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Neuro > DL: Neuro Cases (Holgar and Piercey) > Flashcards

DL: Neuro Cases (Holgar and Piercey) Flashcards

1
Q

What type of neuro problems do horses get?

A
  • spinal/proprioceptive only!!
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2
Q

How does weakness manifest in horses?

A
  • toe drag
  • stumbling
  • shuffly steps
    > but can be d/t lameness/other ataxia too
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3
Q

How do proprioceptive tests in cats differ to dogs?

A
  • much less sensitive in cats than dogs
  • use table for concious proprioception in cats
  • extensor postural thrust used more commonly in cats
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4
Q

How do CN reflexes/responses differ in cats cf. dogs?

A
  • ^ Symp tone so poor PLR

- menace badly (make sure you do palpebral in between each meance)

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5
Q

Ddx for CSF with ^ protein, cell count esp neutrophils in a kitten?

A

> infectious

  • FIP (viral) test for corona virus but hard to dx d/t mutation (new test for specific protein coming out)
  • toxoplasma gondii (protozoa) PCR/serology
  • bacterial meningitis (very rare)
  • fungal [Cryptococcus, hyalohyphomycosis, phaemohyphomycosis] (very rare)
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6
Q

Neuro signs associated with FIP?

A
  • acute painful myelopathy
  • brainstem and cerebellar most common
  • seizures poss
  • dry form = pyogranulomatous and immune complex mediated vasculitis -> gelatinousi nfiltrate into ventricles
  • “inside and outside” affected -> meningitis and ventricles d/t blocked CSF outflow
    (pdf:
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7
Q

How long can a horse be recumbent (down without being able to get up) for before you give up on it

A

24-48hours

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8
Q

What may ^WBCS and neutrophils on bloods be indivcative of?

A

Stress leucogram

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9
Q

Which bones protect the brainstem in horses? When may these be damaged?

A
  • basisphenoid and basioccipital bones, rectus capitus m. underlies these
  • should be in line, v thick bones
  • can be fx if horse goes over backwards and hits head on floor
    > do not ocnfused symphysis of bones for a fx
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10
Q

Damage to what n. may -> DDSP?

A

Glossopharyngeal (IX)

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11
Q

Where does the facial nerve course?

A
  • stylomastoid foramen
  • vertical ramus of the mandible
  • across the masseter
    > if muzzle only place affected = distal portion of facial n. affected (section overlying masseter)
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12
Q

Tx of progressive brainstem lesion?

A
  • ^ dose steroids (no evidence for head trauma but do it anyway?)
  • hyertonic saline/mannitol - only really useful in acute phase of disease
  • NSAIDs
  • ## fluids
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13
Q

What does nystagmus indicate?

A

Acute onset as will compensate after a while
> peripheral vestibular lesion = horizontal
> central vestibular lesion = anything!!

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14
Q

Tx FIP?

A

None

- steroids and IFNw for palliative tx

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15
Q

What does hopping test detect mainly in horses?

A

Strength rather than coordination

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16
Q

Dx of FIP based on..?

A
  • FCov Ab titre/IHC
  • Alb: Glob ratio v (globulins in serum v high, A:G >0.8 r/o FIP, 0.4-0.8 consider other parameters)
  • AGP (acid glycoprotein, an acute phase protein) levels >1500ug/ml
  • haem: lymphopenia, non-regenerative anaemis, HCT
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17
Q

Clinical signs of head trauma in horses

A
  • haemorrhage/CSF from skull (ear, nostril, mouth)
  • blindness (sudden onset, fixed dilated pupils, papilloedema and retinl haemorrhage)
  • longus capitus rupture -> caudo-medial aspect GP
  • basisphenoid bone fx
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18
Q

Tx head trauma in the horse

A
  • NSAIDs
  • IV mannitol/hypertonic saline
  • ?corticosteroids (no evidence, everyone does)
  • IVFT
  • supportive nursing care (decubital/corneal ulcers, pneumonia)
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19
Q

3 [potential diseases classified as MUO?

A

(meningitis of unknown origin)
= meningoencephalomyelitis
> GME: granulomatous meningoencaphalitis
> NME: necoritising meningoencephalitis
> NLE: necrotising leukoencephalomyelitis

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20
Q

PDF for GME

A
  • any breed but esp toy and terriers
  • mean age ~5yrs
  • females
21
Q

3 forms of GME?

A 
> Diffuse 
- most common, multifocal disease
> focal 
- single SOL, ddx neoplasia
> ocular 
- optic n. affected
- can progress -> focal/disseminate
22
Q

Tx GME

A
  • procarbazine +- pred
  • radiation + pred
  • cytarabine + pred
  • cyclosporine +- steroids +- ketoconazole (best outcome)
23
Q

What is NME? pdf?

A

> necortising meningioencaphalitis
= pug dog encephalitis (though other breeds shih Tzu, Lhasa apso, Chihuahua can get)
- 6mo-7yrs, mean 19months
- esp fawn coloured females

24
Q

Clinical course of NME?

A
  • few days/months before presentation
  • FOREBRAIN signs (cerebrum +- thalamus)
  • mean survival 93d (1-680d)
25
Q

What is NLE? pdf?

A

> necrotising leucoencephalitis

  • 1-10yrs mean 4.5yrs
  • no sex predilection
  • esp yorkies but others too
26
Q

Clinical course of NLE?

A
  • highly variable, usually chronic and progressive
  • FOREBRAIN and BRAINSTEM
  • altered mentation, seizures, central blindness, central vestibular signs
27
Q

Viral causes of encephalitis

A

> Canine distemper encephalitis (CDE)
= immature/mature dogs = old dog encephalitis = chronic relapsing encephalomyelitis = post vaccinal CDE
- acute (most common) and chronic forms
- URT/GIT signs + myoclonus rhythmical contractions seen acutely
Rabies
- furious (more common in cats, cerebral signs + aggression)
- dumb/paralytic form (brainstem signs, dropped jaw and swallowing difficulty)

28
Q

Who should be contacted in a suspect rabies case?

A

Defra

29
Q

Protozoal causes of encephalitis?

A

> Toxoplasmosis/Neosporosis

  • toxoplasma gondii [dog and cat], neospora caninum [dog], sarcocystis neurona [horse]
  • pathogenesis by ingestion of infected tissue
30
Q

Clinical signs associated with toxoplasmosis/neosporosis?

A
  • seizures and cerebellar signs, neuromuscular

- systemic and ocular involvement

31
Q

Disgnosis of toxoplasmosis/neopsporosis?

A
  • IgM/G serology
  • MRI/CT
  • CSF mixed cell pleiocytosis
  • PCR on CSF
32
Q

Tx toxoplasmosis/neopsporosis?

A

> 8-12 weeks

  • TMPS 15mg/kg/BID
  • Clindamycin 20mg/kg BID
33
Q

Bacterial causes of encephalitis? Diagnostic indicators and Tx?

A

VERY RARE in dogs, cts and horses

  • haematogenous/local invasion
  • severe neutrophilic pleiocytosis
  • intracellular bacteria/bacterial culture from CSF
  • aggressive Abx to tx, ideally based on culture
34
Q

Parasitic causes of encephalitis?

A

> A. vasorum (metastrongyloid nematode) -> coagulopathy

35
Q

Clinical signs of a. vasorum encephalopathy?

A
  • mainly young dogs
  • cough + dyspnoea (essentially d/t interstitial pneumonia)
  • subcut swelling/haemorrhage
  • coagulopathy and thrombocytopenia
36
Q

Outline the lifecycle of A> Vasorum

A

> L1-L3 development in the snail
eaten by dog
penetrates GIT and develops in mesenteric LNs -> L5
Liver, portal v. -> Pulm a. and RV (10d post infection)
in heart , maturation in ~ 1month post-infect
adults shed eggs
develop -> L1 in pulm aa.
L1 penetrate cepillaries and alveolar walls
coughed up and swallowed
pooped out
-> Cycling beings again

37
Q

How can A. Vasorum cause a coagulopathy? What linical parameter is this associated with?

A
  • eosinophilia -> hypersensitivity
  • cellular response
  • deposition of immune complexes d/t adults irritating BVs
  • inappropriate activation of clotting uses up platelets
  • eggs hatching also inhibit thrombocytopoeisis
    > intravascular consumptive coagulopathy overall
  • prolonged APPT time observed clinically
38
Q

Causes of head tilt in horses?

A
  • trauma eg. basisphenoid bone fx
  • idiopathic
  • temporohyoid osteoarthropathy
  • otitis media/interna (rare)
39
Q

What is head tilt often seen in association with in horses?

A

facial n. signs

40
Q

Aetiology of temporohyoid osteoarthropathy?

A

> theories

  • chronic otitis media/interna
  • infection spreads to tympanohyoid joint and stylohyoid bnoe
  • inflame fuses tympanohyoid joint
  • degenerative hanges over time
  • muscle contraction mechanimal forces (swallowing/mastication) induce pathological fx extending into petrous temporal bone
41
Q

Tx temporohyoid Osteoarthropathy?

A
  • cefquinome/TMPS
  • NSAIDs
  • ceratohyoid bone removal
42
Q

Prognosis for temporohyoid osteoarthropathy?

A 
guarded
- 67% survival 
~ 50% will have residual vestibular +/+- facial deficits 
- recovery takes >1yr 
- risk of relapse
43
Q

How can thiamine levels be assessed ?

A
  • pyridoxal diphosphate assay on whole blood by HPLC (high performance liquid chromatography)
44
Q

Blood thiamine ref range?

A

136-332nmol/l

45
Q

Pathogensis of thiamine deficiency?

A 
> thiamine (vit B1) important for oxidative metabolism of many nutrients 
- 4 reasons: 
> reduced uptake
- anorexia/V+
- thiamine deficient food d/t overheating
- thiaminase activity of fish, bracken etc.
- sulphur dioxide 
> v absorption 
- D+
>altered utilisation 
- hepatopathy
> ^ consumption 
- fever
- infection 
- diuresis
46
Q

Clinical signs of thiamine deficiency?

A
  • anorexia/lethargy
  • vestibular signs
  • pupillary dilation/absent PLR
  • seizures
  • cats = head ventroflexion
47
Q

Diagnostic tools for thiamine deficiency

A
  • MRI: bilat symmetrical lesionin brainstem nuclei
  • transketolase activity in erythrocytes
  • ^ certain urinary organi acids (2-oxo/hydroxyadipate)
48
Q

Tx thiamine deficiency?

A

> thiamine!

  • 12.5-50mg/dog
  • 12.5-25mg/cat
  • sc q24hrs until oral supplemetns can be given
49
Q

What is the difference between LA and SA with vit B1 thiamine deficiency?

A

> Cattle: Polioencephalomalacia

  • thiamine deficiency often d/t ^ carb diet -> overgrowth of thiaminase producing bacteria/ingestion of bracken/high sulphur intake/clostridium
  • young large animals
  • clinical signs: profuse transient D+, listlessness, circling, opisthotonus, muscle tremors

Neuro (30 decks)

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