Specific Neurologic Disorders Flashcards

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1
Q

List the clinical signs for Cerebellar Abiotrophy and provide some differentials for this condition

A
  • Intention tremor
  • Base wide stance
  • Lack of menace & failure to blink in bright light
  • Ataxia
  • Dysmetria and spasticity
    DDX: cranial malformation, congenital spinal malformation (incl atlantoaxial malformation), stenotic myelopathy, cerebellar inflammation/infection and trauma. EEG may help to rule out seizure as a cause for the tremors.
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2
Q

List the breeds commonly affected by cerebellar abiotrophy and the differences between them.

A

Arabian and Gotland foals (and their crosses: generally signs noted by 1 yr of age, most commonly 1-6mo. Signs are generally progressive for several months but once the animal reaches maturity they become static or may improve slightly.
Oldenburgs: generally progressive and fatal with atypical histological findings compared with those of Arabian foals (Arabian foals typically have apoptosis of purkinje cells).

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3
Q

List differentials for cerebellar disease and some defining points for each

A
  • Cerebellar abiotrophy: diagnosed based on signalment (Arabian, Gotland or Oldenburg breeds), typically foals.
  • Gomen Disease: geographically located to New Caledonia, progressive disease in horses at pasture over 3-4 yrs until they die or are euthanised.
  • Dandy-Walker syndrome: defect in the midline of the cerebellum and cystic dilation of the 4th Ventricle. May be abnormal from birth: reported in Arabs and TBs.
  • Cerebellar hypoplasia or dysplasia: reported rarely in TBs with variable clinical signs and ranging from foals to adults.
  • Strep equi equi abscess: history of previous strangles.
  • Aberrant parasitic migration: often accompanied by other neurological deficits
  • Chronic methylmercurial poisoning: signs include cerebellar ataxia, lethargy, anorexia, exudative dermatitis, and laminitis.
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4
Q

List the clinical signs of Shivers and the commonly affected breeds

A

Chronic progressive movement disorder
- Difficulty walking backwards and may have tremors, hyperflexed pelvic limb posture, may progress to involve thoracic limb movement.
- Muscle atrophy and reduced muscle strength
- Exercise intolerance
- Facial twitching and or elevated tail head
Breeds: Draft breeds, TBs, WBs and less commonly Connemara, Welsh, QH, SB, saddlebred, Tennessee Walking horse, Missouri Fox Trotters, Paint and Morgans.

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5
Q

List the 4 gait patterns of shivering

A
  1. Hyperextension when backing and lifting the limb
  2. Hyperflexion and abduction during backward walking
  3. Shivering hyperflexion with abduction during backward walking
  4. Shivering-forward hyperflexion including intermittent hyperflexion and abduction with forward walking
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6
Q

List the breed, age and gender predilection for CVSM

A

Males, young horses (less than 7yrs, often well-fed rapidly growing), TBs, Tennessee Walking horses and WBs.

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7
Q

Define dynamic versus static compression with CVSM including effect of flexion versus extension of the neck.

A

Dynamic: compression is intermittent and occurs when the cervical vertebrae are flexed (cranial vertebral lesions) or extended (caudal vertebral lesions).
Static: compression is continuous regardless of cervical position.

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8
Q

List the common clinical signs of CVSM

A
  • Symmetric ataxia
  • UMN extensor paresis (weak on dynamic tail pull) & dysmetria (usually worse in pelvic than thoracic limbs due to superficial location of pelvic limb spinocerebellar proprioceptive tracts)
  • Circumduction of pelvic limbs on circling
  • Flexor paresis (toe dragging)
  • Forelimb hypometria, particularly up and down a hill/with head elevation
  • May have concurrent OCD/DOD of the appendicular skeleton.
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9
Q

List medical and surgical treatment options for CVSM

A
  • Dietary protein and energy restriction (likely only effective in horses 1-2yrs age) and close monitoring of trace elements such as zinc and copper
  • Stall rest/exercise restriction (more effective in young horses)
  • Supplementation with vitamin E and Se (EDM is a differential in young horses)
  • Anti-inflammatories/corticosteroids (realistically one of the few options in adult horses with acute neuro dz)
  • Medication of DAPJ if evidence of OA
  • Intervertebral fusion (fenestrated basket or threaded cylinder) - most effective if only one site and if only mild neurological disease.
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10
Q

Describe/List the clinical findings, signalment and pathogenesis of equine neuroaxonal dystrophy and equine degenerative myeloencephalopathy

A
  • Diffuse, symmetric degenerative neurologic disease
  • UMN and general proprioceptive deficits including symmetric ataxia, weakness, dysmetria (mostly hypometria), horses may pace. All 4 limbs affected, usually worse in pelvic limbs.
  • May pivot on the inside and circumduct the outside hindlimb when circled
  • Some LMN signs such as hyporeflexia of the trunk and neck with absent or reduced cervical, cervicofacial, cutaneous trunci and laryngea adductor reflexes.
  • No gender or sex predilection; affects young horses, usually in the first yr of life but can be as young as 1 month up to several years.
  • May be inherited as a complex trait that predisposes horses then subject to vit E deficiency
  • Exposure of susceptible horses to diets deficient in vitamin E is thought to be involved in the pathogenesis due to oxidative damage and lipid peroxidation of cell membranes.
  • Vit E deficiency is not consistent among all affected horses, but supplementation during the first year of life may reduce incidence and severity of disease
  • Definitive diagnosis required histo, although low serum vit E in a horse with compatible clinical signs is supportive.
  • Not, or very slowly progressive, but horses don’t recover (usually stabilise by 3yrs but remain neurologically abnormal/unfit to perform).
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11
Q

List the risk factors (incl geographical), common signalment and causative agents for EPM

A

Main risk factors:
- Exposure to opposums
- Housing indoors on straw or corn stalks, and lack of rodent proof feed storage
- Use for racing increased the risk.
- Presence of a stressor such as transport, heavy exercise, injury, parturition etc may increase the risk.
Other risk factors:
- High seroprevalence in the USA, which increases with increasing temperature as well as increasing patient age
- Racing and showing animals are at higher risk than breeding or pleasure horses
Signalment:
- Average age of affected horses is 4yrs, higher risk animals are thought to be 1-5yrs or greater than 13yrs.
- No gender predilection but TB, SB, WB and QH more commonly affected.
Causative agents:
S. neurona is most common, N. hughesi is less common and seroprevalence is much lower to this parasite.

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12
Q

Describe the transmission of EPM

A
  • Contamination of feed/water sources with infected opposum faeces.
  • No horizontal transmission in horses of S. neurona
  • Transplacental transfer is very uncommon or absent
  • Some reports of trans-placental transmission of N. hughesi.
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13
Q

List factors contributing to pathogenesis of EPM

A
  • *- Parasite dose is likely a factor - the immune clearance of the parasite is likely very effective given the high rate of exposure relative to disease incidence.
  • Physiologic stress may influence susceptibility to clinical disease
  • Entry into the CNS thought to be either via endothelial cells or leucocytes
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14
Q

List clinical signs of EPM, including 3 A’s of EPM

A
  • Acute-chronic insidious onset neurological signs that may be focal or multifocal
  • Can include brain, brainstem or spinal cord
  • Signs are variable due to random distribution o lesions within the CNS.
  • Grey matter involvement leads to focal muscle atrophy and severe muscle weakness
  • White matter involvement results in ataxia and weakness in limbs caudal to the lesion.
  • Horses are usually bright and alert with no alterations in physical exam findings.
  • Neuro exam typically shows asymmetric ataxia, weakness, spasticity (quadrilateral).
  • If brain or brainstem involvement may see obtundation, head tilt, cranial nerve dysfunction (often facial) and dysphagia.
  • 3 A’s: ataxia, asymmetry and atrophy.
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15
Q

List the diagnostic methods and pathologic findings

A

Diagnosis:
- Presumptive diagnosis based on clinical signs and absence of other causes of neurological dysfunction
- Immunodiagnostic testing of serum and CSF to show intrathecal antibody production.
- Positive serum titre does not confirm disease due to high seroprevalence; likewise detection in CSF alone does not confirm due to passive transfer across the BBB.
Pathology:
- Haemorrhage and foci of malacia mostly in the spinal cord.
- Brainstem more commonly involved than other areas of the brain.
- Lesions characterised by focal to diffuse areas of nonsuppurative inflammation and necrosis with pervascular infiltration of mononuclear cells (can affect grey or white matter)

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16
Q

List the differential diagnoses for EPM

A
  • CVSM
  • Viral encephalitis (WNV, EEEV, WEEV, EHV-1)
  • Meningitis
  • Trauma (TBI or SCI)
  • ENAD/EDM
  • Polyneuritis equi
    Basically any neurologic disease depending on signs shown.
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17
Q

List treatment options for EPM and likelihood of success

A
  • Pyrimethamine and sulphonamides (caution with addition of folic acid - may increased toxicity - used to reduce risk of anaemia)
  • Ponazuril (benzeneacetonitrile compound) broad spectrum anticoccidial
  • Anti-inflammatories symptomatically to treat acute neurological disease
  • Regardless of treatment method, approximately 60-75% improvement rate is generally seen with standard therapies.
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18
Q

List clinical signs of EHV-1 Myeloencephalopathy

A
  • May be preceded or accompanied by URT disease, fever, inappetence or hindlimb oedema.
  • Acute onset neuro signs, predominantly of spinal white matter (hence flexor reflexes are normal and perineal reflexes are preserved).
  • Ataxia and paresis
  • Hypotonia of tail and anus or tail elevation
  • Urinary incontinence
  • Conscious proprioceptive deficits
  • Limb weakness (can become recumbent)
  • Severe case may become recumbent, and may die in coma or convulsion.
  • signs generally stabilise after 1-2 days and don’t progress.
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19
Q

List the 5 herpesviruses of horses and 3 of asinines and the disease associated with each (briefly)

A
Alpha-herpes:
- EHV-1 (abortion and myelopathy)
- EHV-4 (equine rhinopneumonitis; rarely abortion & myeloencephalopathy)
- EHV-3 (equine coital exanthema)
Gamma-herpes:
- EVH-2 (rhinitis)
- EHV-5 (EMNPF)
Asinine alpha-herpes:
- AHV-1
- AHV-2
- AHV-3
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20
Q

Describe infection and immune evasion of EHV-1

A
  • Inhalation or ingestion of virus in respiratory, abortion, salivary, ocular and faecal products.
  • Attaches to and replicates on nasopharyngeal epithelium where it infiltrates phagocytic cells
  • Incubation is 2-10 days
  • Migration of infected phagocytes into circulation results in viraemia (predominantly T lymphocytes of the buffy coat)
  • Transfers to the vascular endothelium of the CNS
  • Results in vasculitis and thrombosis of arterioles of the brain and spinal cord, hence development of neuro Dz.
  • Evades host immune system in part by downregulating major histocompatibility complex class I expression at the cell surface.
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21
Q

List epidemiologic factors of EHV-1 myeloencephalopathy

A
  • Virus shed by clinically affected, subclinically affected and carrier animals for 3+ weeks
  • Survives in the environment for 14 days
  • Survives on horses hair for 35-42 days
  • Can occur any time of the year but highest incidence in late winter, spring and early summer
  • Restrict movement for at least 3 weeks after resolution of clinical signs in the last clinical case
  • Demonstration of stable or declining titres in affected or exposed horses helps determine when clinical spread has ceased.
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22
Q

List the diagnostic methods and their challenges for EHV-1 Myeloencephalopathy

A
  • Virus isolation from nasopharyngeal swabs or buffy coat (PCR)
  • Virus isolation from CSF (rare)
  • Presence of antibodies to EHV-1 in CSF (but, need to take into account the albumin and serum IgG concentrations as it can simply reflect leakage of antibodies across a damaged BBB with vasculitis)
  • Rising tire on paired samples (but, many horses don’t show the prescribed rise because of rapid antibody production within 6-10 days of infection hence they may have peaked by the time of developing clinical signs).
  • Testing paired serum samples from in-contact horses is a good means as many seroconvert despite not showing clinical signs, or may go on to develop clinical signs.
  • Many tests don’t differentiate between EHV-4 and EHV-1.
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23
Q

List differential diagnoses for EHV-1 Myeloencephalopathy

A
  • EPM
  • CVSM
  • Trauma/fracture
  • Polyneuritis equi
  • Fibrocartilagenous infarction
  • Aberrent parasite migration
  • ENAD/EDM
  • Viral encephalitis (flaviviruses and alphaviruses
  • Rabies
  • Botulism
  • CNS abscess
  • Plant & chemical intoxicoses
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24
Q

List the ocular changes seen in some foals with EHV-1

A
  • Uveal vasculitis with perivascular mononuclear cuffing in the ciliary body and optic nerve
  • Retinal degeneration & hypopyon
  • Chorioretinopathy without anterior segment involvement
  • Occassionally you see ocular and neural damage in the absence of gross signs of neurologic or visual impairment.
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25
Q

What suggests involvement of the immune system in polyneuritis equi?

A

Circulation of antibodies to P2 myelin protein.
Inflammatory lesions contain both T and B lymphocytes, suggesting the possibility of an immune-mediated reaction to myelin.

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26
Q

What are the two forms of polyneuritis equi?

A

Acute/early signs include hyperaesthesia of the perineal or head regions (or both)
The chronic form involves paralysis of the tail, anus, rectum and bladder, often accompanied by urinary or faecal retention.

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27
Q

List possible neurologic abnormalities with polyneuritis equi

A
  • Tail, anus, bladder paralysis (may have faecal/urinary retention)
  • Ataxia (pelvic limbs usually worse and symmetric)
  • Muscle atrophy (gluteals and head - head often asymmetrically)
  • Cranial nerve dysfunction (often asymmetric) primarily of CNV, CNVII and CNVIII; note these are peripheral; no alteration in mentation
  • Head tilt, ear droop, lip droop and ptosis are common signs.
  • Typically lesions involve extradural nerve roots but can also involve intradural nerve roots
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28
Q

What is the primary finding in Acquired Equine Polyneuropathy in Scandinavia?

A

Acute onset bilateral pelvic limb digital extensor dysfunction and knuckling.

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29
Q

List the most frequently isolated alphaviruses (encephalitis viruses), their distribution, vector, pathogenesis and clinical signs

A

EEEV, WEEV, VEEV: western hemisphere, mosquitoes, virus multiplies in muscle, enters the lymphatics, localises in lymph nodes. It replicates in macrophages and neutophils and is shed in small numbers at which time many viral particles are cleared. If clearance is incomplete remaining virus infects endothelial cells and concentrates in vascular organs (liver and spleen) where it replicates further, causing viraemia and early clinical signs. Infection of the CNS occurs within 3-5 days.
Clinical signs include fever, anorexia, stiffness, obtundation, hyperesthaesia, altered behaviour, compulsive walking, cranial nerve dysfunction; death is preceded by recumbency 1-7days

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30
Q

List diagnostic methods for togaviruses

A

Clinical signs, IgM antibody capture enzyme-linked immunosorbent assay (not produced by vaccination), paired samples are not always reliable as titres increase within 24 hours of viraemia, PCR, FAT and ELISA for necropsy specimens.

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31
Q

List the vaccination protocol for EEEV/WEEV recommended by AAEP

A

Adults: 2 doses 4-6 weeks apart. Annually or biannually depending on climate/mosquito prevalence, and timed to be before mosquito season starts
Foals: 3 doses with a 4 week interval (start at 2-3mo if high risk and unvaccinated mare); 4 th dose at 10-12mo or before mosquito season starts

32
Q

List important flaviviruses

A
  • Japanese encephalitis virus (mosquito)
  • St. Louis encephalitis (mosquito)
  • West Nile virus (mosquito)
  • Murray Valley encephalitis (mosquito)
  • Kunjin virus (mosquito)
  • Powassan (tick)
  • Louping Ill virus (tick).
33
Q

List clinical signs of WNV

A
  • ~90% of horses seroconvert without clinical signs.
  • Weakness (LMN in SC)
  • Ataxia (LMN in SC)
  • Altered mentation (grey matter of mid brain and hind brain)
  • Fever in early phase
  • Muscle fasciculations (commonly of the face, neck and muzzle)
  • Cranial nerve deficits (due to effects on grey matter of mid brain and hind brain)
  • Recumbency
  • Anorexia
  • Bruxism
  • Hyperexcitability, apprehension or aggression may be seen (if thalamic involvement)
  • Sleep like states resembling narcolepsy may occur in rare cases.
34
Q

What is the prognosis for recovery with WNV?

A

In horses that improve, 90% recover completely within 1- -6mo.
Residual weakness and ataxia are common complications in those that don’t recover completely. Mild-moderate persistent fatigue on exercise is reported in some horses.

35
Q

List the transmission of Borna virus

A

Virus shed in body secretions gains access to a host via exposed nerve endings in nasal and pharyngeal mucosa. GP43 protein facilitates internalisation to cells via endocytosis; virus migrates to olfactory bulbs and has tropism for the limbic system.
Virus causes progressive severe immune-mediate nonsuppurative meningoencephalitis

36
Q

List the clinical signs of Borna virus

A

Variable signs; may include:

  • Slow-motion chewing or chewing motions of the mouth
  • Head pressing
  • Somnolence and stupor
  • Hyperexcitability
  • Fearfulness or aggressiveness
  • Hypokinesia
  • Abnormal posture
  • Hyporeflexia
  • Head tilt
  • neurogenic torticollis
  • Inability to swallow
  • Death in 1-4 weeks.
37
Q

List the transmission routes for rabies

A
  • Saliva through bites
  • Droplet/aerosolisation inhalation
  • Oral transmission
  • Transplacentally
38
Q

Where does rabies virus replicate?

A

Spinal and dorsal root ganglia of the peripheral nerve it has travelled up.

39
Q

What is the incubation period for rabies virus

A

14-90 days and up to 1 year.

40
Q

List the three forms of rabies and the clinical signs of each

A
  1. Cerebral/Furious form: aggressive behaviour, photophobia, hydrophobia, hyperaesthesia, self-mutilation, straining, muscle tremors, convulsions and blindness.
  2. Brainstem/Dumb form: obtundation, anorexia, head tilt, circling, excess salivation, facial and pharyngeal paralysis.
  3. Paralytic/Spinal form: progressive ascending paralysis, ataxia, shifting lameness with hyperaesthesia, self mutilation of an extremity, flaccid tail and anus and urinary incontinence.
    More than one form can occur concurrently. Anti-inflammatories delay virus progression but death occurs within 5-10 days of clinical signs.
41
Q

List diagnostic tests for rabies

A
  • Direct fluorescent antibody test
  • Lymphocytic pleocytosis in CSF is supportive
  • Histology of the brain
  • Mouse inoculation test (inoculate intracerebrally with salivary or brain tissue and observe for development of disease)
42
Q

Which muscle groups are primarily affected by wasting with EMND?

A

Quadriceps, triceps and gluteals

43
Q

What ocular changes are seen with EMND?

A

Yellow-brown-black pigment with a reticulated appearance above the optic disc on fundic exam (at the tapetal-non-tapetal junction. Seen in 30% of cases

44
Q

Where are degenerative changes primarily localised to with EMND?

A

Ventral horn cells (LMN) of the grey matter, nucleus ambiguous, and all brainstem cranial nerve somatic motor nuclei except III, IV and VI.

45
Q

Which muscle fibres are affected with denervation atrophy?

A

Type I and Type II. EMND primarily affects type I.

46
Q

What is the prognosis for treatment with EMND?

A

20% continue to deteriorate and are euthanased
40% have stabilisation of clinical signs but the muscle mass does not return and they may develop severe gait abnormalities.
40% show dramatic improvement with treatment and may regain normal muscle mass. They may then remain stable for 1-6 yrs+ however many relapse on return to exercise.

47
Q

List the three tetanus exotoxins and which one is most clinically relevant.

A

Tetanolysin, tetanospasmin, nonspasmogenic toxin.

Tetanospasmin is most clinically important.

48
Q

Where does tetanospasmin localise? And what is the effect?

A

Ventral horn of the grey matter of the spinal cord binding to inhibitory interneurons called Renshaw cells.
Tetanospasmin blocks the postsynaptic inhibitory signal of the spinal cord motor neurons by preventing release of the inhibitory neurotransmitters glycine and GABA. Hence you get continued stimulation of motor and reflex arcs causing muscle spasms and contractions, convulsions and respiratory arrest leading to death.

49
Q

List the function of tetanolysin and nonspasmogenic toxin

A

Tetanolysin facilitates spread of infection by increasing local tissue necrosis. The role of non-spasmogenic toxin is not well understood but may involve blocking transmission in peripheral neuromuscular junctions.

50
Q

Does tetanospasmin affect the sympathetic NS, parasympathetic NS or both?

A

Both. Adrenergic stimulation can cause tachycardia, cardiac arrhythmias and peripheral vasoconstriction. Parasympathetic hyperactivity increases vagal tone that may cause bradyarrhythmias, AV block and sinus arrest.

51
Q

What is the treatment for tetanus?

A
  • Binding is almost irreversible
  • Local & parenteral antibiotics to stop further production of toxin (penicillin is drug of choice, others are tetracyclines, macrolides in foals and metronidazole)
  • Tetanus antitoxin to neutralise unbound toxin (500o-2.5x10^6 IU/animal) can be intrathecal although questionable advantages?
  • Muscle relaxants such as phenothiazins, benzodiazepines, alpha2-agonists all may be helpful. Magnesium sulphate. Methocarbamol.
  • Quiet environment and general nursing (catheterisation, rectal evacuation etc if required)
52
Q

What is the vaccination protocol for tetanus?

A

Adults: 2 vaccines 4-6 weeks apart then annually.
Foals: 2 vaccines 4-6 weeks apart starting at 4-6mo age then a third vaccine at 10-12 mo then annual if mare was vaccinated; if unvaccinated mare start at 1-4mo age, boost 4 weeks later then a 3rd dose 4 weeks later.

53
Q

What are the 3 routes of infection with botulism toxin?

A
  1. food borne - ingestion of pre-formed toxin in feed.
  2. toxicoinfectious - release of toxin from the GIT, typically in foals 2wk-8mo age (Shaker foal syndrome); toxins are then absorbed into the blood stream.
  3. wound botulism - infection of a wound with C. botulinum that then germinate and release toxin under anaerobic conditions
54
Q

Where do botulism toxins exert their effects?

A

Peripheral nerve terminals, primarily of skeletal and autonomic cholinergic nerves (can’t cross the BBB).

55
Q

Describe the effects of botulism toxin at their site.

A

Act presynaptically at the peripheral cholinergic neuromuscular junction resulting in inhibition of neurotransmitter (acetylcholine) release and hence neuroparalysis. This is reversible.

56
Q

What are the characteristic clinical signs of botulism?

A

Mydriasis and ptosis, sluggish PLR, reduced tongue tone and slow tongue retraction, delayed prehension of feed (grain test - 8ounces of sweet feed should be eaten in under 2 mins, but may take much longer +/- be dropped out of the mouth with botulism), generalised weakness and low head carriage, muscle fasciculations that start at the shoulder and progress to severe generalised trembling. Usually dysphagic and reduced tail tone.

57
Q

Where are the neuronal lesions found in horses with EGS?

A

Most severe in the autonomic ganglia (cranial cervical, stellate and celiacomesenteric) and enteric nerves. Also seen in the brainstem nuclei and the somatic efferent LMN of the spinal cord.

58
Q

What specific findings will you see on biopsy with EGS?

A

Neuronal loss in both the submucosal and myenteric plexuses throughout the GIT and reduction of interstitial cells of Cajal in the myenteric plexus regions of the GIT

59
Q

What does the phenylephrine test show in cases of EGS?

A

Application of 0.5% phenylephrine topically to the cornea should abolish the ptosis thereby confirming the presence of smooth muscle paralysis.

60
Q

What are the common seasons for Lymes disease?

A

Spring, summer and fall; peak incidence in June and July.

61
Q

List the clinical signs of Lymes (Borrelia burgdorferi).

A

Chronic weight loss, sporadic lameness, laminitis, mild fever, swollen joints (may develop chronic arthritis), muscle tenderness, anterior uveitis, encephalitis and abortion.

62
Q

List differential diagnosis for equine borreliosis (lymes)

A

Anaplasma phagocytophilia, chronic disease, vasculitis, immune mediated-arthritis.

63
Q

Which nerves are commonly blocked for diagnosis of headshaking in horses

A

Infraorbital nerve (part of the maxillary branch) & caudal nasal nerve/posterior ethmoidal nerve (branch of the ophthalmic nerve).

64
Q

What is the proposed mechanism of photic headshaking?

A

Optic-trigeminal summation: stimulation of the optic nerve results in referred sensation to parts of the nose innervated by the trigeminal nerve.

65
Q

What are the therapeutic/medical treatments for headshaking?

A

Cyproheptadine: antihistamine and serotonin antagonist with anticholinergic effects. Also blocks calcium channels.
Carbamazepine: sodium channel blocker and antiepileptic drug - drug of choice for trigeminal neuralgia in people.
Steroids, antihistamines NSAIDs have also been used.

66
Q

What are the common sites affected by Halicephalobus gingivalis? And what are the typical lesions?

A

Brain, spinal cord, nasal and oral cavities, pituitary gland and kidneys.
Malacia, granulomatous and lymphohistiocytic inflammatory infiltration, meningitis and vasculitis.

67
Q

What stage of strongyles cause strongyle encephalomyelitis and how do they enter the CNS?

A

Fourth and fifth stage larvae.
They are present in the intima of the aorta or left ventricle, causing endothelial damage, stimulating the clotting cascade and formation of a thrombus that contains the parasitic larvae. Hence they are transferred to the CNS in the thrombus.

68
Q

List suitable antiparasitics for treatment of verminous encephalomyelitis.

A

Benimidazole compounds (oxfenbendazole, thiabendazole, fenbendazole, mebendazole), diethylcarbamazine and ivermectin for nematodes (ivermectin has delayed killing so may not be ideal); organophosphates have been advocated for warble fly but should be used with caution. 3 day course of fenbendazole might be appropriate.

69
Q

What is the common site for cholesterol granuloma?

A

Choroid plexus of the fourth ventricle. Less commonly in the lateral ventricles, but these may be more likely to result in clinical signs.

70
Q

What specific clinical signs would make cholesterol granuloma a more likely diagnosis?

A

Waxing and waning forebrain signs.

71
Q

What is the most common secondary neoplasm of the CNS? List other common secondary neoplasms.

A

Lymphoma.

Melanoma of the SC, meninges, and brain; adenocarcinoma and carcinoma.

72
Q

List the two syndromes associated with equine leukoencephalomalacia and their associated signs.

A
  1. More common neurologic syndrome: incoordination, aimless wandering, intermittent anorexia, lethargy, obtundation, blindness and head pressing; followed by hyperexcitability, belligerance, extreme agitation, profuse sweating, delerium, recumbency with seizure and death.
  2. Hepatotoxic syndrome with swelling of the lips and muzzle, somnolence, icterus, petechial haemorrhage, abdominal breathing and cyanosis - resembles hepatic or intestinal encephalopathy.
73
Q

What is the causative agent of equine leukoencephalomalacia?

A

Fumonisin B1 intoxication (metabolite of mycotoxin fusarium moniliforme, usually from corn).

74
Q

What are the prominent signs of nigropallidal encephalomalacia associated with Yellow Star Thistle and Russian Knapweed?

A

Impairment of eating and drinking - lack of coordination of movements of prehension, mastication and deglutition. Can swallow if food/water is positioned at the back of the pharynx - may immerse their muzzle deeply in water to force it to the back of the pharynx. Often the mouth is held partially open with the lips retracted and the tongue protruding.

75
Q

What differences on histology would you expect between acute and chronic hepatic encephalopathy?

A

Acute: astrocyte swelling, acute cytotoxic cerebral oedema and intracranial hypertension.
Chronic: evidence of Alzheimer type II changes in addition to the above findings.