Cerebellar and vestibular disease - problem solving - neurology videos Flashcards

1
Q

How easy is it to differentiate ataxia and weakness in horses?

A

very difficult: weakness in horses short shuffle steps, knuckling over and toe dragging but can be seen with ataxia too. For ataxia look for hypermetria.

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2
Q

How common are cerebellar diseases in horses?

A

rare

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3
Q

Which regions do you test for facial sensation?

A
  • palpebral
  • in ear
  • nasal planum
  • upper lip
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4
Q

How do dogs and cats differ in the lesions that cause them to hop? Versus hrse?

A

In cats, you need quite large lesions to cause hopping defects unlike dogs where these defects are more obvious with smaller lesions. Hopping in horse – testing strength, in small animals you are looking more for proprioceptive dysfunction.

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5
Q

Which species is usually tested for extensor postural thrust most commonly?

A

cats - d/t size

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6
Q

How do you detect a headache in dogs/ cats?

A

you press head down and press on area where you would take CSF. If headache, this makes pain worse.

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7
Q

What might cause a feline CSF tap to have increased protein, increased TNCC and neutrophilic pleocytosis?

A
•	VIRAL
o	Coronavirus (FIP)
•	PROTOZOAL
o	Toxoplasma
•	BACTERIAL
•       FUNGAL
o	Cryptococcus
o	Phaeohyphomycosis
o	Hyalohyphomycosis
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8
Q

How do you test for Toxoplasma gondii?

A
  • ELISA
  • serology
  • PCR
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9
Q

How can you test for FIP coronavirus?

A

test for abnormal spike protein – new more specific test (for mutated virus which causes FIP versus the normal coronavirus which doesn’t cause FIP)

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10
Q

CS - FIP

A
  • other neuro signs common (seizure, cerebellar signs)

- systemic and ocular involvement

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11
Q

Pathogenesis - FIP

A

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12
Q

Dx - FIP

A
  • FCoV Ab titre > 128-
  • Albumin: Globulin (A:G) ration raised to globulin to over 40g/L. Ratio of >0.8 rule out FIP, if between 0.4-0.84 consider other parameter
  • Acid glycoprotein level (AGP): this is an APP, usually >1500 in FIP
  • Haematology
  • MRI or CT imaging
  • CSF (+PCR)
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13
Q

Haematology findings - FIP

A

Classically lymphopaenia, a non-regenerative anaemia with a haematocrit of 30% or less and often a neutrophilia with a shift to the left.

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14
Q

MRI or CT imaging of FIP

A

meningeal and ependymal enhancement

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15
Q

CSF - FIP

A

neutrophilic pleocytosis

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16
Q

Tx - FIP

A

SUPPORTIVE ONLY:

  • steroids
  • IFN
  • prognosis: tx only offers a short prolongation of life
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17
Q

If a horse likes having all 4 feet on the ground, does this suggest it is most likely ataxic or weak?

A

weak

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18
Q

If a horse doesn’t look in the direction of being turned, what does it suggest?

A

the horse doesn’t like turning

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19
Q

Are you more likely to get a nystagmus with an acute or chronic onset of brainstem problem?

A

acute - more likely to have nystagmus

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20
Q

How common is it to have a vascular lesion causing an acute onset neuro disease in horses?

A

Rare

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21
Q

Where does facial nn exit skull?

A

stylomastoid foramen

22
Q

Which CN controls soft palate?

23
Q

Tx - equine head trauma causing haematoma in GP

A
  • steroids contraindicated
  • drugs to limit oedema formation (hypertonic saline much more economical in horses than mannitol)
  • NSAIDs
  • euthanasia (realistic)
24
Q

Which skull bones are most commonly fractured in head trauma in horses? 2

A

Basisphenoid and basioccipital bone

25
Prognosis - equine CNS trauma
- Most horses that are recumbent for more than 24-48 hours don't get up. - Deal with things 24 hours at a time
26
Other names for precubital ulcers
pressure ulcers/ pressure sores
27
Different types of meningoencephalitis in dogs
- GME - granulomatous meningoencephalomyelitis - NME - necrotising meningoencephalomyelitis - NLE = necrotising leukoencephalomyelitis - Unknown aetiology (MUA)
28
Dx - meningoencephalitis
- CSF - CT or MRI - R/o infectious diseases
29
Signalment - GME
any breed (especially toy and terriers), mean 5 yo, female predisposition in many studies
30
3 main forms - GME
o Multifocal or disseminated CNS signs o Focal CNS signs o Ocular form: optic nerve, can progress into disseminated or focal forms or can be seen with disseminated form
31
3 main forms - GME
o Multifocal or disseminated CNS signs o Focal CNS signs o Ocular form: optic nerve, can progress into disseminated or focal forms or can be seen with disseminated form
32
Tx - GEM
• Various tx options o initial symptomatic tx  corticosteroids (prednisolone) until remission of signs/ stabilisation (wks) then slowly decrease dose  radiation therapy (selected patient)  ocular form - retrobulbar corticosteroids + oral steroid therapy o Monitoring `
33
Signalment - NME
• Signalment: 6months - 7 years, mean age 19 months (range 8-34), fawn coloured females
34
Clinical course - NME
``` o few days to months before presentation o FOREBRAIN (cerebrum +/- thalamus) o MST = 23 days (range 3-85 months) ```
35
Signalment - NLE
1-10 years (mean age 4.5 years), no sex predilection | • Yorkshire terriers and other breeds
36
Clinical course - NLE
o highly variable, usually chronic progressive o FOREBRAIN and BRAINSTEM o altered mentation, seizures, central blindness, central vestibular signs
37
Forms - Canine Distemper Encephalitis (CDE)
o ACUTE: commonest, associated with URT/ GIT signs, 'myoclonus - rhythmical contractions o CHRONIC: chronic slowly progressive signs o Old dog encephalitis
38
What are the different forms of rabies?
``` • FURIOUS FORM: o more common in cats o aggression, cerebral signs • DUMB/ PARALYTIC FORM: o mainly brainstem signs o dropped jaw o swallowing difficulties ```
39
Dx - toxoplasmosis/ neosporosis - 4
o IgG/ IgM serology o MRI or CT o CSF - mixed cell pleocytosis o PCR on CSF
40
Tx - toxoplasmosis/ neosporosis
o TMPS o Clindamycin o for 8-12 weeks
41
Clinical presentation - Angiostrongylus coagulopathy
* mainly young dogs * coughing * dyspnoea (interstitial pneumonia) * SC swelling or haemorrhage * Coagulopathies, thrombocytopaenia * Sudden death (acute heart failure) * neurological and ocular signs
42
Ddx - head tilt in horses
* Trauma - e.g. baisphenoid bone fracture * Idiopathic * Temporohyoid osteoarthropathy * Otitis interna/ media (rare)
43
Temporohyoid osteoarthropathy - aetiology
* Chronic otitis media/ interna: infection spreads to tympanohyoid joint and stylohyoid bone. The inflammatory process fuses the tympanohyoid joint. * Degenerative changes over time then mechanical forces of mm contraction during swallowing or mastication induce a pathologic fracture that extends into the pertrous temporal bone
44
Tx - temporohyoid osteopathy
* Cefquinome/ TMPS * NSAIDs * Ceratohyoid bone removal
45
Prognosis - temporohyoid osteoarthropathy
* of 33 horses, 67% survival * 95% athletic use * 60% residual facial deficits * 55% residual vestibular deificts * maximal recovery may take a year or more * risk of repeated episodes
46
Why is thiamine important?
Thiamine (vit B1) is important for oxidative metabolism of carbohydrates
47
4 reasons for thiamine deficiency (small animals)
o reduced uptake: d/t anorexia r vomiting, deficiency in food d/t overheating, thiaminase activity of fish or cereals, sulphur dioxide o Decreased absorption (diarrhoea) o Altered utilisation (hepatopathy) o Increased consumption (fever, infection, increased diuresis)
48
CS - thiamine deficiency (SA)
o anorexia and lethargy o vestibular signs o pupilllary dilation with reduced or absent PLR o seizures o cats often also show head ventroflexion
49
Dx - thiamine deficiency (SA) - 3
o MRI bilateral symmetrical lesion in brainstem nuclei o Transketolase activity in erythrocytes o increase in certain urinary organic acids
50
Tx - thiamine deficiency - SA
o Thiamine supplement IM or SC q24 hours until oral supplementation possible