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
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
3
Q
What is the main infectious cause of polymyositis affecting all muscles of the body?
A
Protozoal disease e.g. Toxo, Neospora
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
5
Q
What treatment is used for polymyositis in dogs?
A
Steroids at immunosuppressive doses
6
Q
What is idiopathic polyradiculoneuritis?
A
Coonhound paralysis, unknown cause. Similar to Guillome-Barry syndrome in humans
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
8
Q
How is idiopathic polyradiculoneuritis diagnosed?
A
No tests, only clinical presentation
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
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
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
12
Q
List the common physical causes of behaviour problems in dogs
A
- MSK/dental pain
- Anal sac impaction
- Hypothyroidism
- Congitive dysfunction
- Dietary sensitivity
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
14
Q
What behaviours are commonly seen with ischaemic accidents of the brain in cats?
A
- Severe aggression
- Hypersexual behaviours
15
Q
What are reactivity to noises and agrophobia in animals commonly related to?
A
Painful conditions, generalise very quickly
16
Q
List conditions that are commonly associated with repetitive behaviours and self mutilation
A
- Pain
- Itching
- GI disease
- Seizure activity
17
Q
What physical conditions are fear and anxiety behaviours commonly related to?
A
- Pain
- Hypothyroidism
- reduced sensory ability
- Hyper/hypoadrenocorticism
- Corticosteroid treatment
18
Q
What physical conditions is aggressive behaviour commonly related to?
A
- Pain
- Pruritus
- Inflammatory conditios
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
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)
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
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
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
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
25
Outline ways in which behavioural therapy can be made easier for the owners
- 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
26
Give examples of methods that can be used to build the foundations for behavioural modification
- 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
27
List potential reasons for non-compliance with behavioural modification plan
- 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
28
Describe desensitisation therapy in behaviour modification
- 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
29
Describe counter conditioning therapy in behaviour modification
- 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
30
Compare the 2 methods for counter conditioning of behaviour
- 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
31
Describe the method for desensitisation in behaviour modification
- Ideally when relaxed, may need medication
| - Initial stimulus exposure low, enough to notice but no anxiety attached, very short exposures
32
List non-infectious inflammatory diseases of the nervous system
- GME (granulomatous meningoencephalomyelitis)
- NME (necrotising meningoencephalomyelitis)
- NLE (necrotising leukoencephalitis)
- SRMA
- Cauda equina neuritis
- Pachimeningitis
- Eosinophilic
33
Describe the histopathological appearance of GME
- Characteristic granulomatose, angiocentric encephalitis
- Granuloma is a micture of macrophages, lymphocytes, plasma cells
- Usually white matter and meninges with secondary grey matter involvement
34
What is GME?
An inflammatory, immune mediated disease with unknown aetiology
35
What are the 2 methods of classification of GME?
- Clinical
| - Histopathological
36
What are the 3 clinical classifications of GME?
- Disseminated
- Focal
- Ocular
37
Describe disseminated clinical GME
- Most common
- Acute, rapidly progressive multifocal signs
- Mostly affects cerebrum, caudal brainstem, cerebellum and cervical spinal cord
38
Describe focal clinical GME
- Single granuloma acting as a space occupying lesion
- Most in brainstem
- Acute or slowly progressive
39
Describe ocular clinical GME
- Aka ocular neuritis
| - Affects optic nerves and optic chiasm
40
Where are histolopathological lesions of common disseminated GME typically found?
- Spinal cord
- Brainstem
- Midbrain
- Mainly hemispheric white matter
41
Where are histopathological lesions of focal GME typically found?
- Single discrete mass lesion
- Spinal cord
- Brainstem
- Midbrain
- Thalamus
- Optic nerves
- Cerebrum
42
How to multiple coalescing lesions of GME develop?
Disseminated form with angiocentric expansion
43
Describe the appearance of GME on MRI
- 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
What are the clinical features of GME?
- Young adult dogs (av 4-5yrs)
- Any gender
- But female, toy and terrier breeds over-represented
45
Describe the clinical signs of GME
- 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
List the methods used in the diagnosis of GME
- Rule out systemic disease
- Advanced imaging (MRI)
- CSF tap
- Histopathological confirmation
47
Describe the findings from a CSF tap in a case of GME
Mononuclear mixed pleocytosis, increased total protein
48
Describe the histopathological features that would allow confirmation of GME
- Angiocentric
- Mixed lymphoid
- White matter encephalitis
- Lymphocytic meningitis
49
Describe the treatment of GME
- Supportive e.g. mannitol for increased ICP
- Immunomodulatory
- Prognosis variable, outcome improving through use of polypharmacy
50
Describe NME
- 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
What area of the brain is primarily affected by NME?
Cerebral hemispheres
52
Describe the clinical features of NME
- Young adult dogs, mean age 2yo
- No gender predisposition
- Pug, maltese, pekingese all predisposed but any breed can be affected
53
Describe the clinical signs of NME
- 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
Which methods are used in the diagnosis of NME?
- Rule out systemic disease
- Advanced imaging (MRI)
- CSF
- Histopathology
55
Describe the MRI findings in a case of NME
- 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
What is found in CSF in a case of NME
Lymphocytic, increased total protein
57
Describe the histopathological findings in a case of NME
- Lymphocytic meningitis
- Polioencephalitis
- Necrotising leukoencephalitis
- Holes in brain where affected (fills with CSF)
58
Describe the treatment of NME
- Supportive: antiepileptics, mannitol to reduce ICP
- Immunomodulatory
- Prognosis variable but thorught to be more sinister vs GME due to necrosis
59
What is NLE?
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
Describe the clinical features of NLE
- Young adult dogs, mean 4.5yo
- No gender predisposition
- Yorkie, Pomeranian and Frenchie predisposed
61
Describe the clinical signs of NLE
- Rapidly progressive
- Depression
- Circling
- Vestibulocerebellar signs
- Visual deficits
- Seizures (towards end of disease, secondary grey matter involvement)
- Generally multifocal clinical signs
62
Describe the appearance of NLE on MRI
- Hyperintensities on T2 weighed and FLAIR
- Multiple cystic areas of necorsis
- Hypointense or isotense on T1 weighted images
- Can use contrast enhancement
63
Describe the CSF findings in NLE
Monocytic, increased total protein
64
Describe the histopathological findings in NLE
- 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
Describe the treatment of NLE
- Supportive: mannitol
- Immunomodulatory
- Prognosis is variable
66
What is MUA?
Meningoencephalitis of unknown aetiology
67
Outline the treatment of MUA
Immunosuppression:
- Corticosteroids
- Cytosine arabinoside
- Ciclosporines
- Azathioprine
68
Outline the use of corticosteroids in the treatment of MUA
- 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
Describe the mechanism of action of arabinoside
Synthetic nucleoside analogue, competes for incorporation into nucleic acids and inhibits DNA polymerase in mitotically active cells
70
Discuss the use of arabinoside in the treatment of MUA
- 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
What is an important consideration when using arabinoside in the treatment of MUA?
Likely to be better hospitalised as urine is radioactive for 48 hours
72
Outline the use of ciclosporine in the treatment of MUA
- 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
What is the mechanism of action of ciclosporin?
Suppressing T lymphocyte activation and proliferation
74
Describe the adverse effects of ciclosporin
- GI upset e.g. diarrhoea
- Gingival hyperplasia
- Change in coat (shedding or hirsuitism)
75
Describe the mechanism of action of azathioprine
Thiopurine, interferes with the productions of purine nucleotides leading to decreased lymphocyte proliferation
76
Discuss the use of azathioprine in the treatment of MUA
- 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
What is SRMA?
Steroid responsive meningitis arteritis
- Inflammatory immune mediated disease
- Suppurative inflammation (neutrophilic) affecting the leptomeninges of the spinal cord and causig necrotising fibrinoid arteritis
78
Describe the clinical features of SRMA
- Young dogs 6-18 months
- No gender predisposition
- Any breed, but beagle,, boxer, bernese mountain dog and weimaraner over represented
79
Describe the clinical signs of acute SRMA
- Profound cervical hyperaesthesia, neck pain
- Pyrexia (unless pre-treated with NSAIDs or steroid)
- Depression
- Increased CRP
80
How does chronic SRMA occur?
Is acute disease that either relapses or was treated inadequately
81
Describe the diagnosis of SRMA
- Neutrophilia
- MRI shows longus colli myositis, altered CSF signal (patchy hyperintensities around the spinal cord)
- CSF
82
Describe the CSF findings that would be consistent with acute or chonic SRMA
- 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
What experimental values can be used to test for SRMA in CSF?
- IgA
| - Acute phase C reactive protein (indicate systemic inflammation)
84
Describe the treatment of SRMA
- Immunosuppression e.g. corticosteroids, cytosine arabinoside, ciclosporins, azathioprine
- Prognosis fair to good
85
What is EME?
- Eosinophilic meningoencephalitis
| - Inflammatory, likely immune mediated disease (potentially allergic mechanism
86
Describe the pathophysiology of EME
Severe meningitis and periventriculitis with infiltration of underlying parenchyma
87
Describe the signalment of EME
- Young
- Male Golden Retrievers and Rottweilers may be over-represented
- Any breed and gender can be affected
88
Describe the diagnosis of EME
- MRI shows multifocal changes similar to GME: diffuse white matter inflammation, ventriculitis
- CSF showing eosinophilic ppleocytosis (is diagnostic for EME)
- NO histopathology required
89
Describe the management and prognosis of EME
- Immunosuppressive doses of corticosteroids
- Occasionally needs additional immunosuppressive drugs such as cytosine
- Prognosis variabale
90
What is pachimeningitis?
- Inflammatory, likely immune mediated condition
| - Recently recognised in dogs
91
Describe the pathophysiology of pachimeningitis
Characterised by prominent diffuse thickening of the dura mater by fibrosing inflammatory processes
92
Describe the clinical signs of pachimeningitis
- Reflect multiple cranial nerve deficits
- Present almost like trigeminal neuropathy
- Dropped jaw is most common complaint
93
Outline the diagnosis of pachimeningitis
- MRI: shows subtle changes but highly suggestive, inflammation of dura mater visible on T1 post gad.
- CSF may be inflammatory
94
Outline the treatment and prognosis of pachimeningitis
- 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
What are the potential sources of toxins affecting the nervous system?
- Endogenous (result of metabolic diseases)
| - Exogenous (plants, environmental toxins, envenomation, medications, food)
96
What are the signs of neuroexcitatory toxins affecting the CNS?
Hyperexcitability, seizures, ataxia
97
What are the signs of neuroexcitatory toxins affecting the PNS?
Muscle tremors and fasciculations
98
List common neuroexcitatory toxins
- Ivermectin and macrolides
- Metaldehyde
- Methylxanthines
- Organophosphates and carbamtes
- Permethrin
- Mycotoxins
- Strychnine
- Lead
99
What are the signs of neuroinhibitory toxins affecting the CNS?
Obtundation, stupor, coma
100
What are the signs of neuroinhibitory toxins affecting the PNS?
Weakness, flaccid paralysis
