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Equine Final > Neuro > Flashcards

Neuro Flashcards

1
Q

What is the name of CN I? Is it sensory or motor? What is it involved with?

A

Olfactory nerve; sensory; involved in olfaction

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2
Q

What is the name of CN II? Is it sensory or motor? What is it involved with?

A

Optic nerve; sensory; allows vision

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3
Q

What is the name of CN III? Is it sensory or motor? What is it involved with?

A

Oculomotor; motor; pupil/eye position, innervates majority of extraocular muscles, pupil constriction

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4
Q

What is the name of CN IV? Is it sensory or motor? What is it involved with?

A

Trochlear nerve; motor; pupil/eye position, innervates superior oblique extraocular muscles

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5
Q

What is the name of CN V? Is it sensory or motor? What is it involved with?

A

Trigeminal nerve; mixed function; sensory to face and eyelids, motor to masticatory muscles; 3 branches- maxillary, mandibular, ophthalmic

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6
Q

What is the name of CN VI? Is it sensory or motor? What is it involved with?

A

Abducent nerve; motor; pupil/eye position, innervates lateral rectus extraocular muscle and retractor bulbi, ABDUCTS the eye

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7
Q

What is the name of CN VII? Is it sensory or motor? What is it involved with?

A

Facial nerve; mixed; innervates muscles of expression, involved in taste, salivation, and lacrimation

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8
Q

What is the name of CN VIII? Is it sensory or motor? What is it involved with?

A

Vestibulocochlear; sensory; controls balance and hearing

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9
Q

What is the name of CN IX? Is it sensory or motor? What is it involved with?

A

Glossopharyngeal nerve; mixed; swallowing and taste, motor to swallowing muscles

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10
Q

What is the name of CN X? Is it sensory or motor? What is it involved with?

A

Vagus nerve; mixed; sensation to pharynx and larynx, involved in swallowing and vocalization, recurrent laryngeal is a branch

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11
Q

What is the name of CN XI? Is it sensory or motor? What is it involved with?

A

Accessory nerve; motor; innervates pharyngeal, laryngeal, and cervical muscles

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12
Q

What is the name of CN XII? Is it sensory or motor? What is it involved with?

A

Hypoglossal nerve; motor; lingual muscles, involved in swallowing

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13
Q

What does the dorsal rectus muscle do? What nerve supplies it?

A

Provides upward motion of the globe; oculomotor (III)

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14
Q

What does the ventral rectus muscle do? What nerve supplies it?

A

Provides downward motion of the globe; oculomotor (III)

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15
Q

What does the media rectus muscle do? What nerve supplies it?

A

Provides medial motion of the globe; oculomotor (III)

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16
Q

What does the lateral rectus muscle do? What nerve supplies it?

A

Provides lateral motion of the globe; abducens (VI)

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17
Q

What does the dorsal oblique muscle do? What nerve supplies it?

A

Provides rotation nasally and inferiorly; trochlear (IV)

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18
Q

What does the ventral oblique muscle do? What supplies it?

A

Provides rotation laterally and superiorly; oculomotor (III)

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19
Q

What does the retractor bulbi muscle do? What nerve supplies it?

A

Provides posterior motion of the globe; abducens (VI)

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20
Q

What symptoms would you see of optic (II) nerve dysfunction? How do you test it?

A

Blindness; menace response, PLR, dazzle

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21
Q

What symptoms would you see of oculomotor (III) nerve dysfunction? How do you test it?

A

Lateral strabismus, mydriasis, ptosis; eye position, PLR

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22
Q

What symptoms would you see of trochlear (IV) nerve dysfunction? How do you test it?

A

Dorsomedial strabismus; move head and observe eye position

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23
Q

What symptoms would you see of trigeminal (V) nerve dysfunction? How do you test it?

A

Neurotrophic keratitis; corneal reflex

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24
Q

What symptoms would you see of abducens (VI) nerve dysfunction? How do you test it?

A

Medial strabismus; move head and observe eye position

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25
Q

What symptoms would you see of facial (VII) nerve dysfunction? How do you test it?

A

Exposure keratitis KCS; observation, palpebral reflex, STT

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26
Q

What symptoms would you see of vestibulocochlear (VIII) nerve dysfunction? How do you test it?

A

Spontaneous nystagmus; observation

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27
Q

Define strabismus. What are its causes?

A

Deviation of the globe from its normal orientation in a non-exophthalmic eye. Caused by cranial nerve deficits (III, IV, VI)

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28
Q

What function do UMN have on gait?

A

Gait generation, maintenance of muscle tone/posture against gravity

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29
Q

What function do LMN have on gait?

A

Support of weight

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30
Q

When do spinal/proprioceptive ataxia occur? What are examples?

A

Occur with any injury to sensory (afferent) parts of the CNS, examples include Wobblers, EPM, EDM

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31
Q

What are signs of vestibular ataxia?

A

Truncal sway, wide based stance, nystagmus, head tilt, circling (ex. temporohyoid osteoarthropathy)

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32
Q

Describe cerebellar ataxia

A

Hypermetria, usually worse in thoracic limbs, intention tremors of head, absent menace response; most common in foals; ex. cerebellar abiotrophy (Arabians)

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33
Q

Are reflexes and reactions exaggerated, normal or absent in LMN lesions?

A

Usually decreased to absent

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34
Q

Are reflexes and reactions exaggerated, normal, or absent in UMN lesions?

A

Normal to exagerated

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35
Q

What is the Mayhew scale?

A

Scale for neuro deficits. 0- normal; 1- neuro deficits barely detected at normal gait, worsened w/ tests; 2- neuro deficits easily detected at normal gait; 3- neuro deficits prominent at walk, buckle or fall forward w/ special tests; 4- stumbling, tripping, falling spontaneously; 5- recumbent

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36
Q

What signs will you see with cerebral cortex lesions?

A

Postural deficits, seizures, altered mentation

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37
Q

What signs will you see with brainstem lesions?

A

Ataxia, weakness, dysmetria, dysphagia, anisocoria, dilated pupils

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38
Q

What signs will you see with vestibular lesions?

A

Ataxia, head tilt, postural deficits pronounced

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39
Q

What signs will you see with cerebellum lesions?

A

Ataxia, intention tremors

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40
Q

What signs will you see with spinal cord/UMN lesions?

A

Paresis, ataxia, dysmetria, spasticity

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41
Q

What signs will you see with peripheral nerve/LMN lesions?

A

Weakness predominates, postural deficits

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42
Q

What are signs of a C1-C5 lesion?

A

UMN in all limbs, proprioceptive deficits and weakness in all limbs, possible Horner’s syndrome, hind limbs worse than front

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43
Q

What are signs of C6-T2 lesions?

A

LMN in forelimbs, UMN in hindlimbs, proprioceptive deficits in hindlimbs, possible Horner’s syndrome

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44
Q

What are signs of T3-L3 lesions?

A

Normal gait in forelimbs, UMN and proprioceptive deficits in hindlimbs

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45
Q

What are signs of L4-S1 lesions?

A

Normal gait in forelimbs, LMN in hind limbs

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46
Q

What are signs of sacral/S1-S3 lesions?

A

Urinary incontinence, fecal retention, hypalgesic tail and perineal region, decreased tail tone

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47
Q

Describe UMN paresis/weakness

A

Spastic paresis, hyperreflexia, delayed protraction of limbs when walking or hopping, scuffing of toes

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48
Q

Describe LMN paresis/weakness

A

Short-strided, similar to orthopedic disease, if diffuse, animal may collapse, tremors at rest, proprioception intact, flaccid paralysis

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49
Q

What are signs of a brachial plexus injury?

A

Dropped elbow, inability to bear weight, lateral deviation of shoulder, complete desensitization and flaccidity of limb

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50
Q

What are signs of radial nerve paralysis?

A

Inability to flex shoulder, extend limb, and fix elbow to bear weight, dorsum of foot rests on ground

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51
Q

What are common causes of radial nerve paralysis?

A

Anesthesia or prolonged recumbency, direct trauma from external blow collision

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52
Q

What are signs of obturator nerve paralysis? What are causes?

A

Splay-legged horse; can occur from dystocia or ileal or sacral fractures

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53
Q

What are signs of femoral nerve paralysis?

A

Inability to flex and extend stifle, inability to bear weight, crouched stance with all joints flexed

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54
Q

Describe suprascapular nerve paralysis

A

Atrophy of supra and infraspinatous muscles, abduction of limb during weightbearing, inability to advance shoulder, focal swelling. Called “Sweeney”, caused by direct trauma, often cart horses

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55
Q

What are common neuropathic treatments?

A

Minimize inflammation (NSAIDs, DMSO, corticosteroids), minimize injury (stall rest, wraps/splints), limit exercise, physical therapy

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56
Q

When do horses develop menace response?

A

Around 2-3 weeks old

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57
Q

What nerves does a pupillary light reflex test?

A

CN II and III

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58
Q

How would you assess glossopharyngeal nerve (IX) function? What would its dysfunction look like?

A

Watch them eat or pass a NG tube. Dysfunction would cause dysphagia, feed material in nostrils, coughing while eating

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59
Q

How would you assess vagus nerve (X) function? What would its dysfunction look like?

A

Watch patient eat, slap test of thoracolaryngeal reflex, listen to respiratory noise while working. Dysfunction causes dysphagia, “roaring”, larpar

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60
Q

How would you assess hypoglossal nerve (XII) function? What would its dysfunction look like?

A

Examine tongue for tone and symmetry, ability to retract. Dysfunction would result in failure to retract tongue and atrophy of the tongue

61
Q

What are the parts of a gait analysis evaluation?

A

Walking in straight line, circling, walking with head up, walking over a curb, tail pull, walking backwards, walking up and down hill

62
Q

What are clinical signs of Horner’s syndrome? What are common causes?

A

Signs- miosis (constriction of pupil), ptosis (drooping of eyelid), sweating ipsilateral to lesion. Causes- extravation of irritating substance, guttural pouch disease, EPM, cervical vertebral stenotic myelopathy, trauma

63
Q

How do you diagnose Horner’s syndrome?

A

Clinical signs, localize the lesion, chem/gas panel may show electrolyte changes, acid base derangements, hypocalcemia or hypokalemia

64
Q

Describe CSF analysis

A

Goal is to identify inflammation, trauma, neoplasia, infection, or to rule in/out specific diseases. Perform standing (LS or C1-C2) or under GA (alantooccipital)

65
Q

Describe myelography

A

Antemortem diagnostic of choice for compressive spinal cord lesion, done with rads or CT under GA or standing. Administer contrast, take images in flexed, extended, and neutral positions. Can cause seizures, poor recovery, fever.

66
Q

What is CT good for analyzing? What about MRI?

A

CT- skulls and cervical spine. MRI- brain and cord imaging but not feasible in horses

67
Q

What disease is the leading cause of non-infectious spinal ataxia in horses?

A

Cervical vertebral stenotic myelopathy (AKA Wobbler’s)

68
Q

What are predisposing factors/causes for Wobbler’s?

A

Congenital (occipital atlanto axial malformation in Arabians), environmental + genetic factors

69
Q

What is the classic presentation of a Wobbler’s patient?

A

Rapidly growing, large, history of being “clumsy”, thoroughbred or warmblood

70
Q

What are the clinical signs of Wobblers?

A

Spinal/proprioceptive ataxia worse in hind limbs, symmetric, UMN paresis (spasticity, delayed protraction, increased tone, exaggerated reflexes, minimal muscle atrophy)

71
Q

What is type 1 Wobbler’s?

A

Symmetrical overgrowth of articular processes causes dynamic compression during flexion, develops orthopedic disease, usually mid cervical (C3-C5) region in weanlings or younger horses

72
Q

What is type 2 Wobbler’s?

A

Asymmetrical overgrowth either by direct bony compression or soft tissue hypertrophy, seen in mature horses at C5-C6, C6-C7

73
Q

How is Wobbler’s diagnosed?

A

Neurological examination, radiographs. Calculate sagittal ratios and look for abnormal ossification, malalignment, or degenerative joint disease

74
Q

What are sagittal ratios?

A

Measurements used to identify compression of cord (based on rads)

75
Q

What findings in a myelogram would suggest Wobblers?

A

Complete attenuation of ventral contrast column, at least 50% attenuation of dorsal contrast column

76
Q

Describe medical/conservative treatment of Wobblers

A

Young horses- restrict exercise, restrict protein and carbs (to slow growth rate), alterations in copper and zinc, add vitamin E supplementation. Adults- corticosteroid injections, HA supplementation

77
Q

Describe surgical treatment of Wobblers

A

Ventral stabilization “basket” surgery to stop repetitive trauma to spinal cord. Best candidates are young horses with 1-2 lesions and short duration of clinical signs. Takes 6mos to 1 year to recover, full effects may not be seen until that time. Expect 1-2 grades improved.

78
Q

What is the relationship between vitamin E levels and equine motor neuron disease?

A

Negative- less vitamin E= more risk

79
Q

Describe the clinical signs of equine motor neuron disease?

A

Trembling, muscle fasciculations, weight shifting, base narrow stance, low head carraige, elevation in tail (“elephant on ball stance”), excessive recumbency, muscle atrophy, weight loss despite appetite, not ataxic- walk better than they stand

80
Q

How is Equine motor neuron disease diagnosed?

A

Measure serum or muscle vitamin E, examine retina, muscle biopsy of sacrocaudalis dorsalis medialis- look for neuro atrophy of type 1 oxidative fibers, definitive diagnosis

81
Q

What is the prognosis and treatment for equine motor neuron disease?

A

Treatment leads to improvement over 6 weeks in 40% of cases. 40% cases have permanent disfiguration, 20% have continued atrophy. Treat with vitamin E supplementation (must be active alpha tocopherol 5000-7000 IU/day)

82
Q

What is the most common cause of peripheral vestibular disease in horses?

A

Temporohyoid ostearthropathy (THO)

83
Q

Describe the process and signs of temporohyoid ostearthropathy (THO)

A

Acute onset of peripheral vestibular disease and/or facial nerve paralysis caused by bony proliferation of articulation of stylohyoid and petrous temporal bones leading to fusion of the joint

84
Q

What are potential causes of THO?

A

Extension of inflammation and infection from otitis media/interna, guttural pouch infection, repetitive trauma, nonseptic osteoarthritis, aging change

85
Q

How is THO diagnosed?

A

DV view radiographs, endoscopy to visualize stylohyoid bone, CT/MRI for best image, necropsy

86
Q

Describe the medical treatment of THO

A

Stabilize and provide supportive care, anti-inflammatories, antibiotics (if potential joint infection or otitis), treat the eye

87
Q

Describe surgery for THO

A

Stylohyoid ostectomy (bone can grow back), ceratohyoidectomy- procedure of choice, basihyoid-ceratohyoid disarticulation

88
Q

What is the difference between equine degenerative myelopathy (EDM) and neuroaxonal dystrophy (NAD)?

A

Cell body and axons in the brain and spinal cord undergo degeneration in both, EDM is more widespread, NAD is subset of EDM

89
Q

What are clinical signs of EDM and NAD in young horses?

A

Symmetric ataxia, UMN weakness, may have depressed mentation, absent menace response, base-wide stance, no muscle atrophy, normal tail tone/perineal sensation

90
Q

What are clinical signs of EDM and NAD in adult horses?

A

Ataxia (subtle), rapid behavioral change

91
Q

How are EDM and NAD diagnosed?

A

Increased pNfH on CSF or in blood, low vitamin E levels, postmortem examination

92
Q

How are EDM and NAD treated/prevented? What is the prognosis?

A

Vitamin E supplementation!! Prognosis poor, not reversible

93
Q

What group of clinical signs are described by cauda equine syndrome?

A

Urinary/fecal incontinence, decreased tail tone, analgesia of tail, hypalgesia in perineal region, pelvic limb deficits

94
Q

What are causes of cauda equine syndrome?

A

Inflammatory (polyneuritis equi- auto-immune?), EPM, epidural abscess, EHM, toxic, neoplastic, traumatic (broken tail, secondary to tail block)

95
Q

What breed is predisposed to epilepsy?

A

Egyptian Arabians

96
Q

What are infectious causes of seizures?

A

Bacterial meningitis, brain abscess, verminous encephalitis, EEE/WEE/VEE, WNV, rabies

97
Q

What are traumatic causes of seizures?

A

Skull fracture, basisphenoid fracture, blunt head trauma

98
Q

What are neoplastic causes of seizures?

A

Brain tumor, insulin producing tumor -> hypoglycemia

99
Q

What are toxins that can cause seizures?

A

Moldy corn, castor bean, Jimsonweed, nightshade, hemlock, milkweed

100
Q

What are metabolic and miscellaneous causes of seizures?

A

Hypoglycemia, hypocalcemia, hepatic encephalopathy, hypoxic ischemic encephalopathy, cholesteatic granuloma, pituitary adenoma in PPID

101
Q

How are seizures treated in horses?

A

Short-term control- midazolam or diazepam. Long-term control- KBr, phenobarbital, Keppra, treat underlying cause if obvious. Dont’ ride horse.

102
Q

What are systems to evaluate in a down horse?

A

Musculoskeletal, GI, CV, neuro, metabolic

103
Q

How should you approach a down horse? What is the prognosis?

A

Stay on dorsal side, get TPR. Do neural exam, CBC/chem, blood gas, UA, CSF, imaging. Maintain horse in sling for short-term or flip every 2-6 hours. Prognosis is POOR

104
Q

Describe the lifecycle of Sarcocystis neurona

A

Opossums ingest sarcocysts from intermediate host, sarcocysts reproduce in GI tract, sporocysts are shed in feces and contaminate feed and water. Horse is aberrant host, ingests sporocysts which form sarcocysts in muscle and somehow migrate to CNS

105
Q

What are risk factors for developing EPM?

A

> 5 years old, warmbloods, living in the south

106
Q

What are the clinical signs of EPM?

A

Can be acute or insidious, varied signs based on location of sarcocysts- ataxia, asymmetry, atrophy, inconsistent lameness, LMN signs, brainstem signs, CN involvement

107
Q

What are differential diagnoses for EPM?

A

Wobblers, EEE/WEE/VEE/WNV/EHM, neuroborrelliosis, ortho disease, hepatic encephalopathy, neoplasia, trauma, THO

108
Q

What helps differentiate EPM horses from horses with other diseases?

A

Lack of fever, typically not painful, mentation changes are uncommon, horses are generally pretty happy

109
Q

How is EPM diagnosed?

A

Neuro exam with neurolocalization (often multifocal), serology (only useful if negative), CSF analysis, response to therapy, ruling out other diseases

110
Q

What is the most accurate test for EPM?

A

SAG 2, 4/3 ELISA serum:CSF ratio; ratio <100 consistent with antibody production and active infection

111
Q

How is EPM treated?

A

With ponazuril or diclazuril- both safe, effective, expensive ($1000/month), treat until signs resolve. Can also use folate inhibitors (sulfonamide/pyrimethamine) but less effective. May be more effective if used together. Additionally can use anti-inflammatories or immune stimulants

112
Q

Describe rabies and its 3 phases

A

Arbovirus, ZOONOTIC, reportable. Reservoir- mammals. Phase 1- centripetal, days to weeks, enters CNS and replicates in limbic system, adjacent structures, and spinal cord. Phase 2- spreads to highly vascular organs (ex. salivary glands). Phase 3- centrifugal, unknown

113
Q

What is the incubation period for rabies in horses? What are the common clinical signs of the different forms?

A

Incubation period 2-6 weeks. Most common complaints are lameness and colic. Paralytic form- ascending paralysis, loss of tail/anal tone, ataxia. Brainstem/dumb form- dysphonia, dysphagia, pharyngeal paralysis, head tilt, blidness, drooling. Cerebral/furious form- aggression, photophobia, hydrophobia, hyperesthesia, circling, roaring, bruxism, convulsions, depression

114
Q

How is rabies diagnosed in horses?

A

IFAT on brain tissue, negri bodies on histopathology

115
Q

What kind of viruses are WEE/EEE/VEE? Where are they found? Who carries them?

A

Togavirus (zoonotic, reportable). Carried by rats, birds, snakes, mosquitoes. EEE- SE USA, WEE- Western US and midwest, VEE- northern SA, central America, Mexico

116
Q

What clinical signs are associated with EEE/WEE/VEE?

A

Initial hyperexcitability progressing to somnolence, depression, recumbency, blindness

117
Q

How is EEE/WEE/VEE diagnosed?

A

CSF- neutrophilic to mononuclear pleocytosis, increased protein, antigen specific antibody detection on CSF or serum

118
Q

Describe the prognosis of EEE/WEE/VEE

A

Poor, EEE worst, then VEE, then WEE, tend to have residual neuro deficits

119
Q

How are EEE/WEE/VEE prevented?

A

Vaccines are cross-protective, control mosquitoes

120
Q

What kind of virus is West Nile virus?

A

Flavivirus, zoonotic, not contagious between horses

121
Q

How is WNV carried?

A

Carried by birds with mosquitoes as vectors. Horses and humans are dead end hosts. Peak season is September-November.

122
Q

What clinical signs are associated with WNV?

A

Ataxia, abnormal gait, muscle/muzzle fasciculations, depression, recumbency, +/- mild/mod fever

123
Q

How is WNV diagnosed?

A

IgM capture ELISA on CSF or serum, PCR on tissue

124
Q

How is WNV treated?

A

Supportive care, mannitol (reduce brain edema), corticosteroids, WNV specific immunoglobulin

125
Q

What is the prognosis for WNV?

A

70-80% survival, poor prognosis if recumbent, residual signs possible

126
Q

How is WNV prevented?

A

Vaccinate!

127
Q

Where is equine herpesvirus latently stored?

A

Trigeminal ganglion

128
Q

What are the three forms of equine herpesvirus 1?

A

Respiratory- young horses, most common. Abortion- late term. Neurologic disease- EHM, least common, biggest concern.

129
Q

What are the signs of equine herpes myeloencephalopathy (EHM)?

A

Fever, ataxia, generally worse in pelvic limbs, “dog sitting”, urine dribbling, decreased tail tone, fecal retention

130
Q

How is EHM diagnosed?

A

PCR of nasopharyngeal swab or whole blood in EDTA test of choice, ELISA and VN also available

131
Q

Describe the treatment and prognosis for EHM

A

Supportive care, anti-inflammatories (NSAIDs, corticosteroids), antivirals (valacyclovir), prognosis decent for non-recumbent horses

132
Q

What should you do during an outbreak of EHM?

A

Isolate and test suspected cases, report suspected cases, quarantine until results available, generally 21-28 days after no new cases

133
Q

Why should you vaccinate against equine herpesvirus 1 when it doesn’t protect against myeloencephalopathy?

A

Can still reduce duration of viremia and reduce nasal shed

134
Q

Describe Clostridium tetani

A

Gram positive obligate anaerobe, exists in spore form, has three toxins- tetanospasmin, hemolysin, nonspasmogenictoxin. Tetanospasmin is the toxin that causes clinical signs.

135
Q

How is tetanus transported within the body?

A

Bacteria proliferates in areas with low oxygen tension (wounds), binds to peripheral nerve terminals, is transported within axon and across synapses until it reaches CNS where it is taken up in the axon by endocytosis and blocks the release of GABA

136
Q

What are the clinical signs of tetanus?

A

Diffuse, symmetric hypertonicity and hyperresponsiveness of all muscle groups, third eyelid prolapse, saw horse stance, tachycardia, dysphagia

137
Q

What is a differential diagnosis for tetanus?

A

Hypocalcemia- causes tetany in horses, flaccid paralysis in cattle

138
Q

What is the treatment for tetanus? What is it’s prognosis?

A

Metronidazole, procaine penicillin, hyperbaric oxygen therapy, tetanus antitoxin, muscle relaxants, supportive care. Mortality ~75%

139
Q

Where do the four types of Clostridium botulinum endotoxin occur?

A

Type A- West of Rockies; Type B- mid-Atlantic; Type C- FL, CA, AZ, NE, Canada; Type D- rare

140
Q

Describe the pathophysiology of Clostridium botulinum

A

Blocks ACh release, toxin is taken up into vesicle, acidification leads to toxin being pushed into cytoplasm, toxin cleaves SNARE proteins and prevents cells from releasing vesicle neurotransmitter

141
Q

What are the three different Clostridium botulinum syndromes?

A

Forage poisoning- ingestion of pre-formed toxin (adult horse); Wound botulism- castration site, injection site, umbilicus; Toxicoinfectious- ingestion of spores that proliferate in GI tract and produce toxin, seen in foals

142
Q

What are the clinical signs of botulism?

A

Diffuse, flaccid paralysis, LMN weakness rather than ataxia, dysphagia, slow to eat or retract tongue, constipation, urine dribbling, bladder distension, mydriasis, ptosis, slow PLR, loss of corneal sensation/palpebral reflex

143
Q

How is botulism diagnosed?

A

Difficult- “grain test”- can a horse finish 8oz of grain in <2 minutes? Or finding toxin in feed, GI contents, or wounds.

144
Q

How is botulism treated?

A

Neutralize circulating toxin, use type B/C plasma or polyvalent plasma, debride wounds, provide supportive care and nutritional support

145
Q

What is the vector of lyme disease?

A

Ixodes ticks vector it (Borrelia burgdorferi)

146
Q

What clinical signs are associated with neuroborreliosis/Lyme disease?

A

Lethargy, anorexia, pyrexia, ataxia, hyperesthesia, uveitis, polysynovitis, neck pain, poor performance, tremors, weight loss, mentation changes

147
Q

How is neuroborreliosis/lyme disease diagnosed?

A

Definitively on histopathology (ID of organisms in CNS tissue). Seroprevalence is so high that test is not helpful.

148
Q

How is neuroborreliosis treated?

A

Minocycline can be used, maybe oxytetracycline- successful treatment rare, prognosis poor

149
Q

How is neuroborreliosis prevented?

A

Tick control, deer eclusion. Can use topical cypermethrin, permethrin, pyrethrins, or piperonyl butoxide

Equine Final (5 decks)

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