Equine neurology Flashcards

(34 cards)

1
Q

CENTRAL NS -
EXTRACRANIAL lesion refers to?

A

spinal cord lesion

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2
Q

Age-related diseases that cause neuro signs in young horses e.g. (2)

A

Cervical stenotic myelopathy, “wobbler syndrome”

equine degenerative myelopathy

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3
Q

Cervical stenotic myelopathy (CSM), commonly known as “wobbler syndrome,” is a

A

neurological disorder in horses characterized by compression of the spinal cord within the cervical vertebrae, leading to ataxia and weakness, particularly in the hind limbs.

It typically affects young, rapidly growing horses, especially Thoroughbreds and Warmbloods, and can result from congenital malformations, developmental orthopedic diseases, or degenerative changes that cause narrowing of the vertebral canal.

Clinical signs often include a “wobbly” gait, stumbling, and difficulty in backing up or turning sharply.

Diagnosis is based on neurological examination, radiographs, and advanced imaging such as myelography or MRI. Treatment may involve surgical intervention like vertebral stabilization or conservative management with dietary adjustments and controlled exercise, but prognosis varies depending on severity and response to therapy.

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4
Q

Equine degenerative myelopathy (EDM) is a

A

progressive neurological disease that affects young horses, typically between six months and three years of age, causing symmetrical incoordination (ataxia) and weakness in all four limbs.

It is believed to have a genetic basis, often associated with vitamin E deficiency during early development, which leads to degeneration of neurons in the spinal cord, particularly in the thoracic and lumbar regions.

Clinical signs are usually subtle at first, including stumbling, dragging of the toes, and difficulty with changes in direction or terrain, gradually worsening over time.

Diagnosis is challenging and often based on ruling out other causes of ataxia, vitamin E levels, and sometimes confirmed post-mortem through histopathology. There is no cure for EDM, but supplementation with vitamin E may help slow progression if started early, though the long-term prognosis for athletic performance is generally poor.

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5
Q

Age-related diseases that cause neuro signs in older horses e.g.

A

Facet joint arthrosis + other degenerative changes in the cervical region: older horses (under the “wobbler” umbrella).

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6
Q

Facet joint arthrosis in horses is

A

a degenerative condition affecting the articular processes (facet joints) of the vertebrae, leading to joint inflammation, cartilage deterioration, and bone remodeling.

It most commonly occurs in the cervical and thoracolumbar regions, often resulting from chronic wear and tear, poor conformation, or repetitive strain associated with athletic activities.

Clinical signs can include neck or back stiffness, pain on palpation, reduced range of motion, reluctance to work, performance issues, and sometimes neurological deficits if nerve roots or the spinal cord are compressed.

Diagnosis typically involves a combination of clinical examination, diagnostic imaging such as radiography, ultrasonography, or nuclear scintigraphy, and sometimes diagnostic analgesia (nerve blocks).

Treatment may include anti-inflammatory medications, physiotherapy, intra-articular injections (such as corticosteroids), and management of workload, although in advanced cases, the condition may significantly affect the horse’s performance and quality of life.

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7
Q

Congenital disease that causes neuro signs in horses.

A

cerebellar abiotrophy in horses is a hereditary neurological disorder characterized by the premature degeneration of Purkinje cells in the cerebellum, leading to incoordination, head tremors, and balance issues.

It is most commonly seen in Arabian horses but can occur in other breeds as well, usually manifesting in foals or young horses shortly after birth or within the first few months of life.

Affected horses display signs such as a wide-based stance, exaggerated movement, intention tremors (especially when trying to eat or focus), and difficulty in precise movements, although they remain mentally alert.

Diagnosis is primarily based on clinical signs, breed predisposition, and exclusion of other neurological diseases, with definitive confirmation through post-mortem histopathology.

There is no cure or effective treatment for CA, and affected horses are generally unsuitable for riding or athletic careers; management focuses on ensuring a safe environment to prevent injury.

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8
Q

Draft horse shivers, often simply called “shivers,” is

A

a chronic neuromuscular disorder seen most commonly in heavy breeds like Clydesdales, Shires, and Percherons, characterized by involuntary, rhythmic muscle contractions and difficulty moving the hind limbs, especially when backing up or lifting a leg.

Affected horses display exaggerated, trembling movements of the tail and hindquarters, and may have episodes triggered by stress, excitement, or specific movements.

The exact cause of shivers is not fully understood, but it is thought to involve abnormalities in the cerebellum or spinal cord affecting motor control.

Diagnosis is based on observing characteristic clinical signs, as there are no definitive diagnostic tests available. There is no known cure, and while some horses can be managed with adjustments in exercise, diet, and stress reduction, the condition is progressive and may eventually limit the horse’s ability to work or perform.

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9
Q

Juvenile idiopathic epilepsy (JIE) in Arabian horses, particularly in Egyptian-bred Arabians, is

A

a condition characterized by recurrent seizures that typically begin between a few days to six months of age. The seizures often involve sudden collapse, stiffening, paddling of the limbs, and sometimes temporary blindness or disorientation after the episode, but affected foals are usually normal between seizures and continue to grow and develop typically.

The exact cause is unknown, but a genetic component is strongly suspected. Diagnosis is mainly based on clinical history, exclusion of other causes of seizures (such as trauma, infection, or metabolic issues), and breed predisposition.

Most foals with JIE outgrow the seizures by about one to two years of age without long-term effects, and treatment may involve short-term anticonvulsant therapy if seizures are frequent or severe.

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10
Q

Equine juvenile spinocerebellar ataxia (EJSCA), identified in 2024 in Quarter Horses, is

A

a newly recognized hereditary neurological disorder characterized by progressive incoordination (ataxia) and balance issues beginning in young horses, typically within the first year of life.

Affected foals exhibit signs such as a wide-based stance, clumsy or exaggerated limb movements, stumbling, and difficulty navigating tight turns or uneven ground, while remaining mentally alert.

The disease involves degeneration of the spinal cord and cerebellum, impacting fine motor control and proprioception.

Diagnosis is based on clinical signs, breed predisposition, exclusion of other neurologic diseases, and now genetic testing, given its hereditary nature.

There is currently no cure for EJSCA, and management focuses on supportive care, but most affected horses are unsuitable for athletic careers, and severe cases may require humane euthanasia for welfare reasons.

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11
Q

Name 3 infectious disease that could cause neuro signs in horses which prevalence will vary dependent on location.

A
  • EHV1 (EHM) (vaccination history?)
  • Borreliosis
  • West Nile virus
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12
Q

Name 3 infectious disease that could cause neuro signs in horses which prevalence will vary dependent on travel or import history.

A
  • West Nile Virus
  • Equine Protozoal Myeloencephalitis
  • Rabies
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13
Q

Acquired Equine Polyneuropathy (AEP), also known as

A

“Scandinavian knuckling horse syndrome,” is a rare neurological disorder primarily reported in horses from Scandinavian countries.

It is characterized by a sudden onset of limb weakness, abnormal stance, and a “knuckling” gait, particularly affecting the hind limbs. Affected horses may stumble, drag their toes, or even collapse.

The exact cause of AEP remains unclear, but environmental factors, such as ingestion of toxins from forage (especially wrapped silage or haylage), have been suspected.

Histopathological examination typically reveals degeneration of peripheral nerves and axons. Although some horses recover partially or fully over time, others may require euthanasia due to severe disability. Early diagnosis and supportive care are critical to improving the prognosis.

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14
Q

Feeding bad silage to horses can cause these 2 neuro diseases

A

Acquired Equine Polyneuropathy aka “Scandinavian knuckling horse syndrome”

botulism

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15
Q

Equine Motor Neuron Disease (EMND) is a

A

progressive neurodegenerative disorder in adult horses linked to prolonged vitamin E deficiency. Vitamin E, a potent antioxidant, protects nerve cells from oxidative damage; when deficient, oxidative stress leads to degeneration of lower motor neurons in the spinal cord and brainstem.

Clinically, affected horses often display muscle atrophy, generalized weakness, trembling, weight loss despite a good appetite, a low head carriage, and frequent lying down.

EMND typically occurs in horses with limited or no access to fresh pasture, relying instead on stored feeds that may lack sufficient vitamin E.

Diagnosis is based on clinical signs, history of poor vitamin E intake, blood tests showing low plasma vitamin E levels, and sometimes muscle or nerve biopsies.

Supplementation with vitamin E and providing pasture access can help manage the disease, although nerve damage may be irreversible if advanced.

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16
Q

Head pressing is related to the

17
Q

Head posture such as head turn tells you?

A

Head trauma: central

Vestibular/ guttural pouch disease: peripheral

Head tilt: vestibular disease, also: circling, vestibular ataxia, sometimes difficulty standing

18
Q

Tremors in horses can indicate?

A

Intracranial: cerebellar disease
Cerebellar abiotrophy: mostly head tremor

Extracranial: peripheral nerves/ muscles

19
Q

Describe cervical and cervicofacial reflex testing in horses.

20
Q

Paresis characterization:

A

Paresis: reduction in motor function (weakness or spasticity)

Upper motor neuron (brain – axons travel to spinal cord): initiation of movement; keeping of tone and posture
* UMN disorder: spastic paresis

Lower motor neuron (spinal cord to periphery): signals from CNS to peripheral muscles
* LMN disorder: flaccid paralysis, loss of muscle activation

Graded mild….moderate….severe

21
Q

All limbs affected.
Pelvic limbs generally worse than thoracic limbs.

Localize.

22
Q

Pelvic limb ataxia and paresis. Thoracic limbs normal.

Localize.

23
Q

Paretic pelvic limbs, dragging toes.
Potential cauda equine signs with urinary and fecal incontinence.

Localize.

24
Q

Both pelvic and thoracic limbs affaected but thoracic limbs appear particularly weak, dragging toes, then muscle atrophy.

Localize.

25
Rhodococcus equi is now called
Rhodococcus hoagii
26
All neuro patients should be given?
Vit E orally 6000 IU SID * Anti-oxidant B1 (thiamine) 1-5 mg/kg IV * Potentially improves neuronal metabolism In order to attempt to support the brain and its healing.
27
Explain what cervical vertebral stenotic myelopathy (“Wobbler” syndrome) is.
Developmental abnormality of the spinal cord at C1-T1, stenosis of the vertebral canal. * Stenosis compresses the sensory and motor pathways – hind limb spinocerebellar tracts more peripheral in the white matter. Most common cause of non-infectious spinal ataxia in the horse. * Genetic component likely * Any fast-growing breed or fast-growing young horse predisposed. Essentially 2 types of wobbler because type 1 is super rare, euthanized after birth usually. * type II - young horses/foals * type III - often adults
28
Wobbler presentation in young, growing horses vs adult horses.
Young, growing horse * Onset of ataxia: Sudden or gradual! * Periods of worsening and stabilisation Adult horse * Gradual onset of ataxia * Hind limb lameness * Neck stiffness and local muscle loss Differentials for both above groups: * Trauma * Young horse: Equine degenerative myeloencephalopathy * Equine Herpes Myelopathy (EHV1 caused) * Aberrant parasite migration * Equine Protozoal Myeloencephalopathy or other infection (geography!) * Abscess, neoplasia, hepatic encephalopathy, spinal hematoma, discospondylitis etc.
29
Flowchart for equine neuro signs localization.
30
EHM: Equine Herpesviral Myeloencephalopathy
* Severe, potentially fatal CNS infection: ataxia, paresis, urinary incontinence * EHV1, rarely EHV4 (Neuropathic genotype of EHV1) * Estimated over 80% world equid population latently infected. Re-activation and viral shedding during periods of stress (illness, transport, hospitalisation, competitions). * More at risk horses over 3 yrs, especially older broodmares EHM signs develop in the end stages of viremia (6th – 10th day of infection) * 10-40% of EHV1 horses * Development sudden, worsens over 2-3 days * Spinal cord vasculitis, hemorrhage and thrombosis
31
Once you've diagnosed equine herpes virus. What do you do?
* Quarantine The stable as a whole * Call local state veterinary office * Separate sick horses from healthy ones * All horses: temperature taken 2x day Treatment * NSAIDs: All stages of dz – full dose when febrile, then half dose. * Consider Valacyclovir? 30 mg/ kg PO TID for 2 days, then 20 mg/kg PO BID 14 days * Heparin/ LMW heparin? Only during viremia; caution – will exacerbate CNS hemorrhage. * Lidocaine? CRI 0.05 mg/kg/min - Lowers endothelial cell infection and lysis. * Nursing care Neurological signs can last several weeks to months. Quarantine ends 28 days after last recorded fever – ideally all horses also PCR swab negative.
32
EHV vaccination
does not prevent equine herpes myeloencephalopathy BUT - * Prior whole herd vaccination may lower the number of infected horses and decreases nasal shedding. * Evidence about vaccination efficacy for prevention of EHM extremely scarce. ## Footnote All new horses arriving at any stable should be quarantined for 3 weeks in general.
33
West Nile Virus infection overview:
West Nile Virus has arrived to the baltics, 1st occurrence in Estonia and Latvia 4th Oct 2024! * Vectors: Culiseta spp. mosquitoes * Susceptible: birds, humans, horses, several mammalian species * Disease: sublinical to mild, to severe encephalitis * 33% mortality rate in horses with clinical signs * Equine vaccine available – not yet in Estonia, but ordered (recombinant canarypoxvaccine: 2-shot base, then annual booster). You can get it from a mosquito, not from a horse!
34
What to prescribe and test for in a horse neuro patient when youre not yet sure whats up:
* Box rest * NSAIDs * Vit-E If Viral infection suspicion: * Dry nasal swabs: EHV 1 and 4 (PCR) * Serum: West Nile Virus antibodies (ELISA) * Cerebrospinal fluid: WNV PCR (best) – can be taken post mortem.