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Neurology > Cerebellar and vestibular disease - problem solving - neurology videos > Flashcards

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?

A

CN 9

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
Q

Prognosis - equine CNS trauma

A
  • Most horses that are recumbent for more than 24-48 hours don’t get up.
  • Deal with things 24 hours at a time
26
Q

Other names for precubital ulcers

A

pressure ulcers/ pressure sores

27
Q

Different types of meningoencephalitis in dogs

A
  • GME - granulomatous meningoencephalomyelitis
  • NME - necrotising meningoencephalomyelitis
  • NLE = necrotising leukoencephalomyelitis
  • Unknown aetiology (MUA)
28
Q

Dx - meningoencephalitis

A
  • CSF
  • CT or MRI
  • R/o infectious diseases
29
Q

Signalment - GME

A

any breed (especially toy and terriers), mean 5 yo, female predisposition in many studies

30
Q

3 main forms - GME

A

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
Q

3 main forms - GME

A

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
Q

Tx - GEM

A

• 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
Q

Signalment - NME

A

• Signalment: 6months - 7 years, mean age 19 months (range 8-34), fawn coloured females

34
Q

Clinical course - NME

A 
o	few days to months before presentation
o	FOREBRAIN (cerebrum +/- thalamus)
o	MST = 23 days (range 3-85 months)
35
Q

Signalment - NLE

A

1-10 years (mean age 4.5 years), no sex predilection

• Yorkshire terriers and other breeds

36
Q

Clinical course - NLE

A

o highly variable, usually chronic progressive
o FOREBRAIN and BRAINSTEM
o altered mentation, seizures, central blindness, central vestibular signs

37
Q

Forms - Canine Distemper Encephalitis (CDE)

A

o ACUTE: commonest, associated with URT/ GIT signs, ‘myoclonus - rhythmical contractions
o CHRONIC: chronic slowly progressive signs
o Old dog encephalitis

38
Q

What are the different forms of rabies?

A 
•	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
Q

Dx - toxoplasmosis/ neosporosis - 4

A

o IgG/ IgM serology
o MRI or CT
o CSF - mixed cell pleocytosis
o PCR on CSF

40
Q

Tx - toxoplasmosis/ neosporosis

A

o TMPS
o Clindamycin
o for 8-12 weeks

41
Q

Clinical presentation - Angiostrongylus coagulopathy

A
  • mainly young dogs
  • coughing
  • dyspnoea (interstitial pneumonia)
  • SC swelling or haemorrhage
  • Coagulopathies, thrombocytopaenia
  • Sudden death (acute heart failure)
  • neurological and ocular signs
42
Q

Ddx - head tilt in horses

A
  • Trauma - e.g. baisphenoid bone fracture
  • Idiopathic
  • Temporohyoid osteoarthropathy
  • Otitis interna/ media (rare)
43
Q

Temporohyoid osteoarthropathy - aetiology

A
  • 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
Q

Tx - temporohyoid osteopathy

A
  • Cefquinome/ TMPS
  • NSAIDs
  • Ceratohyoid bone removal
45
Q

Prognosis - temporohyoid osteoarthropathy

A
  • 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
Q

Why is thiamine important?

A

Thiamine (vit B1) is important for oxidative metabolism of carbohydrates

47
Q

4 reasons for thiamine deficiency (small animals)

A

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
Q

CS - thiamine deficiency (SA)

A

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
Q

Dx - thiamine deficiency (SA) - 3

A

o MRI bilateral symmetrical lesion in brainstem nuclei
o Transketolase activity in erythrocytes
o increase in certain urinary organic acids

50
Q

Tx - thiamine deficiency - SA

A

o Thiamine supplement IM or SC q24 hours until oral supplementation possible

Neurology (26 decks)

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