Neuro

Question 1

DDX of vestibular disease in horses ?

Answer 1

• Temporohyoid osteoarthropathy (+++)
• Otitis media and interna (bacterial, viral, fungal, parasitic or neoplasia)
• Trauma (collision, kick, or flipping over)
• Infectious : EPM in USA, Lyme (Borrelia burgdorferi), aberrant parasite migration (Halicephalobus gingivalis), meningitis, brain abscess

Vestibular disease in horses: Recognition, localisation and common causes
(Clinical commentary) EVE 2024

Question 2

What is Juvenile Idiopathic Epilepsy ? (breed, age, clinical signs, prognosis)

Answer 2

Juvenile idiopathic epilepsy (JIE) is a self-limiting disorder in Egyptian Arabian foals, with an early onset of seizures ranging from 2 days to 6 months of age, with apparent resolution within 1 to 2 years of life with no known long-term neurologic sequelae. Prognosis for life and athletic performance generally is good provided no life-threatening complications occur.

Electroencephalographic evaluation under standing sedation using sublingual detomidine hydrochloride in Egyptian Arabian foals for investigation of epilepsy
JVIM 2023

Question 3

What is the suspected mode of inheritance of Juvenile Idiopathic Epilepsy in Arabian foals ?
What is the most common postictal sign ?

Answer 3

JIE in foals has a familial basis and is suspected to be inherited in an autosomal dominant manner with a self-limiting pattern, likely with incomplete penetrance resulting in some asymptomatic foals (siblings of affected foals).
Cortical blindness is the most common postictal sign.

Juvenile idiopathic epilepsy in Egyptian Arabian foals, a potential animal model of self-limited epilepsy in children
JVIM 2024

Question 4

Which breed is most likely to show severe muscular symptoms in cases of anaplasmosis?

Answer 4

Muscle disease was less common, with QH breeds with the variant causing myosin heavy chain myopathy (MYHM) having severe disease.

Common and atypical presentations of Anaplasma phagocytophilum infection in equids with emphasis on neurologic and muscle disease
JVIM 2024

Question 5

What is the current known etiology of shivering in horses?

Answer 5

Our findings support axonal degeneration of Purkinje cells in the cerebellum, without a substantial impact on Purkinje cells soma.

Cerebellar axonopathy in Shivers horses identified by spatial
transcriptomic and proteomic analyses
JVIM 2023

Question 6

What is the current hypothesis when faced with an acute onset of neurological deficits, with decubitus, high GGT and hyperglycemia, in a QH foal (< 1 month) ?
Hypothetical etiology ?

Answer 6

Equine Juvenile Spinocerebellar Ataxia (EJSCA) is a uniformly fatal, rapidly progressive, likely autosomal recessive neurological disease of QHs <1 month of age in North America, that is etiologically distinct from other clinically similar neurological disorders.

Clinicopathological and pedigree investigation of a novel spinocerebellar neurological disease in juvenile Quarter Horses in North America
JVIM 2024

Question 7

What are the key findings regarding juvenile idiopathic epilepsy (JIE) in Egyptian Arabian foals based on EEG and clinical observations?

A) EEG findings showed generalized epileptic discharges in 60% of JIE foals, originating from random cortical regions, and there were no postictal signs like cortical blindness.

B) Most JIE foals experienced focal seizures, with EEG abnormalities being rare and only occurring during wakefulness, unrelated to genetic factors.

C) Focal epileptic discharges originating from the central vertex were observed in 95% of JIE foals. Seizures were mostly generalized tonic-clonic, with postictal signs like cortical blindness, and photic stimulation triggered discharges in 62% of the foals. Asymptomatic siblings also showed EEG abnormalities, suggesting genetic susceptibility.

D) Juvenile idiopathic epilepsy in foals primarily manifests as focal seizures, with generalized tonic-clonic seizures being rare, and all foals responded to antiseizure medications without exception.

Answer 7

Answer: C.

A) INCORRECT-> mentions no postictal signs and generalized discharges in 60% of foals. The paper states postictal signs were observed, and generalized seizures occurred in 86% of foals​

B) INCORRECT->claims focal seizures are common and EEG abnormalities are rare. In reality, generalized seizures were the majority (86%), and 95% of JIE foals had EEG abnormalities​

C)CORRECT
Focal epileptic discharges originating from the central vertex were observed in 95% of JIE foals (n = 35/37) in the form of focal spike-and-wave discharges;
Seizures were mostly generalized tonic-clonic:
Clinically, 41 of 48 JIE foals had generalized seizures… Seizures were characterized as violent generalized tonic-clonic with a facial motor component, trismus, and loss of consciousness.
ostictal signs like cortical blindness:
Postictal signs included disorientation, obtundation, cortical blindness, mydriasis, decreased palpebral reflex, lack of suckle reflex, dysphagia, tongue protrusion, proprioceptive deficits of all limbs, and ataxia.
Intermittent PS [photic stimulation] resulted in photoparoxysmal responses in the form of ED in the central or centroparietal regions in 62% (n = 13/21) of JIE foals.
Asymptomatic siblings also showed EEG abnormalities, suggesting genetic susceptibility:In 3 control foals, focal spike and waves discharges occasionally were observed… None of these 3 control foals had a history of epilepsy, but all had a family history of a sibling with JIE

D)INCORRECT: suggests focal seizures are predominant and all foals responded to treatment, but the paper clearly states that generalized tonic-clonic seizures were more frequent, and 6% of foals were resistant to treatment​

Juvenile idiopathic epilepsy in Egyptian Arabian foals
jvim 23

Question 8

In horses diagnosed with Shivers, which of the following best describes the primary pathological finding in the cerebellum?

A) Degeneration of Purkinje cell (PC) soma with significant gene expression changes.
B) Loss of myelin proteins in the cerebellar cortex.
C) Axonal degeneration in the cerebellar white matter with minimal changes in the Purkinje cell soma.
D) Neurofilament accumulation in Purkinje cell bodies causing axonal atrophy.

Answer 8

answer: C

A) Incorrect. The study found no significant differential gene expression in Purkinje cell soma between Shivers and control horses. The primary pathology was in the axons, not the soma​.

B) Incorrect. While the study did find a reduction in myelin-related proteins, this occurred primarily in the cerebellar white matter, particularly in the axonal regions, not limited to the cortex​.

C) Correct. The primary finding in Shivers horses was axonal degeneration in the cerebellar white matter, particularly in regions rich in axons. There were minimal changes in the Purkinje cell soma, consistent with axonal degeneration without significant soma involvement​.

D) Incorrect. While neurofilament proteins were reduced in Shivers horses, the pathology involved axonal degeneration, not accumulation in the Purkinje cell bodies.​

Cerebellar axonopathy in Shivers horses identified by spatial
transcriptomic and proteomic analyses 2023

Question 9

What is the most common site for a focal lesion to cause progressive obtundation or stupor ?

Answer 9

The thalamus

Question 10

Which neurologic zone is evaluated with the nasal septum sensory perception?

Answer 10

Although nasal sensation is mediated though the trigeminal nerve, this test is really used as a crude assessment of forebrain function.

Detection of slight asymmetry in the behavioral (avoidance) response to a stimulus applied to the nasal septum, that is, hyperalgesia, can take considerable patience but may confirm the presence of asymmetric forebrain disease.

Question 11

What is the first suspicion with a poor tongue tone ?

Answer 11

Botulism

Question 12

What is the neurolocation of ventral strabismus, which is most evident when the head is lifted ?

Answer 12

Disorder of the vestibular system

Photo : right-sided central vestibular lesion

Question 13

What is the neurolocation of a blind horse with normal PLR ?

Answer 13

(1) with optic nerve lesions, both vision and PLR are
abnormal,
(2) with cortical lesions, vision is affected but PLRs are normal,
(3) with efferent arm lesions, the PLR is abnormal and vision is unaffected.

An important caveat here is that PLRs are often maintained even with retinal or optic nerve lesions that result in the loss of vision, so be careful when diagnosing a central lesion in a blind horse with apparently operational PLRs.

Question 14

What are the ophtalmologic signs of cerebellar dysfunction ?

Answer 14

Bilateral mydriasis and PLR deficits

Question 15

What are the clinical signs of a Horner syndrome ?

Answer 15

Horner syndrome, caused by a lesion to the sympathetic input to the eye.

Classic ophthalmic signs of Horner syndrome are ptosis, miosis, and enophthalmos with associated protrusion of the nictitating membrane but in horses ptosis is the most consistent clinical sign and may be the only sign observed.

Lesions in the region of the** guttural pouch** and cranial cervical ganglion will result in sweating of the face (most prominent at the base of the ear) and the cranial neck
down to the level of C2.

Lesions further down the neck involving the sympathetic trunk may result in sweating of the face and the neck extending down to the level of C3 to C4.

Photo : Horse with guttural pouch mycosis resulting in Horner syndrome in the left eye. Note the enophthalmos, ptosis, and particularly the downward pointing eyelashes.

Question 16

What is the suspected neurolocation of a lesion in an ataxic horse of all 4 limbs, with paresis in thoracic limbs ?

Answer 16

C7-T2

C1-C6 vs C7-T2 vs T3-L3 vs L4-S3

Question 17

What is the difference between paresis and ataxia ?

Answer 17

Paresis = reduction in motor function (UMN or LMN), descending upper motor neuron pathways.
Ataxia = deficit in proprioception (hypometria or hypermetria), ascending proprioception pathways.
Usually, spical cord damage is a combination of paresis and ataxia.

Ataxic horses can look remarkably better when excited; it is worth giving the horse time after arrival to the hospital before examining it for mild neurological signs.

Question 18

What are the clinical signs of UMN vs LMN ?

Answer 18

LMN = flaccid paralyis, neurogenic atrophy, electromyography changes of skeletal muscle.
Weakness while standing still, and poor response when the tail is pulled in the standing patient.

UMN = spastic paralysis, absence of voluntary movement, with increased tone and increased reflexes due to the lack on UMN inhibition (ex. cervical lesion)
Easily pulled to the side when walking

Question 19

What is the neurolocation of a lesion in a dog sitting horse ?

Answer 19

Injury caudal to T2

Question 20

What are the intra- and inter-vertebral sagittal ratios to diagnose CVSM ?

Answer 20

Intravertebral sagittal ratios : 0.52 for C3-C6, 0.56 for C6-C7 (Se 84%, Spe 32%)

Intra- and inter-vertebral sagittal ratios : 0.485 for C3-C7 (Se 20%, Spe 100%)

Question 21

What are the ratios to diagnose CVSM using radiographic myelography ?

Answer 21

■ 50% decrease in the height of the dorsal contrast column compared with cranial height (Se 71%, Spe 65%)

↳ 70% in the flexed view (decrease Se, increase Spe)

■ 20% decrease in the total dural diameter of the contrast column compared with cranial diameter, in neutral position.

↳ 25% in the flexed view (Se 100%, Spe 100%)

Question 22

What is the difference between eNAD and EDM ?

Answer 22

eNAD is clinically indistinguishable from EDM.

The disease was classified as eNAD if the histopathologic lesions were confined to the brainstem, whereas a diagnosis of EDM was assigned when axonal necrosis and demyelination extended into the spinocerebellar tracts and the cervicothoracic spinal cord.

The current consensus is that eNAD could be considered a localized form of EDM or EDM a more diffuse form of eNAD.

Question 23

What are the clinical signs of eNAD/EDM ?

Answer 23

In most breeds, eNAD/EDM is characterized by symmetric proprioceptive ataxia in all limbs, often more severe in the pelvic limbs and abnormal base-wide stance at rest, by 6 to 12 months of age in young QH, Morgans…

Another clinical presentation : between 5-15 years in WB, with abnormal behavior, mild to moderate proprioceptive ataxia (grade 1-2/5), and inconsistent menace reflex.

In young horses, concurrent EMND and eNAD/EDM.

Question 24

What is the prevalence of eNAD/EDM ?

Answer 24

In most recent studies :
- first common cause of spinal ataxia = CVCM (TB ++)
- second most common cause of spinal ataxia = eNAD/EDM (QH ++)

Question 25

What is the presumed etiology of eNAD/EDM in QH ?

Answer 25

Both a genetic susceptibility and a temporal ⍺-tocopherol deficiency are required for the phenotype to develop in QH.

• Genetic in QH : hyp of incompletely penetrant autosomal dominant trait
• Vitamin E : low vitamin E levels are not present consistently in all cases. But vitamin E supplementation of genetically susceptible foals lowers the overall incidence and severity of eNAD/EDM. Studies showed that QH with eNAD/EDM had an increased rate of ⍺-tocopherol metabolism → need of high dose supplementation to prevent the clinical phenotype in genetically susceptible horses.
• Excessive oxidative stress due to environmental factors : use of insecticides, exposure to wood preservatives → oxidative imbalance.

Question 26

What is the most frequent in a population of horses located in Oregon (soil deficiencies), with owners’ nutritional supplementation ?
- Selenium deficiency
- Vitamine E deficiency
- β-carotene deficiency
- selenium overdose

Answer 26

- Vitamine E deficiency in Oregon despite most owners providing supplementation.

Inadequate pasture access was associated with alpha-tocopherol deficiency, and reliance on selenium-containing salt blocks was associated with selenium deficiency.

Influence of specific management practices on blood selenium,
vitamin E, and beta-carotene concentrations in horses and risk
of nutritional deficiency
JVIM 2020

Question 27

What is the safety and efficacy of subcutaneous ⍺-tocopherol administration in horses ?

Answer 27

Parenteral administration of ⍺-tocopherol via the subcutaneous route effectively increases serum and CSF ⍺-tocopherol concentrations.

But the tested product is not safe for use in horses due to local tissue reaction and as such cannot be recommended for clinical use at this time.

Safety and efficacy of subcutaneous alpha-tocopherol in healthy
adult horses
eve 2021

Question 28

What have been identified in eNAD/EDM affected QH ?
* decreased α-tocopherol metabolism
* increased α-tocopherol metabolism
* increased α-tocopherol and γ-tocopherol metabolism
* decreased hepatic expression of metabolizer of vitamin E (CYP4F2)

Answer 28

Metabolic rate of α-tocopherol was increased in serum and urine of eNAD/EDM horses, with no difference in the metabolic rate of γ-tocopherol.
Increased expression of CYP4F2 → likely a consequence of the underlying genetic etiology of eNAD/EDM.

Increased α-tocopherol metabolism in horses with equine neuroaxonal dystrophy
JVIM 2021

Question 29

What is the main hypothese(s) associated with increased CSF pNfH (> 3 ng/mL) ?
What is the main hypothese(s) associated with increased blood pNfH (> 1 ng/mL) ?

Answer 29

Increased CSF pNfH concentrations (>3 ng/mL) can be observed with eNAD/EDM or CVCM.
Serum pNfH concentrations are specifically increased (>1 ng/mL) in some horses with eNAD/EDM (but low sensitivity).

Serum and cerebrospinal fluid phosphorylated neurofilament
heavy protein concentrations in equine neurodegenerative
diseases
EVJ 2022

Question 30

What is the impact of vitamin E depletion in healthy juvenile horses ?

Answer 30

Vitamin E depletion may elevate CSF pNfH in otherwise healthy juvenile foals by 6 months of age, compatible with subclinical axonal degeneration.

Vitamin E depletion is associated with subclinical axonal degeneration in juvenile horses
evj 2023

Question 31

True or false : A mutation in CD36 is responsible of eNAD/EDM in QH.

Answer 31

False
2 intronic CD36 SNPs were significantly associated with eNAD/EDM in QHs. However, many postmortem-confirmed cases of eNAD/EDM were wild-type (non-mutated) for these variants. We either identified a false positive association or genetic heterogeneity exists for eNAD/EDM within the QH breed.

Genetic polymorphisms in vitamin E transport genes as
determinants for risk of equine neuroaxonal dystrophy
JVIM 24

Question 32

Which factor is associated with normalization of vitamine E dosage post-supplementation?
Hypothesis of transmission of eNAD/EDM ?

Answer 32

Vitamine E dosage was significantly associated with age, older horses were more likely to respond appropriately to vitamin E supplementation.

Hyp : autosomal dominant transmission with incomplete penetrance or polygenic

Equine neuroaxonal dystrophy/degenerative myeloencephalopathy in Gypsy Vanner horses
JVIM 2024

Question 33

What are the 2 clinical presentations of eNAD/EDM ?

Answer 33

Initial descriptions identified young horses (< 2 years) of specific breeds (Arabians, TB, QH and Morgan), with symmetric ataxia (grade ≧2/5), tetraparesis, and general proprioceptive tract lesions.

Second identified presentation : adult horses (median age 8 yo), majority of Warmbloods, with behavioral changes and proprioceptive ataxia (median grade 2/5).

Clinical and histopathological features in horses with neuroaxonal degeneration: 100 cases (2017-2021)
JVIM 2024

Question 34

Which seems to be the most accurate for discriminating healthy vs eNAD vs CVCM horses : protein test using serum or CSF ?

Answer 34

Modeling indicated that a 2-protein test using CSF had the highest accuracy for discriminating among all 3 groups. CSF R-spondin 1 (RSPO1) and neurofilament-light (NEFL)
Future studies to validate these markers in larger replication cohorts are required before clinical adoption of these biomarkers.

Cerebrospinal fluid and serum proteomic profiles accurately distinguish neuroaxonal dystrophy from cervical vertebral compressive myelopathy in horses
JVIM 2023

Question 35

What is 8-hydroxy-2’-deoxyguanosine (8-OHdG) a biomarker for ? Is it efficient to antemortem diagnose eNAD/EDM ?

Answer 35

8-OHdG is a commonly used biomarker of oxidative damage, extensively studied in humans with neurodegenerative diseases (Parkinson, Alzheimer).
Serum or CSF 8-OHdG did not aid in antemortem diagnosis of eNAD/EDM in this cohort of horses.

Measurement of 8-hydroxy-20-deoxyguanosine in serum and cerebrospinal fluid of horses with neuroaxonal degeneration and other causes of proprioceptive ataxia
JVIM 2024

Question 36

What are the types of Wobbler syndrome ?

Answer 36

Type I : affecting young horses, symmetric overgrowth of the articular processes (male ++, inheritance, diet, trauma, rate of growth). TB ++
C3-C4 ; C4-C5

Type II : older horses, asymmetric overgrowth of one articular process, osteoarthritic changes.
C5-C6 ; C6-C7

Question 37

DDX of spinal ataxia in young horses

Answer 37

• CVCM (most common)
• eNAD/EDM
• EPM
• Trauma
• EHM

Less common :
- Rabies
- Viral encephalitides (WNV, Eastern, Western…)
- Brain abscess
- Neoplasia
- Hepatoencephalopathy

Question 38

Pathogenesis of tetanus

Answer 38

Clostridium tetani (gram + anaerobes) → 2 toxins:
- Tetanolysin: induces local tissue damage → facilitating anaerobic environment

• Tetanospasmin: spreads hematogenously → enters CNS → prevents the release of glycin and GABA neurotransmitters from the inhibitory interneuron (Renshaw cell) in the synaptic cleft
  ⇒ spastic muscle contraction, muscular rigidity

Question 39

DDX of spastic muscle contractions

Answer 39

• Tetanus
• Rabies
• Strychnine intoxication
• Exertional rhabdomyolysis
• Myositis

Question 40

What are the clinical signs of tetanus ?

Answer 40

Question 41

What is the treatment plan of tetanus ?

Answer 41

1- Elimination of infectious agent (peni IV → may worsen, metronidazole PO or IR)

2- Neutralization of circulating neurotoxins → tetanus antitoxin

3- Control of muscular spasms (multimodal → ACP, methocarbamol, diazepam, dantrolen, xylazine…)

4- Establishment of active immunity against neurotoxins → tetanus toxoid (vaccination)

5- High quality supportive care

Question 42

Pathogenesis of botulism

Answer 42

Clostridium botulinum → botulinum neurotoxin (BoNT) type A, B, C (most frequent in Europe)

BoNT → cross epithelial barrier → spreads hematogenously → enters peripheral nerve terminals and the presynaptic nerve → prevent the release of acethylcholine (Ach)
⇒ flaccid neuroparalysis

Question 43

Clinical signs of botulism

Answer 43

Diffuse, symmetric, flaccid paralysis and loss of muscle strenght. First clinical signs → tongue, eyelid, tail, anal sphincter paralysis.
Weakness, dysphagia, poor muscle tone, fasciculations → respiratory failure.

Foals → first signs are muscle fasciculations → shaker foal syndrome

Question 44

DDX muscle fasciculations and weakness

Answer 44

• Botulism
• White muscle disease
• HYPP
• Hypocalcemia
• White snakeroot toxicity
• Ionophore toxicity
• Lead toxicity
• Organophosphate toxicity

Question 45

What are the 3 types of ataxia ?

Answer 45

• Cerebellar ataxia : Hypermetric / dysmetric, intention tremors, wide based stance
• Vestibular ataxia : Head tilt, nystagmus, circling, drifting, falling to one side
• Proprioceptive ataxia : Sensation of where the limbs are (in space) and where the joints are relative to each other

Question 46

What was the main conclusion of the study regarding head-tossing behavior in horses?

A) Head-tossing behavior in horses is primarily caused by trigeminal-mediated head-shaking.
B) All horses with head-tossing behavior had a history of seasonality in their clinical signs.
C) It is important for veterinarians to recognize head-tossing due to musculoskeletal pain and differentiate it from trigeminal-mediated head-shaking.
D) Diagnostic analgesia was ineffective in resolving head-tossing behavior in most horses.

Answer 46

Answer: C) It is important for veterinarians to recognize head-tossing due to musculoskeletal pain and differentiate it from trigeminal-mediated head-shaking.

Head tossing behaviour in six horses: Trigeminal-mediated head-shaking or musculoskeletal pain?
eve 20

Question 47

What is the clinical efficacy of the nose-net in headshakers ?

Answer 47

Improves clinical signs by ≧ 70% in 1/3 of horses

The safety and efficacy of neuromodulation using percutaneous electrical nerve stimulation for the management of trigeminal-mediated headshaking in 168 horses
evj 20

Question 48

What was the main conclusion of the study regarding EquiPENSTM neuromodulation for the treatment of trigeminal-mediated headshaking in horses?

A) EquiPENSTM neuromodulation is not effective in treating trigeminal-mediated headshaking in horses.
B) The treatment was found to be effective and safe in some horses, but further understanding of the condition is needed to optimize the technique.
C) Most horses experienced long-term remission after a single course of EquiPENSTM neuromodulation.
D) The study was inconclusive due to the lack of a control group and long-term follow-up

Answer 48

Answer: B) The treatment was found to be effective and safe in some horses, but further understanding of the condition is needed to optimize the technique.

The safety and efficacy of neuromodulation using percutaneous electrical nerve stimulation for the management of trigeminal-mediated headshaking in 168 horses
evj 20

Question 49

True or False:

EquiPENSTM neuromodulation was shown to be an effective treatment for trigeminal-mediated headshaking in horses, with remission occurring in 53% of horses following the initial treatment course.

Answer 49

Answer: True

The safety and efficacy of neuromodulation using percutaneous electrical nerve stimulation for the management of trigeminal-mediated headshaking in 168 horses
evj 20

Question 50

Which of the following was a key finding of the study on EquiPENSTM neuromodulation for treating trigeminal-mediated headshaking in horses?

A) Most horses remained in remission indefinitely after the initial three-procedure course.
B) Complications from the neuromodulation procedure were common and severe.
C) The median length of remission was 9.5 weeks, with some horses experiencing longer remissions after additional procedures.
D) Predictors for treatment outcomes were easily identified during the study.

Answer 50

Answer: C) The median length of remission was 9.5 weeks, with some horses experiencing longer remissions after additional procedures.

Main results of the study :
- The complication rate was 8.8% of procedures
- Remission of headshaking following the initial course occurred in 53% (72/136) of horses.
- Median length of time recorded in remission was 9.5 weeks.
- Horses were significantly more likely to go into remission at the end of the first three-procedure course if they went into remission after the first procedure and second procedures, but horses could still respond if the first procedure was unsuccessful.

The safety and efficacy of neuromodulation using percutaneous electrical nerve stimulation for the management of trigeminal-mediated headshaking in 168 horses
evj 20

Question 51

Which of the following conclusions can be drawn from one study on computed tomography (CT) findings in 101 horses with headshaking?

A) CT examination is highly effective in diagnosing the cause of headshaking, and it can replace other diagnostic tools.
B) CT revealed causative pathology in only a few cases, and the study emphasizes that headshaking is most commonly due to trigeminal-mediated causes, requiring exclusion of other conditions.
C) CT identified significant differences in the proximity of maxillary cheek teeth to the infra-orbital canal between headshaking and non-headshaking horses.
D) The study concluded that CT imaging should not be used for investigating headshaking in horses due to its high diagnostic yield.

Answer 51

Answer: B) CT revealed causative pathology in only a few cases, and the study emphasizes that headshaking is most commonly due to trigeminal-mediated causes, requiring exclusion of other conditions.

Computed tomographic findings in 101 horses presented for the investigation of headshaking
eve 22

Question 52

A 9-year-old gelding presents to your clinic with a history of intermittent headshaking, which worsens during exercise. The horse has been diagnosed with trigeminal-mediated headshaking, but the owner is concerned about the possibility of other underlying causes. You decide to investigate further by performing a CT scan of the horse’s head under standing sedation.

The CT reveals a periapical infection in one of the maxillary cheek teeth, which had not been identified by previous clinical examinations or radiographs. After appropriate treatment, the horse’s headshaking symptoms resolve.

Based on the study’s findings, which of the following is the most accurate conclusion regarding the use of CT in this case?

A) The CT scan would likely have identified the cause of the headshaking early, avoiding the need for further diagnostic workup.
B) The CT scan was useful in identifying an underlying pathology that was missed by other diagnostic tests, and treatment resolved the headshaking symptoms.
C) The CT scan would have been unlikely to detect any underlying pathology, as trigeminal-mediated headshaking is not associated with any structural changes in the head.
D) CT scans are not valuable in cases of headshaking, and the findings in this case are purely coincidental.

Answer 52

Answer: B) The CT scan was useful in identifying an underlying pathology that was missed by other diagnostic tests, and treatment resolved the headshaking symptoms.

Main results of the study :
- 70% gelding, mean age : 9 yo
- majority of idiopathic or trigeminal-mediated HSK (in this study)
- Main causes of HSK : periapical infections and fracture of the paracondylar process of the occipital bone
- Infra-orbital canal (IOC) assessment : morphological variations of the IOC on CT are common and not associated with HSK.
- No association between IOC compression by cheek teeth and HSK
- CT improved the diagnostic accuracy of HSK

Computed tomographic findings in 101 horses presented for the investigation of headshaking
eve 22

Question 53

A 10-year-old gelding is referred to your clinic for chronic head-shaking behavior. The signs seem to worsen when ridden and have been present for several months without significant improvement with conservative management. After conducting a detailed examination, you decide to perform a CT scan of the horse’s head. The CT scan reveals a temporo-mandibular joint arthritis. The horse is treated for the arthritis, and after a few weeks, the head-shaking symptoms completely resolve.

Based on the study’s findings, which of the following conclusions can be drawn from this case?

A) The CT scan was not useful in identifying the cause of head-shaking, as the diagnosis of trigeminal nerve-mediated head-shaking (TNMH) was already established.
B) The CT scan was instrumental in identifying a treatable primary condition (temporomandibular joint arthritis) that resolved the head-shaking signs.
C) CT is only useful for diagnosing sinusitis and dental issues, not musculoskeletal conditions like arthritis.
D) The CT scan likely identified a secondary condition unrelated to the head-shaking, and treatment would not resolve the symptoms.

Answer 53

Answer: B) The CT scan was instrumental in identifying a treatable primary condition (temporomandibular joint arthritis) that resolved the head-shaking signs.

This MCQ reinforces the idea that CT can help identify underlying conditions, such as temporomandibular joint arthritis, that can be treated to resolve head-shaking behavior in horses.

Computed tomography findings in horses presented with signs of head-shaking
evj 23

Question 54

Which of the following lesions, identified through CT imaging in horses with head-shaking, is considered clinically relevant and directly linked to the resolution of symptoms upon treatment?

A) Dental fracture
B) Basisphenoid fracture
C) Otitis externa
D) All of the above

Answer 54

Answer: D) All of the above

Explanation:
The study identified several clinically relevant primary conditions on CT that, when treated, led to the resolution of head-shaking symptoms, including:
- dental fractures,
- basisphenoid fractures,
- otitis externa,
- temporo-mandibular joint arthritis,
- nuchal bursitis (but not insertional entesopathy of the nuchal ligament),
- musculoskeletal pathologies,
- sinusitis (primary and secondary),
- mass affecting the IO nerve.

These conditions were linked to the improvement or resolution of the horse’s head-shaking behavior following treatment.

Computed tomography findings in horses presented with signs of head-shaking
evj 23

Question 55

What is the lesion identified on the CT ? Is this relevant in the context of HSK ?

Answer 55

Transverse image of the head at the level of 09s maxillary cheek teeth. There is gas within the infundibulum of both 109 and 209 (arrows). This is considered an incidental finding.

Computed tomography findings in horses presented with signs of head-shaking
evj 23

Question 56

What is the lesion identified on the CT ? Is this relevant in the context of HSK ?

Answer 56

Transverse image at the level of the mandibular 08s cheek teeth. There is a complete longitudinal fracture along 308 (arrowheads), dividing it into two big fragments and exposing the pulp canals that show a heterogeneous appearance with gas.
Clinically relevant

Computed tomography findings in horses presented with signs of head-shaking
evj 23

Question 57

What is the lesion identified on the CT ? Is this relevant in the context of HSK ?

Answer 57

Transverse (B) and dorsal (C) images of the head of a horse with marked enlargement of the left infraorbital nerve (white arrows) that is causing expansion and thickening of the infraorbital canal wall.
Clinically relevant

Computed tomography findings in horses presented with signs of head-shaking
evj 23

Question 58

What is the lesion identified on the CT ? Is this relevant in the context of HSK ?

Answer 58

Transverse image at the level of the tympanic bulla of a horse with a soft tissue attenuating mass within the left external ear canal with secondary otitis media and externa (black arrows).
Clinically relevant.

Computed tomography findings in horses presented with signs of head-shaking
evj 23

Question 59

A study on horses with primary or secondary dental sinusitis assessed the relationship between infraorbital canal (IOC) pathology and the occurrence of headshaking behavior. Based on the findings, which of the following statements is correct?

A) Most horses with dental sinusitis did not exhibit IOC pathology on CT scans.
B) A significant correlation was found between the presence of IOC pathology and the occurrence of headshaking behavior.
C) The majority of horses with dental sinusitis showed common CT findings such as hyperostosis, periosteal proliferation, and osteolysis.
D) Follow-up results revealed that most horses with IOC pathology exhibited headshaking behavior five or more years after diagnosis.

Answer 59

Answer:
C) The majority of horses with dental sinusitis showed common CT findings such as hyperostosis, periosteal proliferation, and osteolysis.

Explanation:
- Option A is incorrect because 65 out of 66 horses (98.5%) with dental sinusitis showed IOC pathology on CT scans.
- Option B is incorrect because the study found no significant correlation between IOC pathology and headshaking behavior.
- Option C is correct. Hyperostosis, periosteal proliferation, and osteolysis were common CT findings, observed in 85-86% of cases.
- Option D is incorrect because only five horses (8%) showed headshaking behavior after follow-up, and there was no strong correlation with IOC pathology.

Photo : CT of IOC pathology with sinusitis, not correlated with HSK

The prevalence of headshaking in horses with primary and secondary dental sinusitis and computed tomographic evidence of infraorbital canal pathology
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Question 60

What is the prevalence of infraorbital canal changes on CT in horses with sinusitis (primary or sencondary to dental disease) ?

Answer 60

A total 65 out of 66 horses (98.5%) diagnosed with primary or secondary dental sinusitis demonstrated IOC changes on CT.

The prevalence of headshaking in horses with primary and secondary dental sinusitis and computed tomographic evidence of infraorbital canal pathology
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Question 61

What is the best tool to objectively evaluate the severity of HSK ?

Answer 61

History, Rest and Exercise Score (HRE-S) consists of three subscores: history score (H-S), resting score (R-S) and exercise score (E-S).
Reliability for HRE-S was excellent, irrespective of observers experience. HRE-S is a valid and reliable score evaluating disease severity in TMHS, independent of observers’ experience.

History, Rest and Exercise Score (HRE-S) for assessment of disease severity in horses with trigeminal-mediated headshaking
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Question 62

Right or wrong ?

1. In the equine population, trigeminal-mediated headshaking is less prevalent compared to photic HSK.
2. Trigeminal neuropathic pain refers to a structural lesion of the trigeminal nerve that is rarely identified post-mortem.
3. Computed tomography changes involving the IO canal cannot predict HSK behaviors in sinusitis secondary to dental disease.

Answer 62

1. Wrong, trigeminal-mediated HSK > 90% cases.
2. Wrong, functionnal rather than structural changes
3. Right, abnormalities are frequent but the clinical significance is unknown.

Question 63

Among the following lesions, which one(s) is/are clinically relevant as primary cause of HSK ?
a- entesopathy of the nuchal ligament
b- enlargement and thickening of the IO nerve
c- otitis media/otitis externa
d- cyst-like lesion of the mandibular condyle
e- primary sinusitis

Answer 63

Among the following lesions, which one(s) is/are clinically relevant as primary cause of HSK ?
a- entesopathy of the nuchal ligament → not in the study of Perrier et al
b- enlargement and thickening of the IO nerve
c- otitis media/otitis externa
d- cyst-like lesion of the mandibular condyle
e- primary sinusitis

Question 64

Owners often claim that seizures are worse at night, what do you suspect?

Answer 64

Vestibular disease

During acute severe vestibular disease, the animal might collapse to one side and be unable to stand despite repeated attempts. If this is the case, obvious nystagmus is present and animals often paddle and trash in attempts to stand. This constellation of signs is often confused with “seizures”.

The clinician can attempt carefully to blindfold or move the animal to a darker area to see if vestibular signs develop. The author does not recommend to blindfold an animal that has obvious vestibular disease.

Question 65

Prognosis of vestibular diseases?

Answer 65

The author recommends practicing caution when considering euthanasia based on severity of signs, because horses might improve depending on cause, anatomic region affected, treatment, and stabilization of signs over time.
Some horses might fully recover.

Provide early supportive or specific treatment, and giving time.

Use of animal lift device in the acute phase of vestibular disease?
Mild intravenous (IV) sedation and keeping the lights on might aid in the management of these cases

Question 66

Difference between unilateral and bilateral vestibular diseases?

Answer 66

Unilateral vestibular disease are ipsilateral to the side of the lesion and include nystagmus (usually both eyes), ventrolateral strabismus (CN III), head tilt, leaning, drifting, tight circles, and ataxia.

Bilateral vestibular disease → wide-based stance, no head tilt, no leaning or drifting, no circling, and lacks both physiologic and pathologic nystagmus. The head in these horses can slowly oscillate or move horizontally like in a pendular fashion from side to side. When horses get startled or try to initiate movement they might lose balance and adopt a wide-based stance. Horses might carry their neck and thorax slightly lower with thoracic limbs abducted in apparent attempts to balance themselves.

Horses with bilateral THO display signs of vestibular disease in the side more severely affected. However, some cases display bilateral vestibular disease as described earlier (no nystagmus, no head tilt, no leaning or circling).

These horses can look like cervical vertebral compressive myelopathy; however, a clue of having bilateral vestibular disease is the lack of physiologic nystagmus.

Question 67

Which nerves are affected with THO?

Answer 67

Cranial nerves: facial, vestibular, and cochlear.

Owing to the anatomy of the temporohyoid joint, alterations in this area result in auditory loss (first alteration), then facial and vestibular deficits.

Other CN deficits → central VD

Question 68

Treatment of THO ?

Answer 68

The best results have been reported with surgical management (ceratohyoidectomy) with some cases with complete resolution of signs and return to previous physical activity.

However, auditory loss seems to be a permanent deficit based on long-term follow up.

It is the opinion of the author that THO is the end result of various causes such as infection of the inner ear, guttural pouch infection, trauma, degenerative joint disease, and a possible component of genetic predisposition in QH (more than 50% have bilateral disease).

Question 69

Peripheral vestibular disease : when could you suspect a THO vs infection?

Answer 69

THO are on average mature adults

Those with historical or recent unilateral ear infection seem to be younger.

Photo : Foal with left peripheral vestibular disease due to otitis media-interna. Note left head tilt and mild ventral strabismus of the left eye.

Question 70

THO predisposed by?

Answer 70

Fracture of the hyoid apparatus and cribbing

Question 71

Gentamicin toxicity what do you think about?

Answer 71

Reported toxic effects of gentamicin include nephrotoxicity, vestibulotoxicity, and cochleotoxicity.

Healthy adult horses using approved dosage of IV gentamicin for 7 consecutive days and found no nephrotoxic or vestibulotoxic effects. However, auditory loss developed in 7 of 10 horses, which was irreversible in 3 horses.
Sensorineural auditory loss was suspected.

Gentamicin-induced sensorineural auditory loss in healthy adult horses
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Question 72

Paradoxical vestibular disease, which signs?

Answer 72

The cerebellum provides ipsilateral inhibition to extensors; its dysfunction leads to contralateral leaning .

These animals present signs of cerebellar and vestibular disease concurrently.

In paradoxic vestibular disease, the signs are contralateral to the side of injury.

The cerebellum normally provides ipsilateral inhibitory input to the extensors. If the cerebellum is affected, the ipsilateral inhibitory input to the extensors will be absent or decreased resulting in tilting and leaning contralateral to the side of the lesion.

These animals present signs of cerebellar and vestibular disease concurrently. Other cerebellar signs are ipsilateral, and the resulting vestibular signs are contralateral to the side of the lesion.

Question 73

When to suspect an idiopathic vestibular disease?

Answer 73

Idiopathic vestibular disease diagnosis requires excluding other causes.
Guttural pouch endoscopy and cross-sectional imaging (computed tomography)
CSF analysis → for S. neurona or bacterial meningoencephalitis
Infectious and inflammatory diseases can affect the vestibular system and mimic peripheral disease.

Question 74

What are the clinical signs of peripheral or central vestibular disease?

Answer 74

Central and peripheral = nystagmus, strabismus, head tilt, leaning/circling, and ataxia

Only central = vertical nystagmus, dysconjugate nystagmus, positional nysgtamus or spontaneous change of direction. Proprioceptive ataxia.

Question 75

What are the common etiologies of vestibular disease ?

Answer 75

Peripheral VD :
- THO (most common cause of PVD, photo)
- Otitis media / interna (bacterial, viral, fungal,+/- parasitic, neoplasia)
- Trauma (fracture the petrous temporal bone)
- Idiopathic

Central VD (brainstem disease) :
- Trauma (common basilar skull bone fracture when horse flips over backwards)
- Infectious :
* Parasitic (EPM → most common cause of VD in USA, Halicephalobus gingivalis → aberrant parasite migration)
* Bacteria (meningitis, meningoencephalitis, neuroborreliosis, equine brain abscess)
- Neoplasia

Vestibular disease in horses: Recognition, localisation and common causes
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Question 76

What are the clinical presentations of rabies ?

Answer 76

“Rabies can look like anything”

• Paralytic form (SC) : weakness, lamenes,, paresis, ascending paralysis
• Dumb form (brainstem) : lethargy, anorexia, head tilt, nystagmus, ataxia, dysphagia, hypersalivation, urinary and fecal incontinence
• Furious form (encephalitis) : aggression, photophobia, hyperesthesia, ataxia, muscle tremors, self-mutilation (donkeys ++), opisthotonos

Question 77

What about antibiotics and tetanus?

Answer 77

penicillin has the capacity to augment inhibitory effects on the neurotransmitter GABA potentially exacerbating the toxic effects of tetanospasmin.

Therapy with metronidazole has been compared with penicillin for treatment of tetanus in people; results suggest that metronidazole yields superior results. Based on these data, metronidazole (25 mg/kg orally [PO] every 12 hours or 10–20 mg/kg IV every 6 to 8 hours) could be considered an alternative to penicillin in treatment of equine patients.
The expense of IV metronidazole formulation may limit its clinical utility to the treatment of foals. Metronidazole may also be administered per rectum (50 mg/kg every 12 hours) if the affected patient is unable to swallow.

In recumbent horses at risk for developing aspiration pneumonia -> Broad spectrum antimicrobial drugs that might be effective for the treatment of both tetanus and resultant aspiration pneumonia in recumbent horses include ceftiofur sodium and oxytetracycline.
The clinician should consider risks of antimicrobial-associated colitis when formulating a treatment plan, particularly as these risks can vary geographically.

Question 78

What are the major viruses causing encephalitis in horses ?

Answer 78

• Herpesviridae : EHV-1
• Rhabdoviridae : lyssavirus → rabies
• Flaviviridae : flavivirus (WNV, USUV, TBEV..)
• Bornaviridae : Bornavirus 1
• Togaviridae : alphaviruses (EEEV, WEEV, VEEV)

Question 79

What about immunization and tetanic horse?

Answer 79

The dose of tetanus toxin that is required to induce disease is so low that it is insufficient to initiate an anamnestic response on its own, rendering recovered, unvaccinated horses susceptible to reinfection once TAT antibodies have been bound or cleared from the body

Question 80

1.

Prognosis of tetanus?

Answer 80

Guarded to poor, especially for recumbent animals.
Horses that are able to stand, drink, and eat voluntarily before therapeutic intervention have a significantly better prognosis for survival.
Mortality is estimated at 54% to 80%.
Mortality increased to 94% for horses with severe or terminal signs of disease.
Another study found that, of horses that were presented with dysphagia, 87% did not survive.

Significant association between survival and prophylactic vaccination
within the prior 12 months -> 75% survival (mild mod CS).

The same study reported similar mortalities between affected foals (66.7%) and adults (68.4%).
Evidence is conflicting on whether the dose of TAT affects survival rate.
Most equids that do survive treatment have the potential to fully recover. In one retrospective study, 93.8% of surviving horses had recovered completely.

Reported sequelae included ataxia and unspecified lameness.

Question 81

What are the protocols for vaccination of tetanus?

Answer 81

A tetanus toxoid vaccine for horses is available (Tetanus Toxoid, Zoetis Animal Health,
Parsippany NJ, USA). Naı¨ve adults should initially receive 2 doses 4 to 6 weeks apart
with annual vaccinations following.36 Broodmares should be vaccinated as normal
adults and boostered 4 to 6 weeks prepartum. Foals born to vaccinated mares should
undergo a 3-dose series: once at 4 to 6 months of age; once 4 to 6 weeks after the first
dose; and once at 10 to 12 months of age.36 Foals from unvaccinated mares should
have a similar schedule, but with the first dose at 3 to 4 months of age.36 An additional
booster around incidents that could lead to a clinical case (eg, puncture wound, surgery)
is recommended as well. Kendall and colleagues37 studied a population of horses
in Sweden that were treated with a tetanus toxoid (Equilis Pretenza Te, Intervet AB,
Stockholm, Sweden) once at 5 to 11 months of age, again 4 weeks after the initial
dose, and then a third dose 15 to 17 months after the second dose. Antibody titers
against tetanus remained above detectable levels in nearly all studied horses after
3 years. Although the study’s findings suggest that vaccine recommendations can
be revised, the American Association of Equine Practitioners (AAEP) currently recommends
that adults be vaccinated annually.

Question 82

What could be related from the owner that will induce suspicion of botulism?

Answer 82

In the very acute or mild case, owners may note that the animal takes longer than “normal” to consume its concentrate

Question 83

You suspect a boltulism case, the horse is tachypneic, what is your opinion?

Answer 83

Affected horses may be dehydrated, as some lose the ability to consume water.
Heart rate can be normal or elevated if dehydration or stress is present. Respiratory rate can be normal but may be decreased as the diaphragm weakens. Tachypnea can be found in horses with concurrent respiratory disease, such as aspiration pneumonia, which is a common sequela to dysphagia.

Question 84

Which muscles groups are mostly affected in botulism?

Answer 84

These muscle groups include those of the tongue, eyelids, tail, and anal sphincter. Muscle groups with relatively high requirements for acetylcholine (Ach) tend to become affected earlier than other groups.

Question 85

Do foals could be affected by botulism?

Answer 85

yes. Clinical signs in foals may appear first as muscle fasciculations, which may become
coarse and involve the entire body. common name “shaker foal syndrome.” These foals can tire and lay down, only to
regain their strength and stand again like affected adults. They too can cycle through
standing and recumbency.

Question 86

How to diagnose botulism?

Answer 86

Complete blood count is usually within normal limits,
although concurrent infection (eg, aspiration pneumonia) may cause changes within the leukogram. Serum biochemistry analysis (SBA) may yield normal findings. However, in some cases of botulism, SBA abnormalities can develop because of secondary disease. Elevations in muscle enzymes are expected if the equid has been recumbent, has had difficulty standing, or is showing signs of colic. Electrolyte disturbances and/ or azotemia may be present if the horse has been dysphagic or unable to drink for an extended period. Endoscopic examination should be performed in horses with
dysphagia to rule out abnormalities within the nasopharynx. Examination of the oral cavity is recommended to rule out dental disease, oral foreign bodies, or tongue abscessation as causes of dysphagia. Cerebrospinal fluid analysis is expected to yield normal results in horses with botulism.
Additional laboratory diagnostics can be used to support the clinical diagnosis of botulism through finding the preformed BoNT or BoNT-producing clostridial organisms in foodstuffs, serum, gastrointestinal tract, or wounds of an affected animal, or detection of serum antibodies against the causative clostridial organisms. A mouse bioassay is currently considered the gold-standard diagnostic for detection of botulism; the assay has a high specificity (97% in one study). In this test, serum from the affected patient is injected into naı¨ve and vaccinated mice, and they are monitored for clinical disease. However, because horses are much more sensitive to BoNT than mice, false-negative results can occur if concentrations are less than the threshold of disease. The low sensitivity (32%) presented by Johnson and colleagues reflects the challenges associated with the mouse bioassay technique. Enrichment cultures can improve the sensitivity of the assay. Unfortunately, the mouse bioassay can take several weeks to yield results.
Detection of BoNT via enzyme-linked immunosorbent assay is possible, but these assays have not yet been validated in the horse.27 Quantitative real-time PCR for BoNT genes has been developed and offers a sensitivity of greater than 88% and
specificity of greater than 98% for BoNT types A, B, and C. In the United States, fecal or feed samples should be submitted to the National Veterinary Services Laboratory in Ames, Iowa. Botulism spores are rarely found in fecal samples from normal
horses, and their detection in feces from suspect cases may be useful. Spores were found in 70% of “shaker foal” fecal samples in one study.

Question 87

dx tetanus?

Answer 87

The small infective dose
required to induce clinical disease in horses heightens the difficulty in isolatingneurotoxins. Successful culture of C tetani from wounds in affected horses has been
reported, but anaerobic culture methods did not yield growth of C tetani in 46% to
70% of cases in people.16,20,21 Gram-stain smears of infected wounds can be attempted,
but spores have been reported in only a minority of cases. Moreover, the similar
morphologic appearance of other clostridial spores lessens the utility of this diagnostic
technique. A real-time polymerase chain reaction (PCR) assay has been developed for
detection of the C tetani neurotoxin gene, facilitating rapid diagnosis in people.22 This
assay is not readily available in veterinary medicine. Antemortem diagnosis is typically
presumptive based on history, physical examination findings, and clinical signs. Identification
of a penetrating or infected wound, especially in an unvaccinated horse,
should increase clinical suspicion of tetanus. Because tetanus is identified as a diagnosis
of exclusion, efforts to rule out differential diagnoses should be made. Disease
states that might result in a similar clinical picture include rabies, strychnine intoxication,
exertional rhabdomyolysis, and myositis.
Clinicopathologic findings in patients with tetanus are generally nonspecific unless
secondary disease is present. Increases in inflammatory markers (white blood cell
count, fibrinogen, serum amyloid A) may be present secondary to wound infection
or concurrent pneumonia. Increases in muscle enzymes (creatine kinase, aspartate
aminotransferase) can be observed secondary to damage caused by wound infection
or recumbency. Cerebrospinal fluid analysis and advanced imaging techniques
(computed tomography, MRI) are expected to yield normal findings.
On postmortem examination, abnormal findings are associated with secondary
complications, including pneumonia, intramuscular (IM) hemorrhage, and decubital ulceration.
Again, identification of tetanus toxins is hampered by the small amount of
toxin needed to induce disease. Of 28 adult horses and foals with presumed tetanus,
definitive diagnosis via postmortem examination was not achieved in any of the cases
in one retrospective

Question 88

```

Treatment of botulism

Answer 88

Treatment
The most important and time-sensitive treatment for botulism is neutralization of circulating BoNT. Through administration of botulism antitoxin, circulating BoNT can be bound and eliminated before translocation into cells. Thirty-thousand IU for a foal or 70,000 IU for an adult can provide protection for 60 days. As the antitoxin only binds free BoNT, that which has entered cells can cause clinical signs to worsen for the following 12 to 24 hours. Although expensive, currently available antitoxins include polyvalent (bivalent for types A and B; Sanofi Pasteur Ltd, Toronto, Ontario, Canada; trivalent for types A, B, and C; Lake Immunogenics, Ontario, NY, USA) and monovalent (type B; EquiPlas, PlasVacc, Templeton, CA, USA; ImmunoGlo, Mg Biologics, Ames, IA, USA).
Elimination of causative organisms is important in cases of toxicoinfectious and wound botulism. Some medications can potentiate neuromuscular weakness (aminoglycosides,
procaine penicillin, tetracyclines) and should therefore be avoided. Potassium penicillin or a cephalosporin may therefore be the best antimicrobial option for treatment in these horses.
Concurrent diseases should also be managed in botulism cases. Broad-spectrum antibiotics are indicated for aspiration pneumonia. Mineral oil and/or cathartics may prevent impactions or can be treatments in actively colicking horses. Nutrition and hydration are essential factors to consider in botulism cases, as most become dysphagic and are unable to adequately eat or drink. Feeding tubes can be used to provide sufficient amounts of water and complete enteral nutrition products (Well-Gel; Purina Animal Nutrition; Platinum Enteral Immunonutrition Formula; Platinum Performance).
IV fluids and/or parenteral nutrition may need to be used in patients that cannot tolerate enteral feeding owing to ileus or lateral recumbency.
Supportive nursing care for equids that become recumbent can be time-consuming, expensive, and labor intensive, but is critical. Provision of supportive nursing care includes moving the equid to prevent decubital ulceration and compartment syndrome, alternating recumbency every 3 to 4 hours to minimize lung consolidation, and sedation to control excessive thrashing. This may be difficult to achieve in many horses but can be successful in foals. A sling might be necessary to lift some affected horses but should not be used tomaintain the horse in the standing position, as this can hasten exhaustion
and can also impede respiration. Severely affected horses may experience such profound respiratory depression that mechanical ventilation becomes necessary.

Question 89

Prognosis of botulism?

Answer 89

• depend on the amount of toxin absorbed or ingested.
• Toxin type may affect prognosis
• Recovery takes at least 7 to 14 days and is dependent on construction of new neuromuscular endplates.
• Dysphagia may take 2 to 14 days to resolve
• The time until full-muscle recovery may be 1 month.
• horses that arrived standing had a 67% rate of survival;
• those that remained standing during hospitalization had a 95% rate of survival.
• Overall survival rates in outbreakand hospitalized cases : 10%–48%
• Complications: pneumonia, diarrhea, and decubital ulceration, occurred in 62% of affected horses in one study, but these complications were not associated with nonsurvival.
• Treatment of foals -> more successful -> survival rate of 96% of treated cases and 90% overall.
• **30% of foals required mechanical ventilation. 87.5% mechanically ventilated foals with botulism survived to discharge. **
• Mechanical ventilation of an adult horse with presumed botulism has been described. Although the horse was successfully weaned off mechanical ventilation after 2 weeks of therapy, euthanasia became necessary when large colon volvulus developed several days later.

Question 90

Prevention of botulism?

Answer 90

A BoNT type B toxoid vaccine is available (BotVax B; Neogen, Lansing, MI, USA). The AAEP recommends annual vaccination of adult horses.

Unvaccinated adults need a 3-dose series, each 1 month apart.
Broodmares should receive a booster 4 to 6 weeks before parturition.

Foals born from vaccinated mares should be given the 3-dose series at 4-week intervals starting at 2 to 3 months of age and then boostered annually.
Foals from unvaccinated mares should receive the same initial 3-dose series, but at 1 to 3 months of age.
As the vaccine targets type B, cross-protection against other types is not guaranteed.
Foals who suffer from failure of transfer of passive immunity should be treated accordingly to ensure that they acquire an adequate serum immunoglobulin G concentration.
Eliminating possible exposures is also key in prevention.

This can be completed via ensuring that hay and feed are of good quality and free of contamination from decaying debris; storing foodstuffs appropriately; and inspection of water sources and pastures for dead animals.

Question 91

What is the difference between eNAD and EDM in terms of histopathologic lesions?

Answer 91

eNAD if the histopathologic lesions were confined to the brainstem, specifically within the lateral cuneate, medial cuneate, and gracilis nuclei,
EDM was assigned when axonal necrosis and demyelination extended into the dorsal and ventral spinocerebellar tracts and ventromedial funiculi of the cervicothoracic spinal cord.

Question 92

What are the typical clinical signs of eNAD/EDM in most breeds?

Answer 92

In most breeds, eNAD/EDM is characterized by symmetric ataxia, abnormal basewide stance at rest and proprioceptive deficits in all limbs, signs that can develop from a few weeks to 3 years of age, although most horses develop clinical signs by 6 to 12 months of age. The ataxia is often more severe in the pelvic limbs than the thoracic limbs.

Question 93

How does the clinical presentation of eNAD/EDM differ in Warmbloods compared to other breeds?

Answer 93

In Warmbloods, eNAD/EDM is often recognized in older horses (5-15 years), with abnormal behavior under saddle, changes in demeanor, and abnormal interactions. These horses often display gait and stance abnormalities consistent with mild to moderate proprioceptive ataxia, most commonly graded 1 to 2/5 on the modified Mayhew scale.

Question 94

What was the estimated heritability of eNAD/EDM in Quarter Horses?

Answer 94

In a family of clinically phenotyped QHs with eNAD/EDM, sharing the same underlying risk factor of α-tocopherol deficiency, heritability was estimated at 70%.

Question 95

Which gene was excluded as a candidate for eNAD/EDM in Quarter Horses?

Answer 95

The candidate gene TTPA=a-tocopherol transfer protein gene (TTPA) was excluded in eNAD/EDM in a family of QHs.

downregulation of glutamate receptor and synaptic vesicle tracking pathways was identified.Cholesterol biosynthesis pathways were also downregulated, with the evidence of upregulation of a specific nuclear transcription factor, the liver X receptor.

Question 96

How did vitamin E supplementation affect the incidence of eNAD/EDM in susceptible foals?

Answer 96

It has been demonstrated that, during the first year of life, vitamin E supplementation of genetically susceptible foals (from a dam/sire that produced affected foals), lowers the overall incidence (40% to 10%) and severity of eNAD/EDM.

Question 97

How is eNAD/EDM definitively diagnosed?

Answer 97

At present, definitive diagnosis of eNAD/EDM is only possible on postmortem histologic evaluation of spinal cord and brainstem tissue.

Question 98

What is the sensitivity and specificity of serum pNfH concentrations greater than 1 ng/mL for diagnosing eNAD/EDM?

Answer 98

Serum pNfH concentrations greater than 1 ng/mL were significantly associated with eNAD/EDM, with only 12% sensitivity but 99% specificity.

Question 99

What is the recommended vitamin E supplementation protocol for preventing eNAD/EDM in susceptible horses?

Answer 99

In families of horses in which eNAD/EDM has been diagnosed, supplementation of pregnant broodmares and foals with α-tocopherol at 10 IU/kg PO once daily during the last trimester (mares) and first 2 years of life (foals) is advisable.

Question 100

How effective is empirical α-tocopherol treatment for horses suspected of having eNAD/EDM?

Answer 100

Horses suspected of having eNAD/EDM are often treated empirically with α-tocopherol; however, this rarely results in any improvement of neurologic status.

Question 101

Is there any way to improve bioavailability of ponazuril?

Answer 101

Coadministration of ponazuril with 2 oz of corn oil resulted in higher concentrations of ponazuril in serum (at steady state) than that found in horses given ponazuril alone.
Cerebrospinal fluid concentrations of ponazuril were also greater in horses that received ponazuril and oil.

Conclusions and Clinical Importance: Results suggest that coadministration of corn oil with ponazuril might enhance the effectiveness of treatment with ponazuril

Effects of coadministration of corn oil and ponazuril on serum and cerebrospinal fluid concentrations of ponazuril in horses
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Question 102

What are the negative prognostic factors for a return to sport in horses with EHM? (several answer)
- Urinary complications
- Vascular complications (vasculitis)
- Ataxia grade ≧ 4/5
- Ataxia grade ≧ 3/5
- Lymphopenia
- Neutrophilia
- Neuropathogenic genotype

Answer 102

• Horses with an ataxia grade at admission ≥4/5 had an increased fatality rate and 10% chance of reaching their preoutbreak performance level.
• None of the horses with both vascular and urinary complications returned to their previous performance level.
• Overall, horses affected by EHM had 68% chance of returning to exercise.

Long-term performance of show-jumping horses and relationship with severity of ataxia and complications associated with myeloencephalopathy caused by equine herpes virus-1
jvim 2024

Question 103

Based on the findings in the study of CT myelography of the cervical spine in horses, which of the following statements is most accurate?

A) Degenerative joint disease was identified in fewer than 50% of horses.
B) Spinal cord compression was observed in more than half of the horses (31/51).
C) The CT myelography technique was found to be unsafe for clinical use in horses.
D) Osteochondral fragments were observed in the majority of horses (over 50%).

Answer 103

Correct Answer:

B) Spinal cord compression was observed in more than half of the horses (31/51).

Explanation:
- Option A is incorrect: Degenerative joint disease was identified in 50/51 horses, which is more than 50% of the horses.
- Option B is correct: The study found spinal cord compression in 31/51 horses, which is greater than half of the horses studied.
- Option C is incorrect: The abstract mentions that CT myelography is a relatively safe and easily performed technique when the correct equipment is used.
- Option D is incorrect: Osteochondral fragments were seen in 11/51 horses, which is less than 25% of the horses studied, not the majority.

Computed tomography myelography is relatively safe and an easily performed technique with the correct equipment, enabling evaluation of the cervical vertebral structures of horses in all planes and volumetrically.
It is possible that lesion extent might be underestimated with this diagnostic modality, hence interpretation should be complimented with flexed and extended views radiographically.

Computed tomographic cervical myelography in horses: Technique and findings in 51 clinical cases
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Question 104

According to the study comparing transcranial magnetic stimulation (TMS), cervical radiography, and neurological examination for diagnosing spinal cord dysfunction in horses, which of the following statements is most accurate?

A) Cervical radiography showed the highest sensitivity and specificity for detecting spinal cord dysfunction in horses.
B) Transcranial magnetic stimulation (TMS) had the lowest specificity for detecting spinal cord dysfunction.
C) Neurological examination had a sensitivity of 97.6% and was found to be the most accurate diagnostic test.
D) The best diagnostic approach for spinal cord dysfunction in horses was a combination of neurological examination (highest sensitivity) followed by confirmation with TMS-MMEP (highest specificity).

Answer 104

D) The best diagnostic approach for spinal cord dysfunction in horses was a combination of neurological examination (highest sensitivity) followed by confirmation with TMS-MMEP (highest specificity).

Explanation:

• Option A is incorrect: The study found that cervical radiography had lower sensitivity (43%) and performed the poorest compared to other diagnostic tests.
• Option B is incorrect: TMS had the highest specificity (97.4%) among the tests evaluated, not the lowest.
• Option C is incorrect: Although neurological examination had the highest sensitivity (97.6%), it was not the most accurate test overall. TMS had the highest specificity and accuracy in diagnosing spinal cord dysfunction.
• Option D is correct: The study concluded that the optimal diagnostic strategy would be to use neurological examination first (due to its high sensitivity) and confirm the diagnosis with TMS-MMEP (due to its high specificity). This combination provided the most reliable diagnosis.

Accuracy of transcranial magnetic stimulation and a Bayesian latent class model for diagnosis of spinal cord dysfunction in horses
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Question 105

Based on the findings in the study of sidewinder gait in horses, which of the following statements is most accurate?

A) The study found that sidewinder gait in horses is only associated with neurologic causes.
B) Electromyography and muscle biopsy were not helpful in localizing the site of lesion in horses with sidewinder gait.
C) Sidewinder gait is most commonly observed in younger horses and typically has a favorable prognosis.
D) The condition had a high case fatality rate, with 79% of horses experiencing a poor prognosis for function and life.

Answer 105

D) The condition had a high case fatality rate, with 79% of horses experiencing a poor prognosis for function and life.

Explanation:

• Option A is incorrect: The study found both neurologic and non-neurologic causes for sidewinder gait, including spinal cord compression, equine protozoal myeloencephalitis, and musculoskeletal issues like osteoarthritis and pelvic fractures.
• Option B is incorrect: Electromyography and muscle biopsy were helpful in diagnosing neurologic causes and further localizing the site of lesion in horses with sidewinder gait.
• Option C is incorrect: Sidewinder gait was most commonly observed in older horses (mean age 18.9 years), not younger ones, and the prognosis was poor, not favorable.
• Option D is correct: The study found that sidewinder gait had a high case fatality rate of 79%, with many horses having a poor prognosis for both function and life.

Sidewinder gait is usually observed in older horses and can have neurologic or musculoskeletal etiologies. Electromyography can be used as a diagnostic aid to determine neurologic versus non-neurologic disease and further localize those of neurologic origin.
The condition often has a poor prognosis for function and life.

Sidewinder gait in horses
jvim 20

Question 106

Cerebrospinal fluid collected from the C1-C2 space had significantly higher protein concentrations and red blood cell counts than fluid collected from the lumbosacral (LS) space.

• True
• False

Answer 106

False

Explanation:
The study found that CSF collected from the C1-C2 space had significantly lower protein concentration and red blood cell count compared to CSF from the LS space.

Cerebrospinal fluid from the C1-C2 space provides an acceptable alternative to LS CSF collection with decreased likelihood of clinically important blood contamination of samples.
Collection time, total nucleated cell count, EPM titers, and serum:CSF EPM titer ratios were not significantly different
between collection sites.

Comparison of 2 collection methods for cerebrospinal fluid analysis from standing, sedate adult horses
jvim 20

Question 107

Repeat cerebrospinal fluid (CSF) collection from either the lumbosacral (LS) or C1-C2 space 14 days apart does not significantly affect CSF analytes such as protein concentration, nucleated cell count, or EPM titers.

• True
• False

Answer 107

True

Explanation:
The study found no significant difference in CSF analytes (including protein concentration, nucleated cell count, and EPM titers) when cerebrospinal fluid was collected from the LS or C1-C2 spaces 14 days apart.
This indicates that repeat thecal puncture does not significantly affect subsequent CSF analysis in healthy horses.

The effect of prior thecal puncture on cerebrospinal fluid analytes in normal adult horses
jvim 20

Question 108

What are the common causes of facial nerve paralysis (FNP) in horses (postanesthetic excluded) ?

Answer 108

Summary of Common Etiologies:
1. Trauma
2. CNS disease (e.g., infections, tumors, strokes)
3. Idiopathic (no clear cause after investigation)
4. Temporohyoid Osteoarthropathy
5. Otitis Media-Interna
6. Iatrogenic (due to medical or surgical intervention)
7. Clostridial Myositis
8. Lymphoma

These etiologies encompass both neurologic and non-neurologic causes, with trauma being the most common in equids. Treatment and prognosis often depend on the underlying cause and the presence of concurrent conditions.

If FNP is the consequence of CNS disease, successful treatment of the primary disease likely leads to resolution of FNP. Most cases of FNP in equids are traumatic in origin. True idiopathic cases are uncommon.

Facial nerve paralysis in 64 equids: Clinical variables, diagnosis, and outcome
jvim 20

Question 109

A 4-month-old male Arabian foal was presented to the veterinary clinic with concerns of progressive incoordination and abnormal gait noted by the owner. The foal had been otherwise healthy since birth, but the owner observed that the foal was increasingly unable to coordinate its movements, especially when trying to stand or walk after short periods of rest.
The foal was described as having difficulty standing after lying down, a wide-based stance, and stumbling while attempting to walk. The owner also noticed that the foal appeared to have a head tilt and exhibited tremors when attempting to eat or drink from the ground.

**Clinical hypothesis ? **

Answer 109

1. Cerebellar Abiotrophy (CA): Given the age of the foal (4 months) and the progressive nature of the ataxia, CA is a likely diagnosis. This condition is common in Arabian horses, where affected foals show cerebellar degeneration, resulting in poor motor coordination.
2. Viral Encephalitis (e.g., EEE, WNV, EHV): Infections causing CNS disease could result in ataxia; however, these typically present with more acute onset and may involve other signs like fever, depression, and cranial nerve deficits.
3. Trauma (e.g., spinal cord injury): Could cause ataxia, but there was no history of trauma, and the foal’s signs appear to be more consistent with cerebellar dysfunction.
4. Metabolic Disorders (e.g., Hypoglycemia): Could present with incoordination and weakness, but would not cause progressive cerebellar signs.

Question 110

What is cerebellar abiotrophy ?

Answer 110

Definition:
Cerebellar Abiotrophy (CA) is a genetic, neurodegenerative disorder affecting the cerebellum, leading to progressive ataxia, coordination deficits, and motor dysfunction due to cerebellar degeneration.

Etiology:
- Hereditary condition, most commonly seen in Arabian horses, though it can also affect other breeds.
- Mutation in the target of EGR1 (TOE1) gene
- Autosomal recessive inheritance

Clinical Signs:
- Ataxia (most pronounced in the hind limbs).
- Hypermetria (exaggerated movement, especially in the forelimbs).
- Head tremors (especially when eating or drinking).
- Wide-based stance and difficulty with balance.
- Progressive incoordination that worsens with age.
- Typically no pain, normal mental status, and no signs of systemic disease.

Diagnosis:
1. Neurologic Examination:
Cerebellar signs: ataxia, tremors, hypermetria.
Exclusion of other causes of ataxia (e.g., CNS infections, trauma, metabolic disorders).

2. MRI/CT Imaging:
   Cerebellar hypoplasia or atrophy, confirming the diagnosis.
3. Cerebrospinal Fluid (CSF) Analysis:
   Normal, rules out inflammation or infection.
4. Genetic Testing:
   Confirms the mutation (TOE1 in Arabians).

Prognosis:
- Progressive and degenerative disease with a poor prognosis.
- Foals typically show initial normal development, followed by a gradual onset of ataxia and coordination loss around 4–6 months of age.
- Most affected horses are euthanized by 1–2 years of age due to severe impairments in movement and quality of life.

Management:
- No cure or treatment to stop the progression.
- Supportive care to help with mobility (e.g., physical therapy, environmental modifications to prevent injury).
- Feeding assistance may be necessary if the foal struggles to eat or drink.

Genetic Counseling:
- Genetic disorder, so breeding affected horses or carriers should be avoided to prevent passing the disease to offspring.

Key Points:
- Cerebellar Abiotrophy primarily affects Arabian horses but can also occur in other breeds (Gotland pony, Oldenburg, Bashkir curly horses, Welsh ponies, Trakehner).
- The disease causes progressive incoordination, primarily affecting balance and coordination, and usually results in euthanasia due to the severe impact on quality of life.

Question 111

DDX auditory loss in adult horses

Answer 111

• THO
• Otitis
• Brainstem disease
• Trauma
• Congenital sensorineural deafness (American Paint Horse)
• Old age

Gentamicin-induced sensorineural auditory loss in healthy adult horses
jvim 21

Question 113

According to the study investigating postmortem diagnoses for spinal ataxia in horses, which of the following is the most accurate conclusion?

A) The most common postmortem diagnosis for spinal ataxia was trauma, with a period prevalence of 2.7%.

B) Horses under 5 years of age were more likely to have cervical vertebral compressive myelopathy (CVCM) or equine neuroaxonal dystrophy/degenerative myeloencephalopathy (eNAD-EDM) than trauma or ataxia of unknown origin.

C) Breed had no significant influence on the likelihood of ataxia, as all breeds were equally affected.

D) The period prevalence of ataxia of unknown origin was higher than that of cervical vertebral compressive myelopathy (CVCM).

Answer 113

Correct Answer:

B) Horses under 5 years of age were more likely to have cervical vertebral compressive myelopathy (CVCM) or equine neuroaxonal dystrophy/degenerative myeloencephalopathy (eNAD-EDM) than trauma or ataxia of unknown origin.

Explanation:

• Option B is correct because the study found that horses under 5 years of age had greater odds of being diagnosed with CVCM (OR 2.82) or eNAD-EDM (OR 6.17) compared to trauma or ataxia of unknown origin. This age-related difference was a key finding in the results.
• Option A is incorrect because the most common postmortem diagnosis was CVCM (2.7%), then eNAD/EMD (1.3%) and trauma (0.9%).
• Option C is incorrect because the study indicated that breed did have an influence on the likelihood of specific causes of ataxia.
  For example, Thoroughbreds were more likely to have CVCM, and American QH were more likely to have eNAD-EDM.
• Option D is incorrect because the prevalence of ataxia of unknown origin (2.0%) was lower than CVCM (2.7%).

Why this MCQ is Effective:

• The question targets key findings from the abstract, such as the age-related prevalence of certain conditions (CVCM and eNAD-EDM) and the breed differences observed in the ataxic group.

Postmortem diagnoses of spinal ataxia in 316 horses in California
javma 21

Question 114

According to the study on computed tomography (CT) and CT myelography in horses with suspected cervical spine pathology, which of the following statements is most accurate?

A) CT myelography was used in all horses and successfully detected spinal cord compression in 100% of cases.

B) The majority of cervical vertebral pathology was located cranial to C5, emphasizing the need for imaging of the cranial cervical vertebrae.

C) The study found that osteoarthritis of the articular process joints was the most common lesion, identified in 83% of the horses.

D) Adverse events occurred in over 50% of horses during CT and CT myelography procedures.

Answer 114

Correct Answer:

C) The study found that osteoarthritis of the articular process joints was the most common lesion, identified in 83% of the horses.

Explanation:

• Option A is incorrect because CT myelography detected spinal cord compression in 85% of cases, not 100%.
• Option B is incorrect because the majority of cervical pathology was found caudal to C5 (90%), not cranial, emphasises the importance of good-quality imaging
  of the most caudal cervical vertebrae in horses with
  suspected cervical spinal pathology and/or spinal cord
  compression.
• Option D is incorrect because adverse events occurred in 7.2% (important !!) of the horses, not over 50%.

Why This MCQ is Effective:

• The question targets key findings from the abstract, such as the prevalence of osteoarthritis, the location of lesions, and the effectiveness of CT and CT myelography in diagnosing cervical spine pathology.
• The distractors highlight common misinterpretations of the study’s results, such as assuming higher complication rates or mislocating the majority of lesions.

Computed tomography and myelography of the equine cervical spine: 180 cases (2013–2018)
eve 21

Question 115

According to a CT myelography study, compression from C1 through C4 were primarily ventral and lateral, whereas from C6 through T1 were primarily dorsal and dorsolateral.

True or false ?

Answer 115

True

Site significantly affected direction of compression, and directions of compression from occiput through C4 were primarily ventral and lateral, whereas from C6 through T1 were primarily dorsal and dorsolateral.

Computed tomographic myelography for assessment of the cervical spinal cord in ataxic warmblood horses: 26 cases (2015–2017)
javma 21

Question 116

True or False: The basihyoid-ceratohyoid disarticulation (BCD) procedure for temporohyoid osteoarthropathy (THO) in standing sedated horses resulted in complications in all the horses that underwent the procedure.

Answer 116

False.

Explanation:

• All horses tolerated the procedure well, with no complications and improved neurologic function after BCD.
• 3/3 horses with acute ataxia prior to BCD reportedly had full resolution of this sign;
• 3/4 horses with facial nerve deficits prior to BCD had mild residual facial nerve deficits at follow-up.
• 5/6 horses had a reported activity level equal to or greater than that prior to having signs of THO.

Ccl° : The BCD procedure was performed safely in this sample of THO-affected horses that were sedated while standing, avoiding risks associated with general anesthesia and resulting in no adverse effects such as iatrogenic injury to neurovascular structures.

This approach demonstrated no intraoperative or postoperative complications and reported resolution of clinical signs for 50% (3/6) of horses and return to previous or greater level of work for 80% (5/6).

Treatment of temporohyoid osteoarthropathy in horses with a basihyoid-ceratohyoid disarticulation technique: 6 cases (2018–2019)
javma 21

Question 117

True or False: All horses treated with partial ceratohyoidectomy for temporohyoid osteoarthropathy (THO) showed complete resolution of neurologic signs.

Answer 117

False.

Explanation:

• The study reports that neurologic signs improved in all 10 horses, with 2 showing complete resolution of signs. Therefore, it is not true that all horses showed complete resolution. Only 2 out of 10 horses had complete resolution of neurologic signs.
• Postoperative complications : obstructed airway, tongue mobility issues, and incisional hemorrhage, rhabdomyolysis.
• 10/11 horses underwent general anesthesia.

Ccl ° : Partial ceratohyoidectomy is a surgical option for treatment of THO that provides similar clinical outcomes to published reports on ceratohyoidectomy.

Partial ceratohyoidectomy as surgical treatment for horses with temporohyoid osteoarthropathy: 10 cases (2010–2021)
javma 23

Question 118

What is the effect of xylazine on intracranial pressure in standing horses ? And anesthetized horses ?

Answer 118

Administration of xylazine to anesthetized horses resulted in an increased cerebral perfusion pressure (CPP) due to decreased intracranial pressure (ICP) with concurrent increased MAP.

Administration of xylazine to standing horses did not result in a change in ICP.

The effect of xylazine on intracranial pressure in anesthetized and standing horses
J Vet Emerg Crit Care 21

Question 119

True or false ?
Morphine-containing sedation is contraindicated for atlantoaxial CSF collection in standing horses.

Answer 119

False

Both deto+xyla and deto+morphine sedation protocols are acceptable for AA CSF collection.

Opioid-free sedation for atlantoaxial cerebrospinal fluid collection in adult horses
jvim 22

Question 120

Is the clinical presentation of TBEV acute or progressive neurological disorders ? How to confirm the clinical suspicion in endemic region ?

Answer 120

Acute TBEV infection should be a differential diagnosis in horses with signs of neurologic disease (ataxia and proprioceptive deficits) and originating from TBEV
endemic areas (Switzerland).

Horses tested positive for TBEV using virus neutralization test and samples were further tested for TBEV-specific IgM.

Neurological disease suspected to be caused by tick-borne encephalitis virus infection in 6 horses in Switzerland
jvim 22

Question 121

True or False: The study recommended that prevention and control efforts for West Nile virus (WNV) should focus on new, non-endemic areas rather than previously infected regions.

Answer 121

False.

Explanation:

• The study recommended that prevention and control efforts should focus on previously infected areas, as these areas show a high recurrence of cases and demonstrate endemicity.
• Efforts should be based on the spatiotemporal regional distribution patterns, which highlight areas with local peaks in risk.

Distribution of West Nile virus cases in horses reveals different spatiotemporal patterns in eastern and western Canada
javma 23

Question 122

True or False: The addition of autologous serum to cerebrospinal fluid (CSF) samples improved the preservation of cell morphology up to 96 hours after collection, but had no effect on protein concentration.

Answer 122

True.

Explanation:

• The study found that the addition of autologous serum (4 drops) to an aliquot of CSF sample (2 mL) improved cell morphology preservation up to 96 hours (4 days) after collection, with no significant effect on protein concentration.
• Total nucleated cell count remained stable over time.
• The cell morphology were significantly different in the control group at T48.

Effect of time and autologous serum addition on the analysis of cerebrospinal fluid in horses
jvim 23

Question 123

Should cervical radiographs be included in a pre- purchase examination (PPE)?

Answer 123

Current evidence suggests that most findings present on cervical radiographs acquired at PPE are of unknown or low significance in a clinically normal horse.

There is also minimal evidence of the progression of subclinical cervical radiographic abnormalities and their future impact on performance.

Due to the high level of superimposition that is inherent to cervical radiographs, the reliability of interpretation of these findings is often variable. Additionally, PPE radiographs are often acquired in the ambulatory setting and the limitations of the equipment and environment can compromise their diagnostic value.

Therefore, at this time, there is little evidence to support the acquisition of cervical radiographs as part of a PPE.

Should cervical radiographs be included in a pre-purchase examination?
eve 24

Question 124

Which of the following statements regarding serum nerve growth factor (NGF) concentration in horses is correct?

A) Serum NGF concentration was higher in sound horses (controls) compared to horses with osteoarthritis-associated lameness.

B) Serum NGF concentration did not increase in horses subjected to short-term stress.

C) Serum NGF concentration was significantly lower in horses with radiographic evidence of osteoarthritis compared to sound horses.

D) Horses with fracture-associated pain had high serum NGF concentrations comparable to lame horses with osteoarthritis.

Answer 124

Answer:
B) Serum NGF concentration did not increase in horses subjected to short-term stress.

Explanation:

• A is incorrect because serum NGF concentration was higher in lame horses with osteoarthritis compared to sound horses, not the other way around.
• B is correct; the study found that serum NGF concentration did not increase with short-term stress in horses.
• C is incorrect because serum NGF concentration was significantly higher in horses with osteoarthritis-associated lameness, including both those with and without radiographic evidence, compared to sound horses.
• D is incorrect because horses with fracture-associated pain had low serum NGF concentrations, unlike lame horses with osteoarthritis.

Serum nerve growth factor in horses with osteoarthritis-associated lameness
jvim 23

Question 125

What did the study conclude about the use of real-time PCR (rtPCR) on cerebrospinal fluid (CSF) for diagnosing equine protozoal myeloencephalitis (EPM)?

A) rtPCR on CSF is highly sensitive and specific for diagnosing EPM.
B) The rtPCR assay demonstrated low sensitivity (0%) for EPM diagnosis.
C) The rtPCR assay had high sensitivity and specificity, especially for presumptive EPM diagnoses.
D) The study found that rtPCR was a useful diagnostic tool for differentiating EPM from other neurologic conditions.

Answer 125

Answer:
B) The rtPCR assay demonstrated low sensitivity (0%) for EPM diagnosis.

Evaluation of real-time polymerase chain reaction for the diagnosis of protozoal myeloencephalitis in horses using cerebrospinal fluid
jvim 23

Question 126

What were the main findings regarding the skeletal neuromuscular junctions (NMJs) in horses with equine grass sickness (EGS), as compared to control horses and a horse with botulism?

A) EGS NMJs showed significantly higher synaptic vesicle (SV) density than controls, suggesting enhanced neurotransmitter release.
B) EGS NMJs exhibited a significantly higher percentage of abnormal morphology and a lower mean volume fraction of SVs compared to controls.
C) The skeletal NMJs in horses with botulism displayed the same morphological changes as those in EGS horses, indicating that both conditions affect the NMJ similarly.
D) EGS NMJs showed no significant differences in morphology or synaptic vesicle content compared to control horses, suggesting that EGS does not affect the NMJ.

Answer 126

Correct Answer:
B) EGS NMJs exhibited a significantly higher percentage of abnormal morphology and a lower mean volume fraction of SVs compared to controls.

Explanation:
- The study found that horses with EGS had a significantly higher percentage of NMJs with abnormal morphology (72.2% in EGS horses vs. 6.9% in controls).
- EGS NMJs also had a lower mean volume fraction of synaptic vesicles (18.7%) compared to controls (36.3%), indicating disruptions in synaptic function. SV depletion may reflect increased exocytosis coupled with reduced repopulation of SVs via anterograde axonal transport and endocytosis, consistent with the action of an excitatory presynaptic toxin and/or neurotransmitter reuptake inhibitor.
- Additionally, NMJs from the botulism horse showed different characteristics, specifically dense packing of synaptic vesicles, which is consistent with botulinum toxin action but not seen in EGS.

Equine grass sickness is associated with major abnormalities in the ultrastructure of skeletal neuromuscular junctions
evj 24