Neuro Flashcards

Question

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

Answer 1

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.

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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). ## Footnote Serum and cerebrospinal fluid phosphorylated neurofilament heavy protein concentrations in equine neurodegenerative diseases EVJ 2022

Answer 6

Vitamin E depletion may **elevate CSF pNfH** in otherwise healthy juvenile foals by 6 months of age, compatible with **subclinical axonal degeneration**. ## Footnote Vitamin E depletion is associated with subclinical axonal degeneration in juvenile horses evj 2023

Answer 7

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

Answer 8

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

Answer 9

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

Answer 10

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

Answer 11

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

Answer 12

**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**

Answer 13

- **CVCM** (most common) - eNAD/EDM - EPM - Trauma - EHM Less common : - Rabies - Viral encephalitides (WNV, Eastern, Western...) - Brain abscess - Neoplasia - Hepatoencephalopathy

Answer 14

**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

Answer 15

- **Tetanus** - Rabies - Strychnine intoxication - Exertional rhabdomyolysis - Myositis

Answer 16

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

Answer 17

**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

Answer 18

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**

Answer 19

- **Botulism** - White muscle disease - **HYPP** - Hypocalcemia - White snakeroot toxicity - Ionophore toxicity - Lead toxicity - Organophosphate toxicity

Answer 20

- **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

Answer 21

**Answer:** C) It is important for veterinarians to recognize head-tossing due to musculoskeletal pain and differentiate it from trigeminal-mediated head-shaking. ## Footnote Head tossing behaviour in six horses: Trigeminal-mediated head-shaking or musculoskeletal pain? eve 20

Answer 22

Improves clinical signs by **≧ 70%** in **1/3 of horses** ## Footnote The safety and efficacy of neuromodulation using percutaneous electrical nerve stimulation for the management of trigeminal-mediated headshaking in 168 horses evj 20

Answer 23

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

Answer 24

**Answer:** True ## Footnote The safety and efficacy of neuromodulation using percutaneous electrical nerve stimulation for the management of trigeminal-mediated headshaking in 168 horses evj 20

Answer 25

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

Answer 26

**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. ## Footnote Computed tomographic findings in 101 horses presented for the investigation of headshaking eve 22

Answer 27

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

Answer 28

**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. ## Footnote Computed tomography findings in horses presented with signs of head-shaking evj 23

Answer 29

**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. ## Footnote Computed tomography findings in horses presented with signs of head-shaking evj 23

Answer 30

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**. ## Footnote Computed tomography findings in horses presented with signs of head-shaking evj 23

Answer 31

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

Answer 32

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

Answer 33

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.** ## Footnote Computed tomography findings in horses presented with signs of head-shaking evj 23

Answer 34

**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 ## Footnote The prevalence of headshaking in horses with primary and secondary dental sinusitis and computed tomographic evidence of infraorbital canal pathology evj 23

Answer 35

A total 65 out of 66 horses (**98.5%**) diagnosed with primary or secondary dental sinusitis demonstrated **IOC changes on CT**. ## Footnote The prevalence of headshaking in horses with primary and secondary dental sinusitis and computed tomographic evidence of infraorbital canal pathology evj 23

Answer 36

**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. ## Footnote History, Rest and Exercise Score (HRE-S) for assessment of disease severity in horses with trigeminal-mediated headshaking evj 23

Answer 37

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.

Answer 38

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**

Answer 39

**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.

Answer 40

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

Answer 41

**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**.

Answer 42

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**

Answer 43

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).

Answer 44

**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.

Answer 45

**Fracture** of the hyoid apparatus and **cribbing**

Answer 46

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

Answer 47

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. Other **cerebellar** signs are **ipsilateral**, and the resulting **vestibular** signs are **contralateral** to the side of the lesion.

Answer 48

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.

Answer 49

**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**.

Answer 50

**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 ## Footnote Vestibular disease in horses: Recognition, localisation and common causes eve 24

Answer 51

"Rabies can look like anything" - **Paralytic form (SC)** : weakness, lameness, 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

Answer 52

**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.

Answer 53

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

Answer 54

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

Answer 55

**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.**

Answer 56

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.

Answer 57

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

Answer 58

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.

Answer 59

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.

Answer 60

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.

Answer 61

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.

Answer 62

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

Answer 63

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.

Answer 64

- 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.

Answer 65

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.

Answer 66

**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.**

Answer 67

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.

Answer 68

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.

Answer 69

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%.

Answer 70

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.

Answer 71

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.

Answer 72

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

Answer 73

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

Answer 74

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.

Answer 75

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

Answer 76

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 ## Footnote Effects of coadministration of corn oil and ponazuril on serum and cerebrospinal fluid concentrations of ponazuril in horses jvim 20

Answer 77

* 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. ## Footnote 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

Answer 78

**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**. ## Footnote Computed tomographic cervical myelography in horses: Technique and findings in 51 clinical cases jvim 20

Answer 79

**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. ## Footnote Accuracy of transcranial magnetic stimulation and a Bayesian latent class model for diagnosis of spinal cord dysfunction in horses jvim 20

Answer 80

**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. ## Footnote Sidewinder gait in horses jvim 20

Answer 81

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

Answer 82

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

Answer 83

**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. ## Footnote Facial nerve paralysis in 64 equids: Clinical variables, diagnosis, and outcome jvim 20

Answer 84

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.

Answer 85

**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.

Answer 86

- **THO** - **Otitis** - Brainstem disease - Trauma - Congenital sensorineural deafness (**American Paint Horse**) - Old age ## Footnote Gentamicin-induced sensorineural auditory loss in healthy adult horses jvim 21

Answer 87

**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. ## Footnote Postmortem diagnoses of spinal ataxia in 316 horses in California javma 21

Answer 88

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

Answer 89

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

Answer 90

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

Answer 91

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

Answer 92

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

Answer 93

**False** Both **deto+xyla** and **deto+morphine** sedation protocols are acceptable for AA CSF collection. ## Footnote Opioid-free sedation for atlantoaxial cerebrospinal fluid collection in adult horses jvim 22

Answer 94

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

Answer 95

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

Answer 96

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

Answer 97

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**. ## Footnote Should cervical radiographs be included in a pre-purchase examination? eve 24

Answer 98

**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. ## Footnote Serum nerve growth factor in horses with osteoarthritis-associated lameness jvim 23

Answer 99

Answer: **B) The rtPCR assay demonstrated low sensitivity (0%) for EPM diagnosis.** ## Footnote Evaluation of real-time polymerase chain reaction for the diagnosis of protozoal myeloencephalitis in horses using cerebrospinal fluid jvim 23

Answer 100

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