Neurology

Question 1

What clinical signs indicate neurologic disorders in horses ?

Answer 1

Ataxia, loss of coordination, paresis, toe dragging, dysmetria, and general proprioceptive deficits

Question 2

Name the 5 core vaccination for infectious equine neurologic disease.

Answer 2

Rabies, Tetanus, West Nile Virus, Eastern equine encephalomyelitis (EEE) and Western equine encephalomyelitis (WEE)

Question 3

What are the key components of a neurologic examination in horses?

Answer 3

Gait deficits (Ataxia, loss of coordination, general proprioceptive deficits), paresis (toe dragging, falling, recumbency), dysmetria (extent of joint flexion), and distinguishing LMN and UMN

Question 4

Describe Cervical Vertebral Compressive Myelopathy (CVCM).

Answer 4

Also known as Wobbler’s Syndrome, CVCM involves symmetric ataxia in all Horus limbs (usually worse in back) dysmteria, undisturbed mentation, and intact peripheral nerve functions. It’s cause by cervical vertebral malformation or stenosis
(narrowing)

Question 5

What are the risk factors of CVCM?

Answer 5

Young, fast-growing male horses, particularly Thoroughbreds, Tennessee Walking Horses, and Warmbloods. Diagnosis is confirmed through radiographs and myelography​

Question 6

How does rabies progress in horses?

Answer 6

Rabies causes progressive encephalomyelitis caused by virus starts in autoimmune disease that affects CNS, with clinical signs including ataxia, paresis, lameness, pharyngeal paralysis, colic, and recumbency. Death occurs within 10 days of recumbency onset​

Question 7

What is the incubation period for rabies, and how is it transmitted?

Answer 7

The incubation period is 3-6 months, transmitted via saliva through bites or contact with nervous tissue. The virus travels 1 cm per day to the CNS

Question 8

Describe the pathophysiology and clinical signs of tetanus.

Answer 8

Caused by Clostridium tetani, which produces tetanospasmin, a neurotoxin that blocks GABA and glycine. Clinical signs include a stiff gait, sawhorse stance, lockjaw, protrusion of third eyelid, and altered face expressions

Question 9

How is tetanus diagnosed and treated?

Answer 9

Diagnosis is clinical. Treatment includes antibiotics, tranquilizers, tetanus antitoxin, and toxoid. Prevention is via vaccination with tetanus toxoid

Question 10

What are the primary vectors and reservoirs for equine encephalitides?

Answer 10

Mosquitoes are vectors, and the birds are the reservoir host and horses and human are dead ends

Question 11

What are the mortality rates for EEE, WEE, and WNV?

Answer 11

EEE: 75–95%, WEE: 19–50%, WNV: 30–40%. Recumbency usually indicates poor prognosis​

Question 12

What clinical signs are associated with West Nile Virus (WNV) encephalitis?

Answer 12

Muscle fasciculation, gait abnormalities, cranial nerve deficits, fever, anorexia, and lethargy. Only 10 percent oa horses develop Encephalitis

Question 13

How is WNV diagnosed and treated?

Answer 13

Diagnosed via IgM capture ELISA, PCR, and virus isolation. Treated with anti-inflammatories. Prevention includes mosquito control and vaccination​

Question 14

What are the risk factors for Equine Herpes Myeloencephalopathy?

Answer 14

Outbreaks occur after events, in fall-winter-spring, and affect tall breeds. Clinical signs include asymmetrical ataxia, paresis, and dysmetria​

Question 15

Describe botulism and its clinical signs in horses.

Answer 15

Caused by Clostridium botulinum , dead carcasses, which blocks acetylcholine release, leading to flaccid paralysis. Signs include tongue weakness, dysphagia, poor tail tone, and recumbency​

Question 16

How is botulism treated and prevented?

Answer 16

Treatment involves antitoxin administration. Prevention includes good husbandry, rodent control, avoiding spoiled feed, and vaccination of mares with Type B botulism toxoid in endemic areas

Question 17

What causes Equine Protozoal Myeloencephalitis (EPM)?

Answer 17

EPM is caused by Sarcocystis neurona or Neospora hughesi, with opossums acting as definitive hosts. Sporocysts ingested by horses may lead to CNS invasion in rare cases

Question 18

What are the clinical signs of EPM?

Answer 18

Asymmetry, ataxia, dysmetria, muscle atrophy, and possible cranial nerve involvement. Multifocal progressive lesions affect both gray and white matter​

Question 19

How is EPM Diagnosed and treated?

Answer 19

Diagnosed via detection of antibodies in serum and cerebrospinal fluid (CSF). Treated with antiprotozoal drugs like ponazuril and supportive therapy​

Question 20

What steps does a veterinarian take to determine if a horse has a neurologic disease?

Answer 20

History and Signalment
Physical Exam
Neurologic Examination (gait and proprioception, assess cranial nerve function by vision swallowing facial symmetry,test reflexes and muscle)
Blood Work, CSF, Imaging Pathogen testing
Observation of progression

Question 21

During a neurologic examination, a horse shows signs of ataxia, paresis, and dysmetria. What part of the nervous system is most likely affected?

Answer 21

Spinal Cord

Question 22

A veterinarian suspects Equine Herpes Myeloencephalopathy (EHM) in a horse that recently returned from a competition. What is the most critical first step in management to prevent further spread?

Answer 22

Quarantine the affected horse and monitor others for fever or neurologic signs.