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Equine Medicine Final > Neurologic disorders in foals > Flashcards

Neurologic disorders in foals Flashcards

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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
REM sleep in foals
- > in preemies - Paddling and chomping - can be easily aroused
26
Narcolepsy/cataplexy
- May be stimuli elicited
27
"Fainting foal syndrome"
- Mini's - flaccid limbs, eyes open
28
Seizures threshold of foals
- Inherently low
29
Clinical signs of seizures in foals
- 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
30
Etiologies for seizures
- Perinatal complications - Metabolic - idiopathic epilepsy - Infection - Iatrogenic/drug associated - Developmental - Heat stroke
31
Perinatal complications in foals with seizures
- Perinatal asphyxia, intracranial hemorrhage, cerebral contusions
32
metabolic derangements in foals with seizures
- Decreased Na+, Mg+, Ca2+, or glucose - Increased Na+ - metabolic acidosis
33
Idiopathic epilepsy in foals
- most often in Egyptian Arabs
34
Infectious etiologies in foals with seizures
- Sepsis without meningitis - Septic meningitis - Bacterial or viral encephalitis - Tyzzer's - Clostridium piliformis
35
Iatrogenic or drug associated etiologies in foals with seizures
- Theophylline, toxins, intracarotid injection
36
Developmental diseases leading to seizures in foals
- Hydrocephalus, storage disease
37
Diagnostic options for foals with seizures
- Imaging: CT, MRI, Xray | - CSF Tap
38
CSF tap in foals cons
- Not benign procedures - 5-10 mL considered safe - If you take too much, you can kill a foal
39
CSF tap test in foals
- Fluid analysis and cytology | - UA strips have been used - beware blood contamination (???)
40
Neonatal vs adult CSF normal
- Trace glucose in neonates | - 1st 40 hours protein will be higher than in adults
41
Perinatal asphyxia syndrome other names
- Neonatal multisystem maladaptation syndrome - Hypoxic ischemic encephalopathy - Neonatal maladjustment syndrome - "Dummy" foals - Wanderers/barkers
42
What types of disturbances can occur in perinatal asphyxia syndrome in foals?
- Renal, GI, cardiopulmonary, endocrine, behavioral, and neurologic disturbances
43
What does the hypoxic ischemic event in the foal cause that ultimately leads to all of the cell death and clinical signs?
- Failure of the Na/K+ ATPase pump
44
Perinatal Asphyxia Syndrome Pathogenesis
See the image in the notes
45
4 Prenatal causes of periparturient hypoxia
1. Reduced maternal oxygen delivery 2. Reduced maternal blood flow 3. Placental disease 4. Reduced umbilical flow
46
Reduced maternal oxygen delivery
- anemia, lung disease, cardiovascular disease in dam
47
Reduced maternal blood flow
- Maternal hypotension/hypertension, endotoxemia, colic
48
Placental disease
- PPS, placental insufficiency, twins, placental dysfunction, placentitis
49
Reduced umbilical flow
- General anesthesia, congenital CV disease
50
Placentitis on ultrasound
- Very thick placenta
51
Intrapartum issues
- Dystocia - Premature placental separation - Uterine inertia - Oxytocin induced labor - C-section - Anything prolonging stage II labor
52
Premature placental separation appearance
- "Red bag" | - If you saw this, pull the foal immediately
53
Neonatal causes of hypoxia
- Prematurity/dysmaturity - Any cause of recumbency - Thoracic disease - Recurrent episodes of apnea - Septic shock - neonatal anemia - Congenital cardiovascular disease
54
What determines the severity of the hypoxic injury?
- Duration - Repeated insult? - When it occured
55
What are the most common signs in perinatal asphyxia syndrome?
- CNS is most vulnerable to altered metabolism
56
What regions are most susceptible to hypoxia?
- CNS>kidney>GI>heart>lungs>liver
57
What are the two categories of PAS?
1. born normal, develop within 48 hours | 2. Born abnormal
58
What is the most prominent clinical sign of PAS?
- Cerebral dysfunction | - Category 2 can show signs of brainstem and spinal cord dysfunction
59
Other clinical signs of PAS
- 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
CBC/Chem/UA of uncomplicated foals with PAS
- Normal often | - CAN have metabolic/blood gas derangements
61
CSF in foals with PAS
- Normal or xanthochromic
62
Post-mortem findings in foals with PAS
- CNS necrosis - CNS edema - CNS hemorrhage - NOT always evident
63
Overarching therapy goals treatment for PAS
- Adequate cardiac output/perfusion - Prevent further hypoxic-ischemic episodes - Prevent inflammatory mediators
64
How do you measure adequate cardiac output/perfusion in a foal being treated for PAS?
- Consistent urine output - Perfusion to limbs (warm) - Perfusion to brain (mental status) - Perfusion to bowel (GI function)
65
What can develop if severity of PAS worsens?
- Multiple organ dysfunction | - may need inotrope and pressor therapy
66
How to prevent further hypoxic-ischemic episodes in foals with PAS?
- Put the mon oxygen
67
What does preventing inflammatory mediators do for PAS?
- Support organ system function - Allow recovery - Prevent secondary sepsis - Prevent other complications (bed sores, corneal ulcers, aspiration, self-injury)
68
What should you monitor daily with PAS?
- Body weight
69
Fluid goals with treating PAS
- 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
Specific treatments in foals with PAS
- IVF - Enteral nutrition or parenteral nutrition (enteral preferred) - Control seizures - Maintain cerebral perfusion - CNS protectants
71
Enteral nutrition for foals with PAS
- If tolerable - beneficial to enterocytes - fresh colostrum and mare's milk best - Parenteral nutrition if unable to eat
72
How to maintain cerebral perfusion?
- Careful fluid management | - Maintain blood pressure (inotropes/prssors)
73
CNS protectants
- DMSO, mannitol, thiamine**, MgSO4 - Steroids?? - NSAIDs - Pentoxyfylline
74
Cocktail treatment for initial bag of fluids with foals with PAS
- 1 L lactated Ringers - MgSO4 - Ascorbic acid - Thiamine - DMSO
75
Anti-oxidants to give to foals with PAS
- Vitamin E | - Allopurinol (anti-oxidant)
76
Prognosis of Category 1 PAS foals
- 75-80% survival - Typically milder abnormalities and clinical signs - Generally improve within 48-72 hours
77
Prognosis of Category 2 PAS foals
- 50-75% survival - Typically more severe abnormalities/clinical signs - Foals that don't survive generally deteriorate within 48 hours
78
Negative prognostic indicators for PAS foals
- MOD | - Seizures
79
Madigan squeeze
- Maybe reducing pregnane levels? - Foals return to normal within a few days - More studies needed
80
Bacterial meningitis: stats in septic foals
- up to 10% of septic foals
81
Pathophysiology of bacterial meningitis in foals (3 big contributing factors)
- Immature immune system - lack adequate IgG and complement in CSF - More permeable BBB in neonate; even worse with bacterial induced inflammation
82
CNS signs with bacterial meningitis
- Cerebral signs > cervical pain > spinal signs | - Rapidly progressive to seizure
83
Treatment for bacterial meningitis
- Bactericidal antimicrobials
84
Prognosis for bacterial meningitis
- Guarded to poor prognosis
85
Causes of cerebral trauma
- +/- frontal or parietal bone fractures
86
Cerebral trauma clinical signs
- Blind, depressed, wander to side of cerebral lesion
87
Midbrain trauma causes
- Compression from hemorrhage/cerebral edema
88
Midbrain trauma clinical signs
- CNN deficits (??)
89
Poll trauma causes
- Can result in hemorrhage around brain stem | - DO NOT PULL ON A FOAL IN A HARNESS
90
Poll trauma signs
- CNN deficits (??)
91
What are the signs of neurologic trauma from?
- Immediate injury and secondary tissue reaction to injury
92
Imaging neurologic trauma
- Rads - CT - MRI
93
Supportive treatment for neurologic trauma (for brain vs spinal lesions)
- brain: steroids, hypertonic saline | - Spinal: steroids
94
Neurologic trauma with a closed head prognosis?
- Fair to good prognosis
95
Prognosis of neurologic trauma with an open fracture
- Guarded
96
Metabolic neurologic disorders (4)
1. Hyponatremia 2. Hypernatremia 3. Hypocalcemia/Hypomagnesemia 4. Hypoglycemia/metabolic acidosis
97
Hyponatremia injury to brain
- cerebral edema
98
Hyponatremia value
- <120 mEq/dL
99
Hypernatremia injury to brain
- Dehydration
100
Hypernatremia value
>160 mEq/dL
101
Hypocalcemia/hypomagnesemia clinical signs in foals
- Tetanic rigidity
102
Hypoglycemic/metabolic acidosis signs in foals
- Seizures
103
Idiopathic epilepsy signs
- intermittent psychomotor seizures - Normal interictal periods - Some may have temporary blindness
104
Which breed is predisposed to idiopathic epilepsy?
- Arabian foals
105
Potential pathology with idiopathic epilepsy
- laminar cerebrocortical necrosis secondary to repeated seizures
106
Prognosis for idiopathic epilepsy
- usually resolves with age (6-12 months) - Some require anticonvulsants - Majority become safe useful life
107
Breed predisposition for narcolepsy/cataplexy
- Minies and Ponies
108
Signs of narcolepsy/cataplexy
- Fainting (may be exaggerated version of normal response to restraint) - Collapse, suddenly hypotonic, hyporeflexic state, REM - May last several minutes
109
Pathogenesis of narcolepsy/cataplexy
- Human work may lead to decreased arousal peptide
110
Diagnosis of narcolepsy/cataplexy
- Physostygmine test
111
Treatment for narcolepsy/cataplexy
- None - Imipramine - Atropine
112
Cerebellar abiotrophy breed
- Arabians and Oldenburgs
113
Cerebellar abiotrophy pattern of inheritance
- Recessive genetic defect
114
Pathologic lesion in cerebellar abiotrophy
- Cerebellum degenerates AFTER full development
115
Signs in CA
- No menace, symmetrical without weakness
116
Diagnosis of CA
- MRI shows small cerebellum
117
Treatment for CA
- Most euthanized - Not treatment - Unsafe
118
Occipitoatlantoaxial malformation breed predisposition
- Inherited in Arabians, spontaneous in all others
119
Occipitoatlantoaxial malformation primary lesion
- Occipital, atlas, and axis | - Instability and stenosis of vertebral canal
120
Sign in Occipitoatlantoaxial malformation
- Tetraparesis and ataxia in all four limbs | - may hear clicking with head/neck movement
121
Diagnosis of Occipitoatlantoaxial malformation
- Radiographs | - Hypoplastic dens, fusion of occipito/atlas
122
Treatment for Occipitoatlantoaxial malformation
- Most euthanized
123
Botulism AKA "Shaker foal" etiology
- botulinum toxin - Exotoxin of C. botulinum B or C - Prevents release of acetylcholine at NMJ
124
How do foals typically get botulism?
- 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
Where is botulism typically found?
- Endemic in eastern US but sporadic elsewhere
126
Clinical signs of botulism in foals
- 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
Diagnosis of botulism
- presumptive from toxin in feces or blood | - Can do PCR of GI contents too
128
Treatment for botulism
- Polyvalent antitoxin for B and C | - Mechanical ventilation
129
Mechanical ventilation with foals with botulism
- 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
Prognosis for botulism without treatment
- 90% die within 72 hours without treatment
131
Prognosis for botulism if treated with antitoxin within several hours of onset
- 80% survive
132
Prevention of botulism
- Vaccination - Commercial toxoid available for pregnant mares (type B) - Significantly reduce the endemic incidence

Equine Medicine Final (10 decks)

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