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NEU2 > Neurological diseases of small animals 2 > Flashcards

Neurological diseases of small animals 2 Flashcards

1
Q

Discuss why the use of immunosuppressive doses of steroids may be contraindicated in the treatment of myasthenia gravis

A

Common side effect of MG is megaoesophagus, risk of aspiration pneumonia and immunosuppression would be dangerous in this situation

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2
Q

Describe the clinical signs of polymyositis

A
  • Pain in all muscles
  • refusal to move
  • Masticatory myositis (most common) leading to inability to open jaw, atrophy of jaw, appearance of sunken in head
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3
Q

What is the main infectious cause of polymyositis affecting all muscles of the body?

A

Protozoal disease e.g. Toxo, Neospora

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4
Q

How is non-infectious polymyositis of the dog diagnosed?

A
  • May have autoantibodies but no test available for generalised
  • Blood: proteins/globulins and creatine kinase markely increased
  • Pain on squeezing muscle
  • Electrophysiology and biopsy
  • Pain and elevated CK usually enough
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5
Q

What treatment is used for polymyositis in dogs?

A

Steroids at immunosuppressive doses

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6
Q

What is idiopathic polyradiculoneuritis?

A

Coonhound paralysis, unknown cause. Similar to Guillome-Barry syndrome in humans

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7
Q

Describe the clinical signs of idiopathic polyradiculoneuritis in the dog

A
  • Hindlimb weakness/ataxia progressing to paresis/paralysis
  • Continues to ascend up the body
  • May affect phrenic nerve and cause respiratory failure
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8
Q

How is idiopathic polyradiculoneuritis diagnosed?

A

No tests, only clinical presentation

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9
Q

Describe the treatment for idiopathic polyradiculoneuritis

A
  • Conservative therapy
  • Intensive nursing (but will maintain bowel and bladder control) to ensure they can eat and are comfortable
  • Frequently good recovery
  • Poor prognosis with megoesophagu
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10
Q

Describe the presentation, diagnosis and treatment of distal denervating disease in dogs

A
  • Sudden onset weakness
  • No diagnostic method
  • No specific treatment, respond to nursing
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11
Q

List your differential diagnoses for unilateral facial paralysis with abnormalities confined to the facial nere

A
  • Neoplasia in brainstem/ear/peripheral affectin CNVII
  • Otitis media/interna
  • Abscess around nerve
  • Inflammation of brainstem (would expect other signs)
  • Idiopathic facial nerve paralysis (most likely)
  • Trauma to facial nerve
  • Ivermectin toxicity (in collie)
  • FCE/embolism
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12
Q

List the common physical causes of behaviour problems in dogs

A
  • MSK/dental pain
  • Anal sac impaction
  • Hypothyroidism
  • Congitive dysfunction
  • Dietary sensitivity
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13
Q

List common physical causes of behaviour problems in cats

A
  • Upper and lower urinary tract conditions
  • Pain focus
  • Cognitive dysfunction
  • Ischaemic accident in brain
  • Hyperthyroidism
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14
Q

What behaviours are commonly seen with ischaemic accidents of the brain in cats?

A
  • Severe aggression

- Hypersexual behaviours

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15
Q

What are reactivity to noises and agrophobia in animals commonly related to?

A

Painful conditions, generalise very quickly

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16
Q

List conditions that are commonly associated with repetitive behaviours and self mutilation

A
  • Pain
  • Itching
  • GI disease
  • Seizure activity
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17
Q

What physical conditions are fear and anxiety behaviours commonly related to?

A
  • Pain
  • Hypothyroidism
  • reduced sensory ability
  • Hyper/hypoadrenocorticism
  • Corticosteroid treatment
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18
Q

What physical conditions is aggressive behaviour commonly related to?

A
  • Pain
  • Pruritus
  • Inflammatory conditios
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19
Q

What physical conditions is house soiling commonly related to?

A
  • Cystitis
  • GI disease
  • Sensory perception problems
  • Arthritis, other causes of pain on movement
  • Diabetes mellitus/insipidus, hyperadrenocorticism, other causes of PUPD
  • Anatomical abnormalities and other causes of incontinence
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20
Q

Describe the different types of pain related affect

A
  • Emotional reactions (stimulus bound, short lived)
  • Moods (response to series of events/pervasive changes, bias cognition)
  • Temperament; irritability (largely depends on genetics and early experience, affective style arising from characteristics of early environment)
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21
Q

What are the key points in the treatment of behavioural problems?

A
  • Ensure safety of animal and people
  • Prevent worsening of problem
  • Resolve/reduce problem
  • Provide foundations for longer term interventions in some cases
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22
Q

Outline the aspects of ensuring safety of the patient with regards to behavioural problems

A
  • Minimise risk of self injury e.g. self mutliation
  • Minimise distress
  • Minimise risk of abandonement by building owner understanding
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23
Q

Outline the aspects of ensuring the safety of people with regards to a pet with behavioural problems

A
  • Restrict access of other people to animal
  • Avoid confrontation by learning to understand warning signals, may need to let animal “get away with it”
  • Muzzle training
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24
Q

Outline how to prevent worsening of an unwanted behaviour

A
  • Avoid triggers
  • Manage (distraction)
  • Stop confrontation (distraction, prevention of access to trigger)
  • Stop punishment
  • Reinforce appropriate behaviour
  • Implement the obvious e.g. litter trays, scratch posts, chews, toys, games
  • Owner consistency important
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25
Q

Outline ways in which behavioural therapy can be made easier for the owners

A
  • Ensure owners are aware that they are not alonge
  • Management of public/neighbours
  • Educate on benefits of muzzle, allow owner to tell strangers to not tough dog
  • Use of food can be positive
  • Explain how to manage emergencies with neutral response
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26
Q

Give examples of methods that can be used to build the foundations for behavioural modification

A
  • Meal feeding, use of food toys
  • Establish obedience responses: set up expectations in dog and owner, relationship building to allow working relationship, build skills in dog
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27
Q

List potential reasons for non-compliance with behavioural modification plan

A
  • No confidence in counsellor
  • Competing advice
  • Treatment too much bother/unnatural/seems cruel
  • Problems may have “secondary gains”
  • Family dynamics where one person implements, another does not
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28
Q

Describe desensitisation therapy in behaviour modification

A
  • Raising the threshold at which an animal response to a stimulus/reduction in response to a stimulus
  • Can teach relaxation protocol to dogs but owner often prefers desensitisation protocol which does not require relaxed state before starting
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29
Q

Describe counter conditioning therapy in behaviour modification

A
  • Substituting a response to a simulus with one that is incompatible with the current, unwanted response
  • Can be at a behavioural or emotional level
  • Emotional level often needs to be changed
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30
Q

Compare the 2 methods for counter conditioning of behaviour

A
  • Respondent: bar open/bar closed i.e. stimulus starts = good stuff starts, stimulus stops = good stuff stops. Stimulus must be at level at which animal can disregard it and the negative emotion is not triggered
  • Operant: response substitution, teach away from the stimulus first by teaching wanted response to a stimulus
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31
Q

Describe the method for desensitisation in behaviour modification

A
  • Ideally when relaxed, may need medication

- Initial stimulus exposure low, enough to notice but no anxiety attached, very short exposures

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32
Q

List non-infectious inflammatory diseases of the nervous system

A
  • GME (granulomatous meningoencephalomyelitis)
  • NME (necrotising meningoencephalomyelitis)
  • NLE (necrotising leukoencephalitis)
  • SRMA
  • Cauda equina neuritis
  • Pachimeningitis
  • Eosinophilic
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33
Q

Describe the histopathological appearance of GME

A
  • Characteristic granulomatose, angiocentric encephalitis
  • Granuloma is a micture of macrophages, lymphocytes, plasma cells
  • Usually white matter and meninges with secondary grey matter involvement
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34
Q

What is GME?

A

An inflammatory, immune mediated disease with unknown aetiology

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35
Q

What are the 2 methods of classification of GME?

A
  • Clinical

- Histopathological

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36
Q

What are the 3 clinical classifications of GME?

A
  • Disseminated
  • Focal
  • Ocular
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37
Q

Describe disseminated clinical GME

A
  • Most common
  • Acute, rapidly progressive multifocal signs
  • Mostly affects cerebrum, caudal brainstem, cerebellum and cervical spinal cord
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38
Q

Describe focal clinical GME

A
  • Single granuloma acting as a space occupying lesion
  • Most in brainstem
  • Acute or slowly progressive
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39
Q

Describe ocular clinical GME

A
  • Aka ocular neuritis

- Affects optic nerves and optic chiasm

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40
Q

Where are histolopathological lesions of common disseminated GME typically found?

A
  • Spinal cord
  • Brainstem
  • Midbrain
  • Mainly hemispheric white matter
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41
Q

Where are histopathological lesions of focal GME typically found?

A
  • Single discrete mass lesion
  • Spinal cord
  • Brainstem
  • Midbrain
  • Thalamus
  • Optic nerves
  • Cerebrum
42
Q

How to multiple coalescing lesions of GME develop?

A

Disseminated form with angiocentric expansion

43
Q

Describe the appearance of GME on MRI

A
  • Hyperintensities on T2 weighted or FLAIR throughout CNS white matter indicating lesions or oedema
  • Variable intensity on T1 weighted
  • Variable contrast uptake on T1 post gadolinium, may enhance, may not
  • Variable meningeal enhancement
  • Oedema secondary to inflammation
  • Patchy appearance
44
Q

What are the clinical features of GME?

A
  • Young adult dogs (av 4-5yrs)
  • Any gender
  • But female, toy and terrier breeds over-represented
45
Q

Describe the clinical signs of GME

A
  • Pretty much any neurological signs possible
  • Vestibulo-cerebellar
  • Cranial nerve deficits
  • Visual impairment
  • paresis
  • Cervical pain
  • Ataxia, proprioceptive deficits
  • Body turn
  • Altered mentation
  • Seizures (possible but unlikely)
  • May have normal mentation and only show subtle signs
46
Q

List the methods used in the diagnosis of GME

A
  • Rule out systemic disease
  • Advanced imaging (MRI)
  • CSF tap
  • Histopathological confirmation
47
Q

Describe the findings from a CSF tap in a case of GME

A

Mononuclear mixed pleocytosis, increased total protein

48
Q

Describe the histopathological features that would allow confirmation of GME

A
  • Angiocentric
  • Mixed lymphoid
  • White matter encephalitis
  • Lymphocytic meningitis
49
Q

Describe the treatment of GME

A
  • Supportive e.g. mannitol for increased ICP
  • Immunomodulatory
  • Prognosis variable, outcome improving through use of polypharmacy
50
Q

Describe NME

A
  • Inflammatory disease of unknown aetiology, most likely immune mediated
  • Non-suppurative (no neutrophils), necrotising
  • Pan-encephalitis, all CNS structures involved (meninges, grey and white matter)
51
Q

What area of the brain is primarily affected by NME?

A

Cerebral hemispheres

52
Q

Describe the clinical features of NME

A
  • Young adult dogs, mean age 2yo
  • No gender predisposition
  • Pug, maltese, pekingese all predisposed but any breed can be affected
53
Q

Describe the clinical signs of NME

A
  • Rapidly progressive
  • Seizures due to grey matter involvement
  • Depression (diffuse forebrain disease)
  • Circling (lateralisation in effects on hemispheres)
  • Visual deficits
  • Will usually stand with legs splayed rather than sit down
54
Q

Which methods are used in the diagnosis of NME?

A
  • Rule out systemic disease
  • Advanced imaging (MRI)
  • CSF
  • Histopathology
55
Q

Describe the MRI findings in a case of NME

A
  • Hyperintensities on T2 weighted and FLAIR images
  • Isointense to slightly hypointense on T1 weighted
  • Variable contrast enhancement on T1 weighted
  • Loss of grey/white matter demarcation
56
Q

What is found in CSF in a case of NME

A

Lymphocytic, increased total protein

57
Q

Describe the histopathological findings in a case of NME

A
  • Lymphocytic meningitis
  • Polioencephalitis
  • Necrotising leukoencephalitis
  • Holes in brain where affected (fills with CSF)
58
Q

Describe the treatment of NME

A
  • Supportive: antiepileptics, mannitol to reduce ICP
  • Immunomodulatory
  • Prognosis variable but thorught to be more sinister vs GME due to necrosis
59
Q

What is NLE?

A

Inflammatory disease of unknown aetiology, suspected immune mediated causing non-suppurative necrotising encephalitis affecting the hemispheric white matter and brainstem, without cortex or meninges involvement

60
Q

Describe the clinical features of NLE

A
  • Young adult dogs, mean 4.5yo
  • No gender predisposition
  • Yorkie, Pomeranian and Frenchie predisposed
61
Q

Describe the clinical signs of NLE

A
  • Rapidly progressive
  • Depression
  • Circling
  • Vestibulocerebellar signs
  • Visual deficits
  • Seizures (towards end of disease, secondary grey matter involvement)
  • Generally multifocal clinical signs
62
Q

Describe the appearance of NLE on MRI

A
  • Hyperintensities on T2 weighed and FLAIR
  • Multiple cystic areas of necorsis
  • Hypointense or isotense on T1 weighted images
  • Can use contrast enhancement
63
Q

Describe the CSF findings in NLE

A

Monocytic, increased total protein

64
Q

Describe the histopathological findings in NLE

A
  • Asymmetric, bilateral necrotising encephalitis
  • Hemispheric white matter and brainstem affected
  • Overlying cortex and meninges not involve
  • Histiocyte, microglia and macrophage cell infiltrates
  • Lymphocytic perivascular cuffing
65
Q

Describe the treatment of NLE

A
  • Supportive: mannitol
  • Immunomodulatory
  • Prognosis is variable
66
Q

What is MUA?

A

Meningoencephalitis of unknown aetiology

67
Q

Outline the treatment of MUA

A

Immunosuppression:

  • Corticosteroids
  • Cytosine arabinoside
  • Ciclosporines
  • Azathioprine
68
Q

Outline the use of corticosteroids in the treatment of MUA

A
  • Pred 1.5mg/kg BID then progressively reduced over 6 months to maintenance of 0.5mg/kg EOD
  • Dex: 0.2mg/kg SID then progressively reduce over 6 months to maintenance of 0.05mg/kg EOD
  • Need to treat 6 months minimum and progressively reduce the dose depending on the patient
  • Monitor haematology
69
Q

Describe the mechanism of action of arabinoside

A

Synthetic nucleoside analogue, competes for incorporation into nucleic acids and inhibits DNA polymerase in mitotically active cells

70
Q

Discuss the use of arabinoside in the treatment of MUA

A
  • 50gm/m^2 SC q12 h for 2 consecutive days, repeat every 3-6 weeks (or longer intervals according to clinical signs), 4 times, then increase number of weeks between injections
  • Once at 12 week gap, patient may no longer need drug and could discontinue
  • Monitor haematology
  • need to be accurate as is chemotherapeuttic
71
Q

What is an important consideration when using arabinoside in the treatment of MUA?

A

Likely to be better hospitalised as urine is radioactive for 48 hours

72
Q

Outline the use of ciclosporine in the treatment of MUA

A
  • 6mg/kg PO q12h but base on patient
  • Can be combined with ketoconazole to significantly reduce dose of ciclosporin needed, but more impact on liver metabolism
73
Q

What is the mechanism of action of ciclosporin?

A

Suppressing T lymphocyte activation and proliferation

74
Q

Describe the adverse effects of ciclosporin

A
  • GI upset e.g. diarrhoea
  • Gingival hyperplasia
  • Change in coat (shedding or hirsuitism)
75
Q

Describe the mechanism of action of azathioprine

A

Thiopurine, interferes with the productions of purine nucleotides leading to decreased lymphocyte proliferation

76
Q

Discuss the use of azathioprine in the treatment of MUA

A
  • 2mg/kg SID tapered to 0.5-1mg/kg EOD long term
  • Cheaper but needs regular monitoring, more toxic than other treatments
  • Hepatic metabolism affected
  • Side effects include bone marrow suppression and GI disturbance
77
Q

What is SRMA?

A

Steroid responsive meningitis arteritis

  • Inflammatory immune mediated disease
  • Suppurative inflammation (neutrophilic) affecting the leptomeninges of the spinal cord and causig necrotising fibrinoid arteritis
78
Q

Describe the clinical features of SRMA

A
  • Young dogs 6-18 months
  • No gender predisposition
  • Any breed, but beagle,, boxer, bernese mountain dog and weimaraner over represented
79
Q

Describe the clinical signs of acute SRMA

A
  • Profound cervical hyperaesthesia, neck pain
  • Pyrexia (unless pre-treated with NSAIDs or steroid)
  • Depression
  • Increased CRP
80
Q

How does chronic SRMA occur?

A

Is acute disease that either relapses or was treated inadequately

81
Q

Describe the diagnosis of SRMA

A
  • Neutrophilia
  • MRI shows longus colli myositis, altered CSF signal (patchy hyperintensities around the spinal cord)
  • CSF
82
Q

Describe the CSF findings that would be consistent with acute or chonic SRMA

A
  • Acute: marked neutrophilic pleocytosis and raised total protein
  • Chronic: mixed or mononuclear pleocytosis, raised total protein
  • Grossly may appear orange/pink as opposed to the normal clear colour
83
Q

What experimental values can be used to test for SRMA in CSF?

A
  • IgA

- Acute phase C reactive protein (indicate systemic inflammation)

84
Q

Describe the treatment of SRMA

A
  • Immunosuppression e.g. corticosteroids, cytosine arabinoside, ciclosporins, azathioprine
  • Prognosis fair to good
85
Q

What is EME?

A
  • Eosinophilic meningoencephalitis

- Inflammatory, likely immune mediated disease (potentially allergic mechanism

86
Q

Describe the pathophysiology of EME

A

Severe meningitis and periventriculitis with infiltration of underlying parenchyma

87
Q

Describe the signalment of EME

A
  • Young
  • Male Golden Retrievers and Rottweilers may be over-represented
  • Any breed and gender can be affected
88
Q

Describe the diagnosis of EME

A
  • MRI shows multifocal changes similar to GME: diffuse white matter inflammation, ventriculitis
  • CSF showing eosinophilic ppleocytosis (is diagnostic for EME)
  • NO histopathology required
89
Q

Describe the management and prognosis of EME

A
  • Immunosuppressive doses of corticosteroids
  • Occasionally needs additional immunosuppressive drugs such as cytosine
  • Prognosis variabale
90
Q

What is pachimeningitis?

A
  • Inflammatory, likely immune mediated condition

- Recently recognised in dogs

91
Q

Describe the pathophysiology of pachimeningitis

A

Characterised by prominent diffuse thickening of the dura mater by fibrosing inflammatory processes

92
Q

Describe the clinical signs of pachimeningitis

A
  • Reflect multiple cranial nerve deficits
  • Present almost like trigeminal neuropathy
  • Dropped jaw is most common complaint
93
Q

Outline the diagnosis of pachimeningitis

A
  • MRI: shows subtle changes but highly suggestive, inflammation of dura mater visible on T1 post gad.
  • CSF may be inflammatory
94
Q

Outline the treatment and prognosis of pachimeningitis

A
  • Immunosuppressive doses of corticosteroids
  • Occasionally needs additional immunosuppressive drugs such as cytosine
  • Far prognosis, most dogs achieve clinical remission but cure difficult to obtain
95
Q

What are the potential sources of toxins affecting the nervous system?

A
  • Endogenous (result of metabolic diseases)

- Exogenous (plants, environmental toxins, envenomation, medications, food)

96
Q

What are the signs of neuroexcitatory toxins affecting the CNS?

A

Hyperexcitability, seizures, ataxia

97
Q

What are the signs of neuroexcitatory toxins affecting the PNS?

A

Muscle tremors and fasciculations

98
Q

List common neuroexcitatory toxins

A
  • Ivermectin and macrolides
  • Metaldehyde
  • Methylxanthines
  • Organophosphates and carbamtes
  • Permethrin
  • Mycotoxins
  • Strychnine
  • Lead
99
Q

What are the signs of neuroinhibitory toxins affecting the CNS?

A

Obtundation, stupor, coma

100
Q

What are the signs of neuroinhibitory toxins affecting the PNS?

A

Weakness, flaccid paralysis

NEU2 (23 decks)

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