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Equine Medicine Final > Neurologic disorders in foals > Flashcards

Neurologic disorders in foals Flashcards

1
Q

What is the best way to observe foals for neurologic behavior?

A
  • From a distance is best

- responses can seem random, variable, and unpredictable

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2
Q

How is a lot of time spent for a foal?

A
  • Sleeping in lateral recumbency

- Should be easily aroused

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3
Q

What should a normal foal be doing even early on with the mare and udder?

A
  • Should be seeking the udder and the mare
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4
Q

Head movements of a foal

A
  • Jerky and exaggerated
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5
Q

Restraint of a foal

A
  • Alternating struggling and flopping
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6
Q

What is the menace response like in the foal?

A
  • CN II and VII

- Not complete

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7
Q

When does the menace response complete in the foal?

A

2 weeks

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8
Q

Which CN control eye position?

A

III, IV, VI

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9
Q

What is the normal pupil axis in a foal?

A
  • Ventromedial

- Dorsomedial if some neurologic dysfunction

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10
Q

CN V/VII in a foal

A
  • Sensory and motor (respectively) to the face
  • Hyperresponsive to tactile stimulation
  • Jerky head movements indicate cerebral perception
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11
Q

CN VIII in a foal

A
  • Postional nystagmus is normal
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12
Q

What nerves are part of the swallow reflex?

A
  • CN IX, X, XI
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13
Q

What nerve is involved in lip movement?

A

CN VII

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14
Q

What nerve is involved in jaw movement in foals?

A
  • CN V
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15
Q

What nerve is involved in tongue movement in foals?

A
  • XII
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16
Q

What if a foal has its tongue stuck out?

A
  • Try to pull on it and put it back in
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17
Q

Which CN are involved in nursing?

A
  • CN IX, X, XI (suckle reflex)
  • CN V
  • CN VII
  • CN XII
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18
Q

“Normal” gait abnormalities in a foal

A
  • Dysmetria
  • Base-wide stance
  • Hypermetric reflexes
  • Crossed extensor reflex takes 3 weeks
  • Increased resting extensor tone
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19
Q

Dysmetria

A
  • Short stride with exaggerated step
  • Normal in foals
  • Adult gait achieved with exercise
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20
Q

How long does the crossed extensor reflex take to develop?

A

3 weeks

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21
Q

How long should the suckle reflex/jaw tone take to develop in the foal?

A
  • Within minutes of birth and strong within an hour
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22
Q

Long spinal reflexes in foals

A
  • Cervicofacial cutaneous trunci

- Slap test is inconsistent in foals

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23
Q

Other reflexes that should be present in foals

A
  • Withers and pelvic strength

- Anal tone and tail tone

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24
Q

What are some differentials for seizures in foals?

A
  • REM sleep
  • Narcolepsy/cataplexy
  • “Fainting foal” syndrome
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25
Q

REM sleep in foals

A
  • > in preemies
  • Paddling and chomping
  • can be easily aroused
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26
Q

Narcolepsy/cataplexy

A
  • May be stimuli elicited
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27
Q

“Fainting foal syndrome”

A
  • Mini’s - flaccid limbs, eyes open
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28
Q

Seizures threshold of foals

A
  • Inherently low
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29
Q

Clinical signs of seizures in foals

A
  • Partial/focal - may not be recumbent
  • Chewing gum fits
  • Nystagmus
  • Muscle tremors/twitches
  • Stretching
  • Altered behavior
  • Generalized with recumbency/unconsciousness: involuntary muscle movement, opisthotonus, paddling, extensor rigidity
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30
Q

Etiologies for seizures

A
  • Perinatal complications
  • Metabolic
  • idiopathic epilepsy
  • Infection
  • Iatrogenic/drug associated
  • Developmental
  • Heat stroke
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31
Q

Perinatal complications in foals with seizures

A
  • Perinatal asphyxia, intracranial hemorrhage, cerebral contusions
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32
Q

metabolic derangements in foals with seizures

A
  • Decreased Na+, Mg+, Ca2+, or glucose
  • Increased Na+
  • metabolic acidosis
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33
Q

Idiopathic epilepsy in foals

A
  • most often in Egyptian Arabs
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34
Q

Infectious etiologies in foals with seizures

A
  • Sepsis without meningitis
  • Septic meningitis
  • Bacterial or viral encephalitis
  • Tyzzer’s - Clostridium piliformis
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35
Q

Iatrogenic or drug associated etiologies in foals with seizures

A
  • Theophylline, toxins, intracarotid injection
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36
Q

Developmental diseases leading to seizures in foals

A
  • Hydrocephalus, storage disease
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37
Q

Diagnostic options for foals with seizures

A
  • Imaging: CT, MRI, Xray

- CSF Tap

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38
Q

CSF tap in foals cons

A
  • Not benign procedures
  • 5-10 mL considered safe
  • If you take too much, you can kill a foal
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39
Q

CSF tap test in foals

A
  • Fluid analysis and cytology

- UA strips have been used - beware blood contamination (???)

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40
Q

Neonatal vs adult CSF normal

A
  • Trace glucose in neonates

- 1st 40 hours protein will be higher than in adults

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41
Q

Perinatal asphyxia syndrome other names

A
  • Neonatal multisystem maladaptation syndrome
  • Hypoxic ischemic encephalopathy
  • Neonatal maladjustment syndrome
  • “Dummy” foals
  • Wanderers/barkers
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42
Q

What types of disturbances can occur in perinatal asphyxia syndrome in foals?

A
  • Renal, GI, cardiopulmonary, endocrine, behavioral, and neurologic disturbances
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43
Q

What does the hypoxic ischemic event in the foal cause that ultimately leads to all of the cell death and clinical signs?

A
  • Failure of the Na/K+ ATPase pump
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44
Q

Perinatal Asphyxia Syndrome Pathogenesis

A

See the image in the notes

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45
Q

4 Prenatal causes of periparturient hypoxia

A
  1. Reduced maternal oxygen delivery
  2. Reduced maternal blood flow
  3. Placental disease
  4. Reduced umbilical flow
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46
Q

Reduced maternal oxygen delivery

A
  • anemia, lung disease, cardiovascular disease in dam
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47
Q

Reduced maternal blood flow

A
  • Maternal hypotension/hypertension, endotoxemia, colic
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48
Q

Placental disease

A
  • PPS, placental insufficiency, twins, placental dysfunction, placentitis
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49
Q

Reduced umbilical flow

A
  • General anesthesia, congenital CV disease
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50
Q

Placentitis on ultrasound

A
  • Very thick placenta
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51
Q

Intrapartum issues

A
  • Dystocia
  • Premature placental separation
  • Uterine inertia
  • Oxytocin induced labor
  • C-section
  • Anything prolonging stage II labor
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52
Q

Premature placental separation appearance

A
  • “Red bag”

- If you saw this, pull the foal immediately

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53
Q

Neonatal causes of hypoxia

A
  • Prematurity/dysmaturity
  • Any cause of recumbency
  • Thoracic disease
  • Recurrent episodes of apnea
  • Septic shock
  • neonatal anemia
  • Congenital cardiovascular disease
54
Q

What determines the severity of the hypoxic injury?

A
  • Duration
  • Repeated insult?
  • When it occured
55
Q

What are the most common signs in perinatal asphyxia syndrome?

A
  • CNS is most vulnerable to altered metabolism
56
Q

What regions are most susceptible to hypoxia?

A
  • CNS>kidney>GI>heart>lungs>liver
57
Q

What are the two categories of PAS?

A
  1. born normal, develop within 48 hours

2. Born abnormal

58
Q

What is the most prominent clinical sign of PAS?

A
  • Cerebral dysfunction

- Category 2 can show signs of brainstem and spinal cord dysfunction

59
Q

Other clinical signs of PAS

A
  • Lack of affinity for the mare
  • Restless
  • Hyper-responsive
  • Abnormal posture
  • Tongue protrusion
  • Abnormal jaw/facial movements
  • “Star-gazing”
  • Head-pressing
  • Obsessive licking
  • Abnormal vocalization
  • Recurrent seizures
  • Lethargy/stupor
  • Head tilt
  • Facial paralysis
  • Abnormal breathing
  • MODS
60
Q

CBC/Chem/UA of uncomplicated foals with PAS

A
  • Normal often

- CAN have metabolic/blood gas derangements

61
Q

CSF in foals with PAS

A
  • Normal or xanthochromic
62
Q

Post-mortem findings in foals with PAS

A
  • CNS necrosis
  • CNS edema
  • CNS hemorrhage
  • NOT always evident
63
Q

Overarching therapy goals treatment for PAS

A
  • Adequate cardiac output/perfusion
  • Prevent further hypoxic-ischemic episodes
  • Prevent inflammatory mediators
64
Q

How do you measure adequate cardiac output/perfusion in a foal being treated for PAS?

A
  • Consistent urine output
  • Perfusion to limbs (warm)
  • Perfusion to brain (mental status)
  • Perfusion to bowel (GI function)
65
Q

What can develop if severity of PAS worsens?

A
  • Multiple organ dysfunction

- may need inotrope and pressor therapy

66
Q

How to prevent further hypoxic-ischemic episodes in foals with PAS?

A
  • Put the mon oxygen
67
Q

What does preventing inflammatory mediators do for PAS?

A
  • Support organ system function
  • Allow recovery
  • Prevent secondary sepsis
  • Prevent other complications (bed sores, corneal ulcers, aspiration, self-injury)
68
Q

What should you monitor daily with PAS?

A
  • Body weight
69
Q

Fluid goals with treating PAS

A
  • AVOID fluid overload (permissive dehydration) –> want to prevent dehydration
  • All compromised neonates benefit from glucose therapy (+/- may need insulin if can’t regulate glucose)
  • Electrolytes - acid/base restoration
70
Q

Specific treatments in foals with PAS

A
  • IVF
  • Enteral nutrition or parenteral nutrition (enteral preferred)
  • Control seizures
  • Maintain cerebral perfusion
  • CNS protectants
71
Q

Enteral nutrition for foals with PAS

A
  • If tolerable
  • beneficial to enterocytes
  • fresh colostrum and mare’s milk best
  • Parenteral nutrition if unable to eat
72
Q

How to maintain cerebral perfusion?

A
  • Careful fluid management

- Maintain blood pressure (inotropes/prssors)

73
Q

CNS protectants

A
  • DMSO, mannitol, thiamine**, MgSO4
  • Steroids??
  • NSAIDs
  • Pentoxyfylline
74
Q

Cocktail treatment for initial bag of fluids with foals with PAS

A
  • 1 L lactated Ringers
  • MgSO4
  • Ascorbic acid
  • Thiamine
  • DMSO
75
Q

Anti-oxidants to give to foals with PAS

A
  • Vitamin E

- Allopurinol (anti-oxidant)

76
Q

Prognosis of Category 1 PAS foals

A
  • 75-80% survival
  • Typically milder abnormalities and clinical signs
  • Generally improve within 48-72 hours
77
Q

Prognosis of Category 2 PAS foals

A
  • 50-75% survival
  • Typically more severe abnormalities/clinical signs
  • Foals that don’t survive generally deteriorate within 48 hours
78
Q

Negative prognostic indicators for PAS foals

A
  • MOD

- Seizures

79
Q

Madigan squeeze

A
  • Maybe reducing pregnane levels?
  • Foals return to normal within a few days
  • More studies needed
80
Q

Bacterial meningitis: stats in septic foals

A
  • up to 10% of septic foals
81
Q

Pathophysiology of bacterial meningitis in foals (3 big contributing factors)

A
  • Immature immune system
  • lack adequate IgG and complement in CSF
  • More permeable BBB in neonate; even worse with bacterial induced inflammation
82
Q

CNS signs with bacterial meningitis

A
  • Cerebral signs > cervical pain > spinal signs

- Rapidly progressive to seizure

83
Q

Treatment for bacterial meningitis

A
  • Bactericidal antimicrobials
84
Q

Prognosis for bacterial meningitis

A
  • Guarded to poor prognosis
85
Q

Causes of cerebral trauma

A
  • +/- frontal or parietal bone fractures
86
Q

Cerebral trauma clinical signs

A
  • Blind, depressed, wander to side of cerebral lesion
87
Q

Midbrain trauma causes

A
  • Compression from hemorrhage/cerebral edema
88
Q

Midbrain trauma clinical signs

A
  • CNN deficits (??)
89
Q

Poll trauma causes

A
  • Can result in hemorrhage around brain stem

- DO NOT PULL ON A FOAL IN A HARNESS

90
Q

Poll trauma signs

A
  • CNN deficits (??)
91
Q

What are the signs of neurologic trauma from?

A
  • Immediate injury and secondary tissue reaction to injury
92
Q

Imaging neurologic trauma

A
  • Rads
  • CT
  • MRI
93
Q

Supportive treatment for neurologic trauma (for brain vs spinal lesions)

A
  • brain: steroids, hypertonic saline

- Spinal: steroids

94
Q

Neurologic trauma with a closed head prognosis?

A
  • Fair to good prognosis
95
Q

Prognosis of neurologic trauma with an open fracture

A
  • Guarded
96
Q

Metabolic neurologic disorders (4)

A
  1. Hyponatremia
  2. Hypernatremia
  3. Hypocalcemia/Hypomagnesemia
  4. Hypoglycemia/metabolic acidosis
97
Q

Hyponatremia injury to brain

A
  • cerebral edema
98
Q

Hyponatremia value

A
  • <120 mEq/dL
99
Q

Hypernatremia injury to brain

A
  • Dehydration
100
Q

Hypernatremia value

A

> 160 mEq/dL

101
Q

Hypocalcemia/hypomagnesemia clinical signs in foals

A
  • Tetanic rigidity
102
Q

Hypoglycemic/metabolic acidosis signs in foals

A
  • Seizures
103
Q

Idiopathic epilepsy signs

A
  • intermittent psychomotor seizures
  • Normal interictal periods
  • Some may have temporary blindness
104
Q

Which breed is predisposed to idiopathic epilepsy?

A
  • Arabian foals
105
Q

Potential pathology with idiopathic epilepsy

A
  • laminar cerebrocortical necrosis secondary to repeated seizures
106
Q

Prognosis for idiopathic epilepsy

A
  • usually resolves with age (6-12 months)
  • Some require anticonvulsants
  • Majority become safe useful life
107
Q

Breed predisposition for narcolepsy/cataplexy

A
  • Minies and Ponies
108
Q

Signs of narcolepsy/cataplexy

A
  • Fainting (may be exaggerated version of normal response to restraint)
  • Collapse, suddenly hypotonic, hyporeflexic state, REM
  • May last several minutes
109
Q

Pathogenesis of narcolepsy/cataplexy

A
  • Human work may lead to decreased arousal peptide
110
Q

Diagnosis of narcolepsy/cataplexy

A
  • Physostygmine test
111
Q

Treatment for narcolepsy/cataplexy

A
  • None
  • Imipramine
  • Atropine
112
Q

Cerebellar abiotrophy breed

A
  • Arabians and Oldenburgs
113
Q

Cerebellar abiotrophy pattern of inheritance

A
  • Recessive genetic defect
114
Q

Pathologic lesion in cerebellar abiotrophy

A
  • Cerebellum degenerates AFTER full development
115
Q

Signs in CA

A
  • No menace, symmetrical without weakness
116
Q

Diagnosis of CA

A
  • MRI shows small cerebellum
117
Q

Treatment for CA

A
  • Most euthanized
  • Not treatment
  • Unsafe
118
Q

Occipitoatlantoaxial malformation breed predisposition

A
  • Inherited in Arabians, spontaneous in all others
119
Q

Occipitoatlantoaxial malformation primary lesion

A
  • Occipital, atlas, and axis

- Instability and stenosis of vertebral canal

120
Q

Sign in Occipitoatlantoaxial malformation

A
  • Tetraparesis and ataxia in all four limbs

- may hear clicking with head/neck movement

121
Q

Diagnosis of Occipitoatlantoaxial malformation

A
  • Radiographs

- Hypoplastic dens, fusion of occipito/atlas

122
Q

Treatment for Occipitoatlantoaxial malformation

A
  • Most euthanized
123
Q

Botulism AKA “Shaker foal” etiology

A
  • botulinum toxin
  • Exotoxin of C. botulinum B or C
  • Prevents release of acetylcholine at NMJ
124
Q

How do foals typically get botulism?

A
  • Ingestion of bacterium with proliferation of toxin in GI tract and ingestion of preformed toxin (or wound infection)
  • Foals typically get toxicoinfectious disease from GI tract (ingest bacterium, which produces the toxin in the tract)
125
Q

Where is botulism typically found?

A
  • Endemic in eastern US but sporadic elsewhere
126
Q

Clinical signs of botulism in foals

A
  • Sudden onset weakness/flaccid paralysis
  • Dribbling milk from nose and mouth
  • Pupillary dilation/ptosis
  • Muscle tremors that progress to recumbency
  • Death can occur within 72 hours (respiratory paralysis)
127
Q

Diagnosis of botulism

A
  • presumptive from toxin in feces or blood

- Can do PCR of GI contents too

128
Q

Treatment for botulism

A
  • Polyvalent antitoxin for B and C

- Mechanical ventilation

129
Q

Mechanical ventilation with foals with botulism

A
  • Recumbent foals are unlikely to survive without mechanical ventilation (BUT they can survive)
  • May require several days to weeks
  • Full recovery may take months
130
Q

Prognosis for botulism without treatment

A
  • 90% die within 72 hours without treatment
131
Q

Prognosis for botulism if treated with antitoxin within several hours of onset

A
  • 80% survive
132
Q

Prevention of botulism

A
  • Vaccination
  • Commercial toxoid available for pregnant mares (type B)
  • Significantly reduce the endemic incidence

Equine Medicine Final (10 decks)

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