Neurologic disorders in foals Flashcards
What is the best way to observe foals for neurologic behavior?
- From a distance is best
- responses can seem random, variable, and unpredictable
How is a lot of time spent for a foal?
- Sleeping in lateral recumbency
- Should be easily aroused
What should a normal foal be doing even early on with the mare and udder?
- Should be seeking the udder and the mare
Head movements of a foal
- Jerky and exaggerated
Restraint of a foal
- Alternating struggling and flopping
What is the menace response like in the foal?
- CN II and VII
- Not complete
When does the menace response complete in the foal?
2 weeks
Which CN control eye position?
III, IV, VI
What is the normal pupil axis in a foal?
- Ventromedial
- Dorsomedial if some neurologic dysfunction
CN V/VII in a foal
- Sensory and motor (respectively) to the face
- Hyperresponsive to tactile stimulation
- Jerky head movements indicate cerebral perception
CN VIII in a foal
- Postional nystagmus is normal
What nerves are part of the swallow reflex?
- CN IX, X, XI
What nerve is involved in lip movement?
CN VII
What nerve is involved in jaw movement in foals?
- CN V
What nerve is involved in tongue movement in foals?
- XII
What if a foal has its tongue stuck out?
- Try to pull on it and put it back in
Which CN are involved in nursing?
- CN IX, X, XI (suckle reflex)
- CN V
- CN VII
- CN XII
“Normal” gait abnormalities in a foal
- Dysmetria
- Base-wide stance
- Hypermetric reflexes
- Crossed extensor reflex takes 3 weeks
- Increased resting extensor tone
Dysmetria
- Short stride with exaggerated step
- Normal in foals
- Adult gait achieved with exercise
How long does the crossed extensor reflex take to develop?
3 weeks
How long should the suckle reflex/jaw tone take to develop in the foal?
- Within minutes of birth and strong within an hour
Long spinal reflexes in foals
- Cervicofacial cutaneous trunci
- Slap test is inconsistent in foals
Other reflexes that should be present in foals
- Withers and pelvic strength
- Anal tone and tail tone
What are some differentials for seizures in foals?
- REM sleep
- Narcolepsy/cataplexy
- “Fainting foal” syndrome
REM sleep in foals
- > in preemies
- Paddling and chomping
- can be easily aroused
Narcolepsy/cataplexy
- May be stimuli elicited
“Fainting foal syndrome”
- Mini’s - flaccid limbs, eyes open
Seizures threshold of foals
- Inherently low
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
Etiologies for seizures
- Perinatal complications
- Metabolic
- idiopathic epilepsy
- Infection
- Iatrogenic/drug associated
- Developmental
- Heat stroke
Perinatal complications in foals with seizures
- Perinatal asphyxia, intracranial hemorrhage, cerebral contusions
metabolic derangements in foals with seizures
- Decreased Na+, Mg+, Ca2+, or glucose
- Increased Na+
- metabolic acidosis
Idiopathic epilepsy in foals
- most often in Egyptian Arabs
Infectious etiologies in foals with seizures
- Sepsis without meningitis
- Septic meningitis
- Bacterial or viral encephalitis
- Tyzzer’s - Clostridium piliformis
Iatrogenic or drug associated etiologies in foals with seizures
- Theophylline, toxins, intracarotid injection
Developmental diseases leading to seizures in foals
- Hydrocephalus, storage disease
Diagnostic options for foals with seizures
- Imaging: CT, MRI, Xray
- CSF Tap
CSF tap in foals cons
- Not benign procedures
- 5-10 mL considered safe
- If you take too much, you can kill a foal
CSF tap test in foals
- Fluid analysis and cytology
- UA strips have been used - beware blood contamination (???)
Neonatal vs adult CSF normal
- Trace glucose in neonates
- 1st 40 hours protein will be higher than in adults
Perinatal asphyxia syndrome other names
- Neonatal multisystem maladaptation syndrome
- Hypoxic ischemic encephalopathy
- Neonatal maladjustment syndrome
- “Dummy” foals
- Wanderers/barkers
What types of disturbances can occur in perinatal asphyxia syndrome in foals?
- Renal, GI, cardiopulmonary, endocrine, behavioral, and neurologic disturbances
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
Perinatal Asphyxia Syndrome Pathogenesis
See the image in the notes
4 Prenatal causes of periparturient hypoxia
- Reduced maternal oxygen delivery
- Reduced maternal blood flow
- Placental disease
- Reduced umbilical flow
Reduced maternal oxygen delivery
- anemia, lung disease, cardiovascular disease in dam
Reduced maternal blood flow
- Maternal hypotension/hypertension, endotoxemia, colic
Placental disease
- PPS, placental insufficiency, twins, placental dysfunction, placentitis
Reduced umbilical flow
- General anesthesia, congenital CV disease
Placentitis on ultrasound
- Very thick placenta
Intrapartum issues
- Dystocia
- Premature placental separation
- Uterine inertia
- Oxytocin induced labor
- C-section
- Anything prolonging stage II labor
Premature placental separation appearance
- “Red bag”
- If you saw this, pull the foal immediately
Neonatal causes of hypoxia
- Prematurity/dysmaturity
- Any cause of recumbency
- Thoracic disease
- Recurrent episodes of apnea
- Septic shock
- neonatal anemia
- Congenital cardiovascular disease
What determines the severity of the hypoxic injury?
- Duration
- Repeated insult?
- When it occured
What are the most common signs in perinatal asphyxia syndrome?
- CNS is most vulnerable to altered metabolism
What regions are most susceptible to hypoxia?
- CNS>kidney>GI>heart>lungs>liver
What are the two categories of PAS?
- born normal, develop within 48 hours
2. Born abnormal
What is the most prominent clinical sign of PAS?
- Cerebral dysfunction
- Category 2 can show signs of brainstem and spinal cord dysfunction
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
CBC/Chem/UA of uncomplicated foals with PAS
- Normal often
- CAN have metabolic/blood gas derangements
CSF in foals with PAS
- Normal or xanthochromic
Post-mortem findings in foals with PAS
- CNS necrosis
- CNS edema
- CNS hemorrhage
- NOT always evident
Overarching therapy goals treatment for PAS
- Adequate cardiac output/perfusion
- Prevent further hypoxic-ischemic episodes
- Prevent inflammatory mediators
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)
What can develop if severity of PAS worsens?
- Multiple organ dysfunction
- may need inotrope and pressor therapy
How to prevent further hypoxic-ischemic episodes in foals with PAS?
- Put the mon oxygen
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)
What should you monitor daily with PAS?
- Body weight
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
Specific treatments in foals with PAS
- IVF
- Enteral nutrition or parenteral nutrition (enteral preferred)
- Control seizures
- Maintain cerebral perfusion
- CNS protectants
Enteral nutrition for foals with PAS
- If tolerable
- beneficial to enterocytes
- fresh colostrum and mare’s milk best
- Parenteral nutrition if unable to eat
How to maintain cerebral perfusion?
- Careful fluid management
- Maintain blood pressure (inotropes/prssors)
CNS protectants
- DMSO, mannitol, thiamine**, MgSO4
- Steroids??
- NSAIDs
- Pentoxyfylline
Cocktail treatment for initial bag of fluids with foals with PAS
- 1 L lactated Ringers
- MgSO4
- Ascorbic acid
- Thiamine
- DMSO
Anti-oxidants to give to foals with PAS
- Vitamin E
- Allopurinol (anti-oxidant)
Prognosis of Category 1 PAS foals
- 75-80% survival
- Typically milder abnormalities and clinical signs
- Generally improve within 48-72 hours
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
Negative prognostic indicators for PAS foals
- MOD
- Seizures
Madigan squeeze
- Maybe reducing pregnane levels?
- Foals return to normal within a few days
- More studies needed
Bacterial meningitis: stats in septic foals
- up to 10% of septic foals
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
CNS signs with bacterial meningitis
- Cerebral signs > cervical pain > spinal signs
- Rapidly progressive to seizure
Treatment for bacterial meningitis
- Bactericidal antimicrobials
Prognosis for bacterial meningitis
- Guarded to poor prognosis
Causes of cerebral trauma
- +/- frontal or parietal bone fractures
Cerebral trauma clinical signs
- Blind, depressed, wander to side of cerebral lesion
Midbrain trauma causes
- Compression from hemorrhage/cerebral edema
Midbrain trauma clinical signs
- CNN deficits (??)
Poll trauma causes
- Can result in hemorrhage around brain stem
- DO NOT PULL ON A FOAL IN A HARNESS
Poll trauma signs
- CNN deficits (??)
What are the signs of neurologic trauma from?
- Immediate injury and secondary tissue reaction to injury
Imaging neurologic trauma
- Rads
- CT
- MRI
Supportive treatment for neurologic trauma (for brain vs spinal lesions)
- brain: steroids, hypertonic saline
- Spinal: steroids
Neurologic trauma with a closed head prognosis?
- Fair to good prognosis
Prognosis of neurologic trauma with an open fracture
- Guarded
Metabolic neurologic disorders (4)
- Hyponatremia
- Hypernatremia
- Hypocalcemia/Hypomagnesemia
- Hypoglycemia/metabolic acidosis
Hyponatremia injury to brain
- cerebral edema
Hyponatremia value
- <120 mEq/dL
Hypernatremia injury to brain
- Dehydration
Hypernatremia value
> 160 mEq/dL
Hypocalcemia/hypomagnesemia clinical signs in foals
- Tetanic rigidity
Hypoglycemic/metabolic acidosis signs in foals
- Seizures
Idiopathic epilepsy signs
- intermittent psychomotor seizures
- Normal interictal periods
- Some may have temporary blindness
Which breed is predisposed to idiopathic epilepsy?
- Arabian foals
Potential pathology with idiopathic epilepsy
- laminar cerebrocortical necrosis secondary to repeated seizures
Prognosis for idiopathic epilepsy
- usually resolves with age (6-12 months)
- Some require anticonvulsants
- Majority become safe useful life
Breed predisposition for narcolepsy/cataplexy
- Minies and Ponies
Signs of narcolepsy/cataplexy
- Fainting (may be exaggerated version of normal response to restraint)
- Collapse, suddenly hypotonic, hyporeflexic state, REM
- May last several minutes
Pathogenesis of narcolepsy/cataplexy
- Human work may lead to decreased arousal peptide
Diagnosis of narcolepsy/cataplexy
- Physostygmine test
Treatment for narcolepsy/cataplexy
- None
- Imipramine
- Atropine
Cerebellar abiotrophy breed
- Arabians and Oldenburgs
Cerebellar abiotrophy pattern of inheritance
- Recessive genetic defect
Pathologic lesion in cerebellar abiotrophy
- Cerebellum degenerates AFTER full development
Signs in CA
- No menace, symmetrical without weakness
Diagnosis of CA
- MRI shows small cerebellum
Treatment for CA
- Most euthanized
- Not treatment
- Unsafe
Occipitoatlantoaxial malformation breed predisposition
- Inherited in Arabians, spontaneous in all others
Occipitoatlantoaxial malformation primary lesion
- Occipital, atlas, and axis
- Instability and stenosis of vertebral canal
Sign in Occipitoatlantoaxial malformation
- Tetraparesis and ataxia in all four limbs
- may hear clicking with head/neck movement
Diagnosis of Occipitoatlantoaxial malformation
- Radiographs
- Hypoplastic dens, fusion of occipito/atlas
Treatment for Occipitoatlantoaxial malformation
- Most euthanized
Botulism AKA “Shaker foal” etiology
- botulinum toxin
- Exotoxin of C. botulinum B or C
- Prevents release of acetylcholine at NMJ
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)
Where is botulism typically found?
- Endemic in eastern US but sporadic elsewhere
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)
Diagnosis of botulism
- presumptive from toxin in feces or blood
- Can do PCR of GI contents too
Treatment for botulism
- Polyvalent antitoxin for B and C
- Mechanical ventilation
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
Prognosis for botulism without treatment
- 90% die within 72 hours without treatment
Prognosis for botulism if treated with antitoxin within several hours of onset
- 80% survive
Prevention of botulism
- Vaccination
- Commercial toxoid available for pregnant mares (type B)
- Significantly reduce the endemic incidence
