2022.Vol38.Iss2.EquineNeurology Flashcards
Clostridial Diseases (botulism & tetanus)
C. tetani spores are characteristcally described as
“drumstick-shaped”
Clostridial Diseases (botulism & tetanus)
C. tetani induces disease through which 2 primary toxins
tetanolysin
tetanospasmin
Clostridial Diseases (botulism & tetanus)
Describe the pathogenesis of tetanospasmin
–binds to ganglia & neuromuscular junctions (somatic ns)
-internalized by endocytosis
–carried along axon retrograde
–acts on vesicle-assoc membrane protein in Renshaw cells (inhibitory neurons) to irreversibly impede the release of inhibitory neurotransmitters: glycine and GABA
SPASTIC MM CONTRACTIONS, mm rigidity
Clostridial Diseases (botulism & tetanus)
What are some classic C/S of tetanus
-stilted gait
-facial mm contraction– resulting in sardonic grin
-prolapase of the 3rd eyelid
Clostridial Diseases (botulism & tetanus)
death with tetanus usually occurs because
of respiratory paralysis
Clostridial Diseases (botulism & tetanus)
tetanus antemortem diagnosis
-presumptive: hx, PE findings/C/S
-R/O: rabies, strychnine intoxication, exertional rhabdomyolysis, myositis
Clostridial Diseases (botulism & tetanus)
what is the first line of treatment with tetanus?
penicillin
-metronidazole can be considered an alternative
**consider broad spectrum antibiotics with aspiration pneumonia
-Tetanus antitoxin & tetanus toxoid
Clostridial Diseases (botulism & tetanus)
Why is it important to treat tetanus cases with tetanus antitoxin?
-allows binding & inactivation of any tetanus toxin that is circulating n the vascular system
Clostridial Diseases (botulism & tetanus)
Tetanus treatment is aimed at circulating toxin, what does toxin not get?
once tetanus toxin is absorbed into a neural body, it cannot be inactivated by TAT
**anticipate clinical disease assoc with tetanus to worsen for 1-2 days before signs begin to improve
Clostridial Diseases (botulism & tetanus)
What disease has tetanus antitoxin been linked with?
theiler disease (fatal hepatitis)
– develops 45-90 days after admin
Clostridial Diseases (botulism & tetanus)
What are consequences of tetanus sustained muscle contraction & spasm?
pain, stress, respiratory paralysis
**recommend treatment with acepromazine and methocarbamol
Clostridial Diseases (botulism & tetanus)
horses that recover from the tetanus, what sequelae are reported
ataxia
unspecified lameness
Clostridial Diseases (botulism & tetanus)
C. botulinum produces what 3 neurotoxins
Type:
A: west of rocky mountains
B: mid-atlantic US & kentucky
C: europe
Clostridial Diseases (botulism & tetanus)
What are the 3 different routes that an equid can acquire botulism?
- animals ingests feed, soil or carrion with clostridial preformed toxin
- wound botulism
- toxicoinfectious botulism– inhabit GI tract; shaker foal syndrome
Clostridial Diseases (botulism & tetanus)
Describe the pathogenesis of botulism
-enter presynaptic nerve (only affect peripheral nerves– cannot cross BBB)
-internalized via endosome
-targets neuronal soluble SNAP receptor SNARE proteins (that function in neurotransmitter exocytosis
-protein cleavage prevents release of acetylcholine & results in neuroparalysis
Clostridial Diseases (botulism & tetanus)
Clinical signs associated with botulism is dependent on which factors?
dose dependent– will presist until new synapses are formed
**type of toxin may play a role in the duration of neuroparalysis
Clostridial Diseases (botulism & tetanus)
what C/S are seen with botulism?
weakness, dysphagia, poor mm tone
acute death
INC time laying down, inability to rise
colic
mm fasciculations
low head carriage
shuffling gait
Weak, but no CP deficits
Clostridial Diseases (botulism & tetanus)
Which mm groups are affected first in botulism cases because of high requirements for acetylcholine?
tongue, eyelids, tail & sphincter
Clostridial Diseases (botulism & tetanus)
how do foals commonly present with botulism?
-muscle fasciculations (shaker foal syndrome)
-cycle through standing & recumbency
-dehyration
-decreased respiratory rate
Clostridial Diseases (botulism & tetanus)
what differentials should be considered in horses presenting like botulism?
white muscle disease
HYPP
Hypocalcemia
white snakeroot tox
ionophore tox
lead toxicity
organophosphate tox
Clostridial Diseases (botulism & tetanus)
What is the most important & time sensitive treatment for horses with botulism?
Neuralization of circulating toxin with BoNT antitoxin
foal: 30,000 IU
Adult: 70,000 IU
**provides protection for 60 days
Clostridial Diseases (botulism & tetanus)
What medications can potentiate neuromuscular weakness and should be avoided in cases of botulism?
aminoglycosides
procaine penicillin
tetracyclines
Clostridial Diseases (botulism & tetanus)
How long does it take for horses to recover from botulism?
-7-14 days, dependent on construction of new endplates
- full muscle recovery in 1 month
Clostridial Diseases (botulism & tetanus)
What is the described survival rate of horses with botulism?
67% survival rate
95% in horses that remained standing
Clostridial Diseases (botulism & tetanus)
What is key to remember about the botulism toxin vaccine?
its a type B toxoid vaccine yearly booster
-initial series: 3-doses, each 1 month apart in unvaccinated adults
-broodmares- booster 4-6 weeks prior to parturition
-foals unvx mares: 3 dose series, start 1-3 m old
***cross protection against other types is not guarenteed
Equine Neuroaxonal dystrophy & degenerative myeloencephalopathy
what is the definitive diagnosis of eNAD/EDM require?
histo evaluation of the spinal cord & brainstem at necropsy
Equine Neuroaxonal dystrophy & degenerative myeloencephalopathy
What is the typical presentation of eNAD/EDM?
young < 2 year old horse with symmetric proprioceptive ataxia, but some horses, particularly Warmbloods are affected later in life & show behavior changes in addition to progressive ataxia
Equine Neuroaxonal dystrophy & degenerative myeloencephalopathy
What neurologic deficits are seen with eNAD/EDM?
abnormal limb positioning
pelvic limb ataxia
thoracic limb hypermetria
decreased strength & spasticity of limbs- UMN and general CP lesions
Equine Neuroaxonal dystrophy & degenerative myeloencephalopathy
describe the phosphorylated nuerofilament heavy, biomarker test for eNAD/EDM
high specificity
low sensitivity
for dx of ENA/EDM in young non-wramblood breeds
Equine Neuroaxonal dystrophy & degenerative myeloencephalopathy
eNAD is clinically indistinguishable from EDM, however is distinguished on histopathology by which features?
eNAD: lesions confined to brainstem, LACN, medial cuneate & gracillis nuclei
EDM: axonal necrosis & demyelination extended to the dorsal & ventral spincereballar tracts & ventromedial fuiculi of the cervicothoracic spinal cord
Equine Neuroaxonal dystrophy & degenerative myeloencephalopathy
When do C/S of eNAD/EDM appear?
6-12 months of age
**can develop from a few weeks to a up to 3 years of age
Equine Neuroaxonal dystrophy & degenerative myeloencephalopathy
in comparison between quarterhorses & warmbloods that develop eNAD/EDM, what is a dufference?
pigment retinopathy– in young warmbloods
**recommend a the full fundic examination in warm bloods
Equine Neuroaxonal dystrophy & degenerative myeloencephalopathy
what does muscle biopsy look like with eNAD/EDM?
No abnormalities
Specific Diagnostic Techniques in Equine Neurology (Raidography, Ultrasonography, CT & MRI)
Describe how the intravertebal sagittal ratio is calculated
Normal intravertebral ratios:
C3-C6: 0.52
C6-C7: 0.56
Specific Diagnostic Techniques in Equine Neurology (Radiography, Ultrasonography, CT & MRI)
For myelography, what are the two most commonly used criteria to recognize extradural spinal cord compression?
-50% reduction in height of contrast column
-20% reduction in total dural diameter of the contrast column compared
Specific Diagnostic Techniques in Equine Neurology (Raidography, Ultrasonography, CT & MRI)
Diagnosis of intra-cranial abnormalities is best accomplished with what modality?
magnetic resonance imaging (MRI)
Arboviral equine encephalitides
Most people and horses infected by togaviral encephalitidies develop what C/S
mild and nonspecific
Arboviral equine encephalitides
What percentage of people develop systemic signs of neurologic disease, infected with togaviral encephalitidies?
less than 10%
Arboviral equine encephalitides
Eastern equine encephalitis (EEE) is seen is transmitted by what vector?
mosquitoes
Arboviral equine encephalitides
Of the togaviruses, which is the deadliest to humans and horses?
EEE, mortality rates:
humans: 50%
horses: 90%
Arboviral equine encephalitides
In North America, EEE persists in an enzootic (sylvatic) cycle between what?
passerine birds and ornithophilic mosquitoes
Arboviral equine encephalitides
What is the main vector of WEE virus?
culex tarsalis
Arboviral equine encephalitides
which immune cells are important for clearing alpha viruses?
B and T cells
Arboviral equine encephalitides
What C/S are seen with alphaviral infections?
nonspecific: fever, anorexia, lethargy
Cerebral: obtundation (sleeping sickness), incoordination, hyperexcitability, head pressing, staggering, aimless awndering, convulsions, death
Brain stem: dysphagis, impaired vision, circling
Arboviral equine encephalitides
As far as alphavirus development in humans, who are teh most susceptible to developing disease?
older humans
young children
infants
Arboviral equine encephalitides
What are differentials to consider for WEE/EEE?
WNV encephalitis
rabies
EPM
EHV-1
toxicities: leukoencephalomalacia
metabolic: hepatic encephalopathy
aberrant parasite migration
others: tumors, abscess
Arboviral equine encephalitides
Why are CVSM and EDM/eNAD an unlikely differential for WEE/EEE?
-b/c clinical findings & disease progression
Arboviral equine encephalitides
What is a consistent CSF finding with EEE?
neutrophilic pleocytosis
WEE: usu mononuclear pleocytosis, inc protein
What is the diagnostic of choice for antemortem diagnosis of EEE/WEE?
IgM capture ELISA
> 1:400
Smith: p1018
Arboviral equine encephalitides
Rarely, WNV affects horses of less than 1 year of age, what age is more likely to die?
> 3 year old
Arboviral equine encephalitides
who are dead end hosts of WNV?
horses & humans
Arboviral equine encephalitides
What are vectors of WNV?
mosquitoes–many spp
Arboviral equine encephalitides
How does WNV enter the CNS?
through dsiruption of BBB, transported by mononuclear cells that migrate into the CNS and retrograde axonal trasnport
**hematogenous spread also important
Arboviral equine encephalitides
What C/S are seen in horses with WNV?
Cerebral: somnolence, usu good mentation, but can be hyperexcitabil
brain stem: blindness, facial paralysis, dysphagia
Msk/spinal cord signs– precede neuro signs; ataxia (symm/assymm) lameness, tremors, muscle fasciculations of head & neck, tremors
recumbency & inability to rise
Arboviral equine encephalitides
In comparison to other viral diseases, what clinical signs are consistent findings in horses with WNV?
muscle fasciculations
tremors
behavioral changes
**spinal cord signs are more evidence
Arboviral equine encephalitides
WNV is seasonal in temperate climates and is seen typically when?
following vector emergence in the spring
Equine Protozoal Myeloencephalitis
What are the causative organisms of EPM?
S. neurona
N hughesi (less frequently)
Equine Protozoal Myeloencephalitis
How do horses become infected with S. neurona?
AFter ingesting food or water contaminated with feces from an ifnected opposum
Equine Protozoal Myeloencephalitis
What is the mode of transmission for N. hughesi?
Uncertain
**foals can be infected by transplacental passage of the parasite
Equine Protozoal Myeloencephalitis
what is the definitive host of S. neurona in N. America?
opossum: diselphis virginiana
Equine Protozoal Myeloencephalitis
what combination of C/S help distinguish EPM from other diseases?
asymmetry of gait & focal muscle atrophy
Equine Protozoal Myeloencephalitis
What treatments are approved for EPM?
sulfadiazine & pyrimethamine: blocks protozoal folate synthesis
diclazuril & ponazuril: coccidiostats
Cervical Vertebral Stenotic Myelopathy
What are the two types of CVSM in horses?
T.1: young horses, multifactorial: gender, inheritance, diet, trauma & rate of growth
T.II: older horses, affects all breeds, OA of articular processes, DJD of articular processes
Cervical Vertebral Stenotic Myelopathy
What neurologic exam findings help distinguish CVSM from other neurologic diseases?
-spinal ataxia- assymm/symm- pelvic limbs» forelimbs
-loss of CP deficits
**usu more visible at the walk
Cervical Vertebral Stenotic Myelopathy
What are differentials for spinal ataxia/CVSM?
young horse: EPM, trauma, EDM, EHV-1
less common: rabies, viral encephalitidies, congenital malformations
less common: rabies, viral encephalitidies, brain abscesses, neoplasia, hepatoencephalopathy
Cervical Vertebral Stenotic Myelopathy
What is the gold standard diagnostic for CVSM?
postmortem examination
Cervical Vertebral Stenotic Myelopathy
What are the 5 characteristic bony malformations of the cervical vertebrae in horses with CVSM?
- flare of the caudal vertebral epiphysis of the vertebral body
- abnormal ossification of the articular processes
- malalignment between adjacent vertebrae
- extension of the dorsal laminae
- degenerative joint disease of the articular processes
Cervical Vertebral Stenotic Myelopathy
Where are the most common sites for static stenosis?
C5-C6 and C6-C7
Cervical Vertebral Stenotic Myelopathy
What are the most common sites for dynamic compression?
C3-C4 and C4-C5
Cervical Vertebral Stenotic Myelopathy
what are the 3 most important nutritional factors that seem to be associated with incidence of developmental orthopedic disease?
- excessive digestible energy
- excessive phosphorus
- Copper deficiency
Equine herpesvirus-1 myeloencephalopathy
What are typical features of EHM in outbreaks?
-suddent onset of neuro deficits: ataxia, paresis & urinary incontinence
-involvement of multiple horses on the premises
-recent history of fever, abortion or viral respiratory disease in affected horse or herd mates
Equine herpesvirus-1 myeloencephalopathy
How id antemortem diagnosis of EHM supported?
-r/o other neurologic conditions
-demonstrate xanthochromia & INC TP in CSF
-ID or siolate EHV-1 from resp tract, buff-coat or CSF
Equine herpesvirus-1 myeloencephalopathy
The treatment of EHM is challenging and directed towards:
-supportive nursing and nutritional care
-DEC CNS inflammation
-minimizing thromboembolic events
-controlling the lymphocyte-assoc. viremia
Equine herpesvirus-1 myeloencephalopathy
Which EHV-1 genotype is more commonly associated with EHM?
D752
Equine herpesvirus-1 myeloencephalopathy
What is the most common EHV-1 genotype within the equine population?
N752
Equine herpesvirus-1 myeloencephalopathy
What are the risk factors associated with EHV-1 and respiratory disease?
Equine herpesvirus-1 myeloencephalopathy
What risk factors are associated with EHV-1 and abortion?
Equine herpesvirus-1 myeloencephalopathy
What risk factors are for EHM?
Equine herpesvirus-1 myeloencephalopathy
EHV-1 infects which immune cells, that are important to establishing EHV-1 latency?
lymphocytes
Equine herpesvirus-1 myeloencephalopathy
What are secondary disease manifestations for EHV-1?
EHM
EHV-1 abortions
neonatal foal death
chorioretinopathies
Equine herpesvirus-1 myeloencephalopathy
What medication has been shown to help decrease viremia and prevent the development of neurologic sequelae?
valacyclovir
Vestibular Disease
What C/S indicate vestibular disease?
head tilt
pathologic nystagmus
ventrolateral strabismus
body leaning
moving in tight circles
ataxia
Vestibular Disease
Why is there increased ipsilateral extensor tone & decreased contralateral extensor tone seen with vestibular disease?
interneurons are facilitatory to the ipsilateral alpha-motor & gamma motor neurons of the extensors of the limb & inhibtory to the ispilateral flexors of the limbs
Vestibular Disease
What two important reflexes are responsible for maintaining balance of the eyes, head, neck, trunk and limbs during rest and movement?
- vestibulo-ocular (physiologic nystagmus) reflex
- vestibulospinal (extensor tone) reflex
Vestibular Disease
Eye movements are coordinated by the extraocular muscles of the eye, through what cranial nerves?
oculomotor (main)
trochlear
abducens motor
Vestibular Disease
Describe how lesions of vestibular system cause strabismus.
-oculomotor nuclei provides input to the most of the extraocular mm
-lesions to oculomotor nuclei or nerve or vestibular system, result in
IPSILATERAL VENTROLATERAL STRABISMUS
Vestibular Disease
How does nystagmus help distinguish vestibular lesions?
slow phase– indicates the side of lesion
fast phase– the side away from the lesion
Vestibular Disease
What is positional nystagmus?
if nystagmus only occurs when the head is placed in an unusual position (eg, lateral, facing up)
Vestibular Disease
list causes of vestibular disease
peripheral disease: trauma, otitis media/interna, temporohyoid osteoarthropathy (THO) & idiopathic vestibular dz
brain stem disease: trauma, bacterial meningoenceaphlitis, neoplasia, EPM
Less commonly: caudal cereballer dz: mass occupying lesions, vascular accidents
Vestibular Disease
How to differentiate from central vs peripheral vestibular disease?
Peripheral: nystagmus is horizontal or rotary, does not change direction & is non-positional
Central: nystagmus is horizontal, rotary, vertical, spontaneous change of direction & is positional
Vestibular Disease
How do you determine the side of the lesion based on clinical signs?
-decreased ipsilateral input to extensor tone & lack of inhibitor of flexors–> tilt, lean, flex and move toward the side of the lesion
Vestibular Disease
The cerebellum contributes to fine motor movement, how can it contribute to vestibular lesions
cerebellum affected, the ipsilateral inhibitor input to the extensors will be absent or decreased resulting in tilting and leaning contralateral to the side of the lesion
**also in paradoxic vestibular disease
Vestibular Disease
What will worsen vestibular signs?
darkness/ covering eyes
Vestibular Disease
What C/S are seen with bilateral vestibular disease?
-wide-based stance
-no head tilt
-no leaning or drifting
-no circling
-lacks both physiologic & pathologic nystagmus
Vestibular Disease
In THO, what cranial nerves are affected?
facial
vestibular
cochlear
Vestibular Disease
List causes of peripheral vestibular disease.
Vestibular Disease
List causes of central vestibular disease
Nonarboviral Equine Encephalitides
what are the 3 forms that rabies can present as?
- paralytic (spinal cord)
- dumb (brain stem)
- furious (cerebral cortex)
Nonarboviral Equine Encephalitides
what is a common sign of rabies in donkeys?
self mutilation
Nonarboviral Equine Encephalitides
which form is the most common presentation of rabies in horses?
paralytic & dumb form
Nonarboviral Equine Encephalitides
what is the antemortem diagnostic for equine rabies?
No
Nonarboviral Equine Encephalitides
what is pathognomonic on histology for lyssavirus infections?
negri bodies
**their absence does not rule out rabies
Nonarboviral Equine Encephalitides
what is the official and gold standard diagnostic method for rabies?
direct fluorescent antibody (DFA) test using monoclonal antibodies on tissue impressions or histologic sections
Movement Disorders and Cerebellar abiotrophy
describe the movement of patients with shivers
abnormal hindlimb hypertonicity during walking forward
Movement Disorders and Cerebellar abiotrophy
describe the movement of patients with stringhalt
consistent hyperflexion during walking forward & trotting
variable difficulty when walking backward
Movement Disorders and Cerebellar abiotrophy
which breeds is cerebellar abiotrophy reported?
Arabian
Gotland pony
Oldenburg
Movement Disorders and Cerebellar abiotrophy
what C/S are seen in foals with cerebellar abiotrophy?
intentional head tremor
hypermetric forelimb gait
symmetric ataxia
wide-based stance & gait
dysmetria
spasticity
limb may be hyperflexed when walking (slamming foot on ground)
+/- menace reflex absent or diminished
Movement Disorders and Cerebellar abiotrophy
When do foals develop a menace response?
by 2 weeks of age
Movement Disorders and Cerebellar abiotrophy
what is the inheritance of cerebellar abiotrophy in arabians?
autosomal recessive
chromosome 2– 4th exon TOE1 & MUTYH antisense strand
Equine Neurologic Examination
head muscle mass is controlled by what cranial nerve (s)?
CN V
Equine Neurologic Examination
What cranial nerve controls tongue tone?
CN XII
Equine Neurologic Examination
What cranial nerves control eye movement?
CN III, IV, VI, VIII
Equine Neurologic Examination
Which cranial nerve/ parts of the brain controls menace response?
-vision
-CN II
-visual cortex
-CN VII
-cerebelum
Equine Neurologic Examination
Which cranial nerves control pupillary light reflex?
CN II
parasympathetic III
Equine Neurologic Examination
Which cranial nerves control palpebral response?
CN V
CN VII
Equine Neurologic Examination
Which cranial nerves control local cervical reflex and cervicofacial reflex?
cervical dorsal and ventral spinal roots
CN VII
Equine Neurologic Examination
Which cranial nerves/nerves control cutaneous trunci reflex?
dorsal roots
cranial thoracic spinal cord
C8 spinal cord lateral thoracic nerve
Equine Neurologic Examination
Which nerves control anal sensation & reflex, tail tone?
caudal equina
Equine Neurologic Examination
What does assessing gait in straight line, circling, zigzagging, walking down slope with head elevated test?
upper & lower motor neurons
general proprioception
cerebellum
vestibular system
Equine Neurologic Examination
When assessing vision, how are lesions localized
- optic nerve lesions, both vision & PLR abnormal
- cortical lesions, vision affected but PLRS are normal
- efferent arm lesions, PLR is abnormal & vision is unaffected
**one caveat is, PLRS are maintained even with retinal or optic nerve lesions that results in loss of vision
Equine Neurologic Examination
What are signs of horners syndrome?
lesion to the sympathetic input to the eye
1. ptosis
sometimes the only C/S seen
2. miosis
3. enophthalmos assoc. with protrusion of the nictitating membrane
Equine Neurologic Examination
Describe the neuroanatomic location of a lesion from:
C1-C6
C7-T2
T3-L3
L4-S3
sacral segments/cauda equina
Equine Neurologic Examination
When assessing a neurologic patient, while patient is standig still and square, and pulling on the tail, what is this testing?
-extensor (patellar, quadriceps) reflex
-poor response or patient will demonstrate weakness while standing still (hypotonia): LMN lesion at L3-5
-UMN lesion– will not show paresis when the tail is pulled when standing
Equine Neurologic Examination
What do tail pulls assess?
UMN axonal damage d/t cervical spinal lesion will easily be pulled
**muscle weakness
Equine Neurologic Examination
What lesions should you consider in recumbent horses?
-assess CN/cerebral function
-assess cutaneous trunci mm, cervico facial reflex
-if horse can adopt dog sitting position– injury caudal to T2 likely
-abnormal respiratory & unable to raise head– proximal cervical spinal cord lesion or diffuse neuromuscular disease (ie botulism– test tongue tone)
-acute unilateral vestibular disease– will be down on affected side, nystagmus
Equine Neurologic Examination
Which reflexes can be tested in the recumbent horse that usually cannot be assessed in the standing horse or reflexes that should be tested?
-flexing carpal/tarsal joints– decreased tone– neuromuscular disease, increased tone– SC lesion & lack of UMN disease
-patellar reflex: tests femoral nerve & L4-5 SC segments– wooden handle of hammer
-Withdrawal reflex: pinching coronary band with hemostat
-pelvic limb flexion: sciatic nerve, caudal & sacral segments
-thoracic limb flexion: brachial plexus n, cervical intumescence
-forelimb withdrawal: brachail plexus, C6-T2 SC segments
-Tail & anal tone
-muscle tone of eyelids/tongue= decreased suggest neuromuscular dz
Neurologic Disorders of the Foal
What is the most common neurologic abnormality seen in equine neonates?
neonatal encephalopathy
Neurologic Disorders of the Foal
What severe disease is a complication of neonatal isoerythrolysis?
kernicterus
Neurologic Disorders of the Foal
AT whta level does kernicterus develop?
bilirubin concentration >19 mg/dL
Neurologic Disorders of the Foal
Is icteric CSF normal/abnormal in faols?
Normal in foal sup to 10 days of age
**needs to be considered when foals have NI
Neurologic Disorders of the Foal
hypoglycemia can be corrected at what rate? (5-10% solution)
4 to 8 mg/kg/minute
Neurologic Disorders of the Foal
Most foals with uncomplicated maladjustment have what kind of prognosis?
85% of foals survive
Pathologic Conditions of the Nervous System in Horses
Which organism transmitts the spirochete bacterium, Borrelia burgdorferi
Ixodes spp
