Equine Neurology

Question 1

Which of the following choices best describes cytological and biochemical properties of normal cerebral spinal fluid?

A. Clear fluid with a total nucleated cell count of 100 cells/μl, a total protein of 50 mg/dl and 2
red blood cells/μl. Cytological examination reveals a pleocytosis.

B. Clear fluid with a total nucleated cell count of 50 cells/μl , total protein of 70 mg/dl and no red
blood cells. Cytological examination reveals predominantly small mononuclear cells

C. Clear fluid with a total nucleated cell count of 4 cells/ μl, a total protein of 70 mg/dl and no
red blood cells. Cytological examination reveals predominately small mononuclear cells.

D. Clear fluid with a total nucleated cell count of 6 cells/ μl, a total protein of 50 g/dl and no red
blood cells. Cytological examination reveals a pleocytosis.

Answer 1

C. Clear fluid with a total nucleated cell count of 4 cells/ μl, a total protein of 70 mg/dl and no
red blood cells. Cytological examination reveals predominately small mononuclear cells.

Question 2

When examining a 6 week old Arabian colt you notice a hypermetric gate in all four limbs when the foal walks along with fine tremors of the head. Mentation appears appropriate. On cranial nerve exam, both direct and indirect pupillary light responses are present; however a menace response is absent bilaterally. Which of the following is the best differential for this foal’s symptoms?

A. Idiopathic juvenile epilepsy
B. Lavender foal syndrome
C. Cerebellar abiotrophy
D. Hydrocephalus

Answer 2

C. Cerebellar abiotrophy

Question 3

You are presented with a 2‐week‐old Arabian colt for seizure like activity. On initial exam you find the foal in lateral recumbency with rigid extension of the hind limbs as well as head and neck. When stimulated the symptoms worsen. The owner wants you to do everything possible for this colt because it is the only colt she has ever had with such a unique and unusual hair color. The foal was born full term to a dam that was vaccinated 1 month prior to foaling with EWT/WNV, Flu/Rhino and Rabies vaccinations. Which of the following is the best differential diagnosis for this foal’s symptoms?

A. Tetanus
B. Idiopathic juvenile epilepsy
C. Lavender foal syndrome
D. Cerebellar abiotrophy

Answer 3

C. Lavender foal syndrome

Question 4

Which bone is most commonly fractured and responsible for some of the clinical signs associated with flipping over injuries in young horse?

A. Stylohyoid bone
B. Basisphenoid bone
C. Frontal sinus bone
D. Zygomatic arch

Answer 4

B. Basisphenoid bone

Question 5

Which of the following cranial nerve deficits are associated with temporohyoid osteoarthropathy in the horse and which answer best explains why these neuropathies develop in this disease?

A. CN V and CN VII deficits, due to their anatomical association with the petrous temporal bone,
these nerves are affected by ankylosis and inflammation of the temporohyoid joint.
B. CN V and CN VII deficits, due to their anatomical association with the guttural pouch, these
nerves are affected by inflammation secondary to microfractures of the stylohoid bone.
C. CN VII and CN VIII deficits, due their anatomical association with the petrous temporal bone,
these nerves are affected by ankylosis and inflammation of the temporohyoid joint.
D. CN VII ad CN VIII deficits, due to their anatomical association with the guttural pouch, these
nerves are affected by inflammation secondary to microfractures of the basiphenoid bone.

Answer 5

C. CN VII and CN VIII deficits, due their anatomical association with the petrous temporal bone,
these nerves are affected by ankylosis and inflammation of the temporohyoid joint.

Question 6

You examine a 10‐year‐old gelding in Missouri for acute onset of neurologic symptoms. On presentation, the horse is aimlessly walking in circles and bumping into the walls. When you try to handle the horse, he seems get more agitated and hyperexcitable despite your attempts to calm him. You inquire about the horse’s diet and find out the horse is fed a mixture of cracked corn and oats. Based on this information, what is the most likely diagnosis and mechanism of toxicity causing the horse’s abnormal behavior?

A. Leukoencephalomalacia caused by ingestion of moldy corn containing Fumonesin B1 toxin
B. Nigropallidal encephalomalacia caused by ingestion of yellowstar thistle or Russian nap weed.
C. Formation of lysosomal vacuoles in the central nervous system caused by accumulation of
Swainsonine alkaloid from ingestion of Locoweed
D. Severe cortical necrosis caused by administration of fluphenazine.

Answer 6

A. Leukoencephalomalacia caused by ingestion of moldy corn containing Fumonesin B1 toxin

Question 7

This tumor is frequently an incidental finding on necropsy in older horses, however, clinical symptoms may result from obstruction of the third ventricle.

A. Pars Pituitary Intermedia melanoma
B. Pars Pituitary Intermedia adenoma
C. Cholesteatoma
D. Neuroglioma

Answer 7

C. Cholesteatoma

Question 8

You examine a 3‐year‐old Thoroughbred horse in July that recently moved to Florida from Minnesota. The horse has an acute onset of ataxia and abnormal behavior. On examination you find the horse has a fever of 103*F and you note that the horse shows intermittent periods of extreme somnolent behavior but when stimulated circles repeatedly. The horse also appears ataxic in all four limbs. You inquire about the horse’s vaccination history and find out that he was vaccinated over one year ago for “everything” according to the owner. You collect several samples to test for common neurologic infectious diseases. You also bravely sedate the horse and collect a CSF sample from the lumbosacral site. On cytological examination, the total nucleated cell count is 100 cells/ul with predominately neutrophils observed. Based on this information, what is your top suspicion for the cause of this horse’s symptoms?

A. Rabies virus
B. West Nile virus
C. Eastern equine encephalomyelitis
D. Equine herpes myeloencephalitis

Answer 8

C. Eastern equine encephalomyelitis

Question 9

Which of the following symptoms are most commonly reported in horses with clinical manifestations of
West Nile Virus?

A. Fever and cranial nerve deficits
B. Muscle fasciculations and ataxia
C. Dysuria and constipation
D. Ataxia and focal muscle atrophy

Answer 9

B. Muscle fasciculations and ataxia

Question 10

Which of the following statements about Rabies disease in horses is true?

A. The onset of clinical signs is no longer than 10 days after exposure to the virus and
progression of disease occurs rapidly after the onset of symptoms
B. The onset of clinical signs is no longer than 10 days after exposure but progression of the
disease is slow with death occurring months after the onset of symptoms.
C. The onset of clinical signs can be up to 6 months after exposure and progression of the
disease is slow with death occurring months after the onset of symptoms.
D. The onset of clinical signs can be up to 6 months after exposure but progression of the disease occurs rapidly after the onset of symptoms

Answer 10

D. The onset of clinical signs can be up to 6 months after exposure but progression of the disease occurs rapidly after the onset of symptoms

Question 11

Which of the following best describes the pathogenesis of Equine Herpes Myeloencephalitis?

A. Active viral infection leads to viremia and infection of the CNS endothelium, causing
vasculitis, microthrombosis and ischemic lesions in the CNS.
B. Active viral infection leads to viremia and infection of the neurons within the spinal cord,
ultimately resulting in neuronal cell death within the CNS.
C. Latent viral infection gets reactivated within the spinal cord and viral replication causes
subsequent neuronal cell death within the CNS.
D. Latent viral infection gets re‐activated within the trigeminal nerve, leading to a viremia and
subsequent infection of neurons within the gray matter of the spinal cord.

Answer 11

A. Active viral infection leads to viremia and infection of the CNS endothelium, causing
vasculitis, microthrombosis and ischemic lesions in the CNS.

Question 12

You are presented with a 13 year old TB gelding for acute onset of ataxic in both hind limbs. When questioning the owner, you find out the horse returned from a horse show 5 days ago and subsequently the horse has had intermittent, biphasic fevers up to 103°F for the last 3 days. As Equine Herpes Myeloencephalitis is on your list of differential diagnoses, which of the following diagnostic tests are most appropriate?

A. Submission of serum for antibody titers to EHV‐1.
B. Submission of cerebral spinal fluid for EHV‐1 PCR testing.
C. Submission of nasopharyngeal swabs and whole blood for EHV‐1 PCR testing.
D. Submission of cerebral spinal fluid to measure intrathecal EHV‐1 antibody production.

Answer 12

C. Submission of nasopharyngeal swabs and whole blood for EHV‐1 PCR testing.

Question 13

Which of the following statements are true concerning EHV‐1 infection in horses.

A. The symptoms caused by EHV‐1 upper respiratory infection are similar to other viral
etiologies of upper respiratory infection in horses including Equine Influenza Virus.
B. The symptoms caused by EHV‐1 upper respiratory infection are unique compared to other
viral etiologies of respiratory infection in horses such as Equine Influenza Virus.
C. EHV‐1 infection is relatively uncommon in horses compared to other viral etiologies of upper
respiratory infection in horses such as Equine Influenza Viral infection
D. The symptoms caused by EHV‐1 upper respiratory infection in horses are less common than
the neurologic manifestations observed in Equine Herpes Myeloencephalitis.

Answer 13

A. The symptoms caused by EHV‐1 upper respiratory infection are similar to other viral
etiologies of upper respiratory infection in horses including Equine Influenza Virus.

Question 14

Of the following equine infectious diseases, which one does not have a vaccine labeled to prevent neurologic disease?

A. Eastern equine encephalomyelitis virus (EEE)
B. Equine Herpesvirus 1 (EHV‐1)
C. West Nile virus (WNV)
D. Rabies virus

Answer 14

B. Equine Herpesvirus 1 (EHV‐1)

Question 15

Which of the following statements concerning Equine protozoan myeloencephalitis (EPM) is true?

A. Compared to a high rate of seroprevalence for Sarcocystis neurona in horses, the incidence
of clinical disease caused by EPM is relatively low in the United States.
B. Compared to the low rate of seroprevalence for Sarcocystis neurona in horses, the incidence
of clinical disease caused by EPM is relatively high in the United States.
C. The high seroprevalence for Sarcocystis neurona is reflective of an overall high rate of clinical
disease caused by EPM in horses in the United States.
D. The seroprevalence for Neospora hughesi is similar to that for Sarcocystis neurona throughout
the United States.

Answer 15

A. Compared to a high rate of seroprevalence for Sarcocystis neurona in horses, the incidence
of clinical disease caused by EPM is relatively low in the United States.

Question 16

Which best describes the mode of transmission of EPM?

A. The opossum is the definitive host for S. neurona. The opossum acquires infection by
ingesting sarcocysts in muscle tissues of intermediate hosts, such as skunks or cats. S. neurona
undergoes sexual reproduction in the opossum’s intestinal epithelium and infectious sporocysts
are passed in the feces. Horses acquire infection by ingesting feed or water sources
contaminated with the opossum feces.
B. The opossum is the definitive host for S. neurona. The opossum acquires infection by
ingesting sarcocysts in muscle tissues of intermediate hosts, such as skunks or cats. Sexual
reproduction occurs in the opossum, leading to extensive sarcocyst formation in muscle tissue.
Horses acquire the infection by eating foodstuffs contaminated with carion (dead animal
carcasses) of the opossum.
C. Small mammals such as dogs, cats and skunks are the definitive hosts of the for S. neurona.
After ingestion, the organism forms infectious sarcocysts in muscle tissues of these hosts.
Horses acquire infection by eating foodstuffs contaminated with carion (dead animal carcasses)
of these small mammals.
D. Small mammals such as dogs, cats and skunks are the definitive hosts for S. neurona. After
these animals ingest sarcocysts found in muscle tissue of the opossum, S. neurona under goes
sexual reproduction in intestinal epithelium of the definitive hosts. Infectious sporocytes are
then passed in the feces and horses acquire infection by ingesting feed or water sources
contaminated with feces from cats, dogs or skunks.

Answer 16

A. The opossum is the definitive host for S. neurona. The opossum acquires infection by
ingesting sarcocysts in muscle tissues of intermediate hosts, such as skunks or cats. S. neurona
undergoes sexual reproduction in the opossum’s intestinal epithelium and infectious sporocysts
are passed in the feces. Horses acquire infection by ingesting feed or water sources
contaminated with the opossum feces.

Question 17

Which of the following are considered risk factors for EPM in horses?

A. Presence of nearby prairie land, cold weather seasons and conditions associated with
diminished immunity
B. Presence of nearby woods, lack of appropriate vaccination for EPM and stressors such as
transport or exercise
C. Presence of nearby prairie land, warm weather seasons and high stocking density
D. Presence of nearby woods, warm weather seasons and conditions associated with
diminished immunity

Answer 17

D. Presence of nearby woods, warm weather seasons and conditions associated with
diminished immunity

Question 18

Which of the following drugs is FDA approved in the United States to treat EPM in horses?

A. Ponazuril (Marquis ™)
B. Toltrazuril (Baycox ™)
C. Levamisole
D. Decoquinate

Answer 18

A. Ponazuril (Marquis ™)

Question 19

A 3 year old QH gelding used for trail riding presents to you for acute onset of stumbling when being
worked under saddle. On examination, you find the horse’s mentation to be normal and vitals
parameters including rectal temperature are within normal limits. Gait analysis reveals a symmetrical
ataxia in the hind limbs (grade 2/5) and significant atrophy of the left gluteal muscle. The horse was
vaccinated 1 month ago for EWT/WNV/Rabies along with Equine Influenza virus and Equine Herpes
virus. According to the owner the horse has not left the farm in the last 6 months. What is your top
differential diagnosis for this horse and how would you best confirm this diagnosis?

A. Equine herpes myeloencephalomyelitis; PCR testing for EHV‐1 on pharyngeal swab and whole
blood.
B. Neuroborreliosis; determination of intrathecal production of antibodies to the outer surface
proteins of Borrelia burgdorferi
C. West Nile Virus; measurement of serologic titers by IgM capture ELISA
D. Equine protozoal myeloencephalomyelitis; determination of intrathecal production of
antibodies to surface antigen proteins (SAGs) of S. neurona.

Answer 19

D. Equine protozoal myeloencephalomyelitis; determination of intrathecal production of
antibodies to surface antigen proteins (SAGs) of S. neurona.

Question 20

Which of the following diagnostic findings would best confirm a diagnosis of cervical vertebral stenotic
myelopathy?

A. A myelogram showing greater than 50% reduction of the dorsal dye column at the area of
suspected compression
B. A myelogram showing greater than 30% reduction of the dorsal dye column at the area of
suspected compression
C. A myelogram showing greater than 25% reduction of the dorsal dye column at the area of
suspected compression
D. A myelogram showing greater than 10% reduction of the dorsal dye column at the area of
suspected compression

Answer 20

A. A myelogram showing greater than 50% reduction of the dorsal dye column at the area of
suspected compression

Question 21

You are asked to examine a 2 year old TB colt for suspected ataxia that was first noted when the colt was
started into training at the track. On examination, the colt appears alert with normal vital parameters.
Further neurologic examination reveals a symmetrical spinal ataxia in the pelvic limbs (grade 3/5) but
normal forelimbs. You note that deficits worsen when the horses is asked to walk with his head
elevated with subtle deficits also noted in the forelimbs under these circumstances. The colt is up to
date on all vaccines including EWT/WNV/Rabies, Equine Influenza and Equine Herpes virus. No other
horses have been reported ill at the track over the past month and this colt has not left the premises for
the last 2 months. Based on this information provided, what is your top differential diagnoses?

A. Equine Herpes Myeloencephalopathy
B. Cervical Vertebral Stenotic Myelopathy
C. Neuroaxonal Degenerative Myelopathy
D. Polyneuritis equi

Answer 21

B. Cervical Vertebral Stenotic Myelopathy

Question 22

You work in an equine practice in Connecticut and you are asked to examine a horse for lethargy and
depressed mentation of 2 months duration. More recently, the owner noted the horse to seem ataxic
and also reports a possible seizure like episode. On examination, the horse has a rectal temperature of
102*F but other vital parameters are normal. On neurologic examination, you appreciate ataxia in all
four limbs, fine muzzle fasciculations and effusion in multiple joints. In addition, you find numerous ticks
in the horse’s mane. Based on these findings what is your top differential diagnosis and recommended
course of therapy?

A. EPM, treat the horse with a 28 day course of Ponazuril (Marquis)
B. EHV‐1, treat the horse with valcyclovir and Banamine
C. WNV, treat the horse with anti‐inflammatories and vitamin E
D. Neuroborreliosis, treat the horse with 7 days of IV oxytetracycline followed by 30 days of
oral minocycline.

Answer 22

D. Neuroborreliosis, treat the horse with 7 days of IV oxytetracycline followed by 30 days of
oral minocycline.

Question 23

Risk factors implicated in the development of equine degenerative myelopathy (EDM) include

A. A lack of dietary intake of vitamin E, dry lot turn and exposure to insecticides
B. Presence of developmental orthopedic diseases such as osteochondrosis in other peripheral
joints increases the risk of vertebral body malformation causing spinal cord compression and
subsequent degenerative myelopathy
C. Farm exposure to opossums, nearby woods and high stocking density
D. Stress and immunosuppression

Answer 23

A. A lack of dietary intake of vitamin E, dry lot turn and exposure to insecticides

Question 24

You are presented with a 10 year old TB gelding because the owner is concerned the horse has lost
significant weight over the past year. The owner has also noted an overall weakness that has progressed
in the past 6 months to the point that she can no longer ride the horse. On examination, the horse
appears to have significant muscle atrophy of the gluteal and quadriceps muscles along with generalized muscle fasciculations. The horse seems anxious when you ask him to stand still and prefers to continue moving. The horse is kept on a dry lot and fed poor quality round bail hay along with 4lb of sweet feed twice a day. The owner reports the horse has maintained an excellent appetite. Based on this
information what is your top differential diagnosis and what diagnostic test would be best to confirm
this diagnosis?

A. EPM; demonstration of intrathecal production of antibodies to surface antigen proteins
(SAGs) of S. neurona.
B. Cervical Vertebral Stenotic Myelopathy; cervical radiographs and myelogram
C. Botulism; collect feed material to perform a mouse bioassay and verify contamination of
feedstuffs with the neurotoxin.
D. Equine Motor Neuron Disease; measure serum vitamin E levels and perform a muscle biopsy
of the Sacrocaudalis dorsalis m.

Answer 24

D. Equine Motor Neuron Disease; measure serum vitamin E levels and perform a muscle biopsy
of the Sacrocaudalis dorsalis m.

Question 25

Which of the following clinical signs can also accompany the more traditional deficits observed with
Equine Motor Neuron Disease in horses?

A. Lipopigment accumulation in the tapetum observed on fundic exam
B. Hyperesthesia to the perineum or head region
C. Dysuria and constipation
D. Mydriasis

Answer 25

A. Lipopigment accumulation in the tapetum observed on fundic exam

Question 26

Which of the following statements best describes the clinical presentation of chronic Polyneuritis equi?

A. Generalized muscle atrophy with weakness in all four limbs characterized by narrow based
stance and short‐strided gait
B. Generalized ataxia in the pelvic limbs with diminished cervical and cervico facial reflexes
C. Initial areas hyperesthesia around the tail head followed by the development of dysuria, ileus
and generalized weakness and muscle fasculations.
D. Initial areas of hyperesthesia around the tail head followed by the development of dysuria,
impaction colic and paralysis of the tail and anus

Answer 26

D. Initial areas of hyperesthesia around the tail head followed by the development of dysuria,
impaction colic and paralysis of the tail and anus

Question 27

You are presented with a 12 year old gelding for acute onset of difficulty ambulating. When you
examine the horse you notice he stands in a rigid, sawhorse stance and he has a grimace appearance in
the face. You also notice an old wound puncture wound in the triceps region. When you inquire about
the horse’s vaccination history, the owner explains she doesn’t believe in vaccinating her animals. Based
on these findings, what would be your best choice of therapy?

A. Clean the wound and start the horse on a course of penicillin and NSAIDs while providing
supportive care.
B. Clean the wound, start the horse on a course of penicillin and administer the Tetanus toxoid
vaccination to the horse while providing supportive care
C. Clean the wound, start the horse on a course of penicillin and administer antiserum for
Tetanus neurotoxin while providing supportive care.
D. Clean the wound, start the horse on penicillin, administer Tetanus antiserum and give the
Tetanus toxoid vaccine at a separate site while providing supportive care.

Answer 27

D. Clean the wound, start the horse on penicillin, administer Tetanus antiserum and give the
Tetanus toxoid vaccine at a separate site while providing supportive care.

Question 28

Which of the following statements concerning the mechanism of action of Tetanus is true?

A. Clostridium tetani is inoculated through a peripheral wound where it releases
Tetanospasmin toxin (TeNT). The toxin is taken up through peripheral nerve terminals at the
neuromuscular junction and transported retrograde along alpha motor neuron axons to the
spinal cord. TeNT then crosses the synaptic cleft and becomes internalized by inhibitory neurons
where it cleaves SNARE proteins. This in turn blocks the release of inhibitory neurotransmitters
resulting in continued activation of alpha motor neurons and tetanic muscle contraction.
B. Clostridium tetani is inoculated through a peripheral wound where it releases Tetanospasmin
toxin (TeNT). The toxin is taken up through peripheral nerve terminals at the neuromuscular
junction and transported retrograde along alpha motor neuron axons to the spinal cord. TeNT
then crosses the synaptic cleft and becomes internalized by inhibitory neurons where it cleaves
inhibitory neurotransmitters. In turn this prevents inhibition of alpha motor neurons resulting in
continued tetanic muscle contraction.
C. Clostridium tetani is inoculated through a peripheral wound. Tetanolysin toxin is released
causing local tissue damage and facilitating the uptake of Tetanospasmin (TeNT) into the
peripheral blood circulation. TeNT then travels to inhibitory neurons within the spinal cord.
Once internalized in these neurons, the toxin cleaves SNARE proteins. This in turn blocks the
release of inhibitory neurotransmitters resulting in continued activation of alpha motor neurons
and tetanic muscle contraction.
D. Clostridium tetani is inoculated through a peripheral wound. Tetanospasmin neurotoxin
(TeNT) diffuses to the neuromuscular junction where it inhibits acetylcholinesterase and thus
prevents the breakdown of acetylcholine, leading to continued tetanic muscle contraction.

Answer 28

A. Clostridium tetani is inoculated through a peripheral wound where it releases
Tetanospasmin toxin (TeNT). The toxin is taken up through peripheral nerve terminals at the
neuromuscular junction and transported retrograde along alpha motor neuron axons to the
spinal cord. TeNT then crosses the synaptic cleft and becomes internalized by inhibitory neurons
where it cleaves SNARE proteins. This in turn blocks the release of inhibitory neurotransmitters
resulting in continued activation of alpha motor neurons and tetanic muscle contraction.

Question 29

There are 7 known serotypes of Botulinum neurotoxin (BoNT A‐G). Which serotypes most often effects
horses in the United States?

A. Serotypes BoNT/A and BoNT/B
B. Serotypes BoNT/B and BoNT/C
C. Serotypes BoNT/A and BoNT/C
D. Serotypes BoNT/D and BoNT/F

Answer 29

B. Serotypes BoNT/B and BoNT/C

Question 30

Which form of botulism is common in foals born to previously unvaccinated mares in the Kentucky?

A. Wound botulism
B. Forage poisoning
C. Toxico‐infectious botulism
D. Ingestion of preformed toxin in feedstuffs contaminated with carion (dead animal carcasses)

Answer 30

A. Wound botulism

Question 31

Which of the following best describes the mechanism of action of Botulinum neurotoxin (BoNT) ?

A. BoNT binds to the end terminal of alpha motor neurons at the neuromuscular junction.
Within the terminal, the toxin cleaves acetylcholine, preventing release of this neurotransmitter
at the neuromuscular junction thus resulting in a flaccid muscle paralysis
B. BoNT binds irreversibly to acetylcholine receptors on muscle cells at the neuromuscular
junction thus resulting in a flaccid muscle paralysis.
C. BoNT cleaves acetylcholine released from alpha motor neurons at the neuromuscular
junction, reducing the amount of acetylcholine available to bind to muscle receptors causing a
flaccid muscle paralysis.
D. BoNT is taken up by alpha motor neuron nerve terminals at the neuromuscular junction
where it cleaves SNARE proteins preventing vesicle tethering and subsequent release of
acetylcholine, resulting in flaccid muscle paralysis.

Answer 31

D. BoNT is taken up by alpha motor neuron nerve terminals at the neuromuscular junction
where it cleaves SNARE proteins preventing vesicle tethering and subsequent release of
acetylcholine, resulting in flaccid muscle paralysis.

Question 32

You are presented with a 9 year old QH gelding because the owner has noted he is slow to eat all of his food and seems to be laying down more than usual for the past 2 days. The owner is very worried
because he found a herd mate dead in the pasture 2 days ago. The horses are fed round bale hay and
sweet feed. The owner also said he found parts of a dead animal in one of the bales of hay last week.
Based on this information, what is your top differential and what other clinical signs would you look for
on physical exam to confirm your suspicions?

A. Tetanus; evidence of rigid muscle contraction, saw‐horse stance, the presence of a sardonic
grin and elevation of the third eyelid
B. Botulism; bilateral mydriasis with sluggish pupillary light reflex and a camped under stance
with generalized muscle fasciculations.
C. Equine motor neuron disease; dark discoloration to the teeth, evidence of retinal lipopigment
accumulation on fundic exam and a camped under stance with generalized muscle
fasciculations.
D. Polyneuritis equi; evidence of hyperesthesia of the perineal region

Answer 32

B. Botulism; bilateral mydriasis with sluggish pupillary light reflex and a camped under stance
with generalized muscle fasciculations.

Question 33

Based on the picture below, what is the likely causative agent of this horse’s gait abnormality? (picture showed an adult horse that appeared to have stringhalt)

A. Grazing a pasture with significant overgrowth of Locoweed
B. Grazing a pasture with significant overgrowth of Yellowstar Thistle
C. Grazing a pasture with significant overgrowth of Russian Knapweed
D. Grazing a pasture with significant overgrowth of Lathyrus spp.

Answer 33

D. Grazing a pasture with significant overgrowth of Lathyrus spp.

Question 34

Which peripheral nerve injury is more commonly observed in foals after assisted deliveries and what
deficits are noted?

A. Femoral nerve, the foal is unable to bear weight in the limb and all joints in the distal limb
are flexed
B. Sciatic nerve, the foal is unable to bear weight in the limb and all joints of the distal limb are
flexed
C. Femoral nerve, the foal is unable to bear weight in the limb and all joints of the distal limb are
extended
D. Sciatic nerve, the foal is unable to bear weight in the limb and all joints of the distal limb are
extended

Answer 34

A. Femoral nerve, the foal is unable to bear weight in the limb and all joints in the distal limb
are flexed