration, necropsy showing multifocal microabscesses; no definitive antemortem test
87
How is listeriosis treated? What is the prognosis?
Antibiotics (tetracycline or penicillin) and supportive care; fair to good prognosis if treated early
88
Which animals most commonly get thromboembolic meningoencephalitis?
Weanling to young adult feedlot cattle
89
What time of year are signs of thromboembolic meningoencephalitis seen most commonly?
Winter, approximately 2-4w after entering a feedlot
90
What is the causative agent of thromboembolic meningoencephalitis?
Histophilus somni
91
What is the probable route of infection for thromboembolic meningoencephalitis?
Respiratory tract, infects vascular tissue and endothelium resulting in inflammation and thrombosis of small vessels
92
What clinical signs are associated with thromboembolic meningoencephalitis?
Anorexia, fever, depression, ataxia
93
How is thromboembolic meningoencephalitis diagnosed?
History of acute onset of neuro disease in young feedlot animals, CSF analysis with neutrophilic pleocytosis and increased protein and xanthochromia, serum titers, necropsy showing multifocal hemorrhage in brain stem, cerebral cortex, spinal cord, and kidney
94
Thromboembolic meningoencephalitis is associated with _________ morbidity and ________ mortality
Low morbidity, high mortality
95
How is thromboembolic meningoencephalitis treated?
Antibiotics (aminopenicillins, ceftiofur, oxytetracycline, florfenicol), electrolytes and glucose, supportive care. Prognosis good for ambulatory animals
96
How can thromboembolic meningoencephalitis be prevented?
Vaccine (killed bacterin, given twice 2-3w apart), metaphylaxis
97
Describe lower motor neuron deficits
Paresis or paralysis, hyporeflexia or areflexia, early and severe muscle atrophy, hypotonia or atonia, eventual contracture and fibrosis
98
Where does evidence of LMN dysfunction localize the lesion to?
Cell body (spinal cord or brain stem) or axon (peripheral/cranial nerve or nerve root)
99
Describe upper motor neuron deficits
Paresis or paralysis of voluntary motor function, normoreflexia or hyperreflexia, increased tone in extensor muscles
100
Where does UMN dysfunction localize the lesion to?
Brain or spinal cord segments cranial to LMNs
101
What signs do mild compressive lesions cause? Moderate lesions? Severe?
Mild- loss of proprioception only Moderate- loss of motor function, inability to bear weight, loss of voluntary movement Severe- loss of nociception (deep pain perception)
102
What are differential diagnoses for spinal cord lesions?
Caprine arthritis encephalomyelitis, verminous encephalomyelitis, vertebral osteomyelitis/diskospondylitis/myelitis, neosporosis, trauma, bovine lymphoma
103
What kind of virus is the causative agent of caprine arthritis encephalomyelitis?
Retrovirus
104
What type of animals are most commonly affected by caprine arthritis encephalomyelitis?
1-6 month old kids after ingesting milk from infected does
105
What is the clinical presentation of animals with caprine arthritis encephalomyelitis?
UMN dysfunction of the limbs progressing cranially, occasional LMN involvement, fever, tachypnea, weight loss, polyarthritis
106
How is caprine arthritis encephalomyelitis diagnosed?
History, evidence of chronic arthritis, pneumonia, mastitis, and weight loss in adults, CSF analysis with mononuclear pleocytosis and elevated protein, ELISA or PCR testing- not specific or sensitive, findings of severe granulomatous perivascular leukomyelitis with demyelination
107
What is the prognosis of caprine arthritis encephalomyelitis?
Poor, no treatment
108
How is caprine arthritis encephalomyelitis prevented?
Separate kids from dams, feed heat-treated colostrum and milk, maintain a closed herd, use serological monitoring
109
What group of animals most commonly develops verminous meningoencephalomyelitis?
Young goats and lambs
110
What is the cause of verminous meningoencephalomyelitis?
Paraelaphostrongylus tenuis- meningeal worm of white tailed deer
111
What intermediate host does verminous meningoencephalomyelitis need?
Mollusk or snail
112
What clinical signs are associated with verminous meningoencephalomyelitis?
Asymmetric gait abnormality, vestibular signs, occasionally cerebellum and forebrain signs
113
How is verminous meningoencephalomyelitis diagnosed?
CSF analysis of neutrophilic or eosinophilic pleocytosis, antibody test at larval proteins is supportive
114
How is verminous meningoencephalomyelitis treated?
Anthelmintic and anti-inflammatory drugs
115
What is the prognosis of verminous meningoencephalomyelitis?
Fair to poor depending on severity; permanent deficits often persist
116
What is the most common cause of spinal cord dysfunction in adult cows?
Bovine lymphosarcoma
117
What is the typical presentation of an animal with bovine lymphosarcoma?
Acute onset paraparesis and recumbency, may have lymphadenopathy, arrhythmias, melena, exophthalmos
118
How is bovine lymphosarcoma diagnosed?
CSF analysis is normal with increased protein, persistent lymphocytosis or atypical lymphocytes in blood, positive AGID test, spinal imaging

Ruminants (10 decks)

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