Neurological diseases of small animals 4 Flashcards
Pain
1
Q
Give examples of pain scales specific for osteoarthritis pain
A
- Canine Brief Pain Inventory
- Liverpool Osteoarthritis in Dogs scale
2
Q
Give examples of drugs licensed for the treatment of osteoarthritis in the UK
A
- Cimicoxib
- Carprogen
- Meloxicam
- Firocoxib
- Grapiprant
- Robenacoxib
3
Q
Give examples of drugs not licensed, but indicated, for the treatment of osteoarthritis in dogs in the UK
A
- Derocoxib
- Etodolax
4
Q
Give examples of nutritional supplements that are indicated in the treatment of chronic pain due to osteoarthritis
A
- Glucosamine
- chondroitin
- Green lipped muscle
5
Q
Describe the histopathological apperance of chromatolysis
A
- Swelling and loss of Nissl substance
- Nucleus pushed to side
6
Q
Explain how chromatolysis of neurones occurs
A
- Axonal damage or toxicity
- Neuronal degeneration
7
Q
What may cause the histopathological appearance of hyperoesinophilic, shrunken neurons?
A
- Ischaemia
- Hypoglycaemia
- Vitamin deficiencies e.g. thiamine
- INtoxications e.g. cyanide, lead, mercur
8
Q
Describe the appearance of necrotic neurones
A
- Cells appear red
- More condensed
- Pyknotic neuclei
- Irreversible
9
Q
What may cause the histopathological appearance of swollen neurons?
A
Lysosomal storage diseases
10
Q
Describe the presentation of animals with storage diseases
A
- Neurological deficits 1-1.5 years old (takes time for metabolites to accumulate to degree where will cause neurosigns)
- Ataxia
- Visual deficits
- Liver condition
11
Q
Describe the histopathological appearance of lysosomal storage diseases
A
- Markedly enlarged neurons with some kind of inclusion
- White metabolite may be seen
12
Q
Describe the different viral inclusion bodies that can occur in neurons
A
- Nuclear: Herpes, Adeno and Borna viruses
- Cytoplasmic: Pox virus, rabies
- Intranuclear and intracytoplasmic: Paramyxovirus (distemper)
13
Q
Describe the inclusion bodies that may be seen in Rabies
A
Negri bodies in cytoplasma (darker purple bodies, often at periphery of cytoplasm)
14
Q
Describe the inclusion bodies seen with distemper
A
Large eosinophilic inclusion bodies in the neuron nucleus
15
Q
What conditions may cause the cytoplasmic vacuolation of neurones?
A
Spongiform encephalopathies - pathognomic
16
Q
What causes the vacuolation of white matter tracts?
A
Trauma to spinal cord leading to the degeneration of white matter tract
17
Q
What causes axonal swellings (spheroids) on histopathology?
A
- Shuttling system of axon non-functional
- e.g. oedema, lack of oxygen
- (Reversible but advanced so survival unlikely)
18
Q
What causes gliosis on histopathology?
A
Acute or ongoing liver failure e.g. hepatic encephalic syndrome in horses
19
Q
Describe the apperance gliosis on histopathology
A
Alzheimer type 2 cells
- Upset astrocytes, round cells with vacuolation (activation and proliferation)
20
Q
What are Gitter cells?
A
Microglia cells that become enlarged
21
Q
What causes the appearance of gitter cells on histopathology?
A
Acute necrosis in the brain e.g. due to ischaemic infarct, migrating larvae. Are required to clean up necrotic damage in malacic areas
22
Q
Describe the histopathological appearance of demyelination
A
- White matter phagocytosed by gitter cells
- Strands visible (remnants of axons)
- WM completely gone
23
Q
Give an example of a disease that causes a demyelination histopathological appearance
A
Distemper (causes death of oligocytes)
24
Q
Compare the histopathology of de- and hypomyelination
A
- Demyelination: had normal myelination, destroyed by gitter cells
- Hypo: never myelination present, no white matter, some axons, no Gitter cells
25
What conditions may cause the hypomyelination apperance on histopathology?
In utero infection with BVDV or Border disease
26
Describe the histopathological appearance of cerebral oedema
- Increased extracellular fluid
| - Seen as white spaces in tissue
27
Describe the histopathological appearance of cytotoxic oedema
Increased intracellular fluid
28
What conditions may cause cytotoxic oedema of neural tissue?
- Vascular leakage e.g. vasculitis, blood thinning, toxic agent
- Low ATP, low oxygen affecting cellular pumps
29
Where and why does brain herniation usually occur in the dog?
- Oedematous fluid in brain due to lack of space
| - Foramen magnum
30
Describe the gross pathological apperance of congenital hydrocephalus
- Expansion of ventricles
| - Loss of CNS tissue (pressure atrophy, necrosis, hypoplasia)
31
Explain the ways in which congenital hydrocephalus can develop
- Fusion of colliculi or agenesis of mesencephalic aqueduct
- OR BVDV, Schmallenberg or border discease infection (porencephaly, hydrancephaly) leading to migration of neurons being disturbed
- In foals: anomaly of mesencephalic aqueduct preventing ventricular fluid flowing from lateral to 4th ventricle so lateral swells increasing pressure on sides of brain
32
What is congenital lissencephaly? Clinical signs?
Smooth brain, may have no clinical signs even with little to no neocortex left esp. if only neocortex affected
33
What causes congenital lissencephaly?
Disturbance of neuronal migration and proliferation during development, common in Lhasa Apso
34
List the potential causes of cerebellar hypoplasia
- In utero BVDV
- congeital malformation
- Parvovirus in dogs possible cause (rare)
35
What is myelomalacia? Aetiology?
- Necrosis of the spinal cord
| - Potential aetiology: FCE
36
Describe the histopathological appearance of myelomalacia
Pale cartilaginous emboli in haemorrhagic spinal cord segment
37
Describe the histopathological appearance of listeriosis
- Caudal brainstem: suppurative foci with numerous neutrophils, some macrophages infiltrating the neuroparenchyma (aka microabscesses)
- Pons affected most
38
How do viral neuro infections often manifest histopathologically?
Non-suppurative (meningo)-encephalo(myel)itis, with or without viral inclusion bodies
- Pure lymphocytic glial disease
- Perivascular accumulations of lymphocytes common
39
Describe the histopathological appearance of Aujesky's disease
- Characterised by perivascular cuffing and intense focal liosis and inflammatory infiltration within neocortex
- Some neutrophils present in the infiltrate
40
Describe the pathological appearance of cerebral cortical necrosis
- Aka polioencephalomalacia
- Liquefactive necrosis with varying degrees of tissue separation
- acute necrosis of grey matter substance
- White matter congested (brown discolourations)
- Autofluorescence of necrotic areas when highlight with UV
41
Name the primary neoplasias of the CNS
- Meningioma
- Astrocytoma and oligodendroglioma
- Ependymoma/choroid plexus tumour
- Neuroblastomas/medulloblastoma (PNET)
42
Briefly describe meningiomas
- Slow growing, surgery often curative
| - Common in cats, 9 different subtypes
43
Briefly describe astrocytomas and oligodendrogliomas
- More common in dogs vs cats
- Astro: lots of interactions with surrounding cells, poorly demarcated
- Oligo: tumour of cells producing myelin, if well differentiated are superbly demarcated
44
Briefly describe ependymomas/choroid plexus tumours
- Ventricular tumours
- If large can obstruct CSF flow
- Leads to acquired hydrocephalus, herniation, severely ill/dead animal
45
How do metastasis in CNS tissue occur?
Haematogenous spread only
46
What are the treatment goals in emergency status epilepticus treatment?
- Terminate seizure activity
| - Identify and treat cause for seizures
47
List the emergency treatment options for status epilepticus
- Diazepam
- Phenobarbital
- Propofol
- Midazolam
- Pentobarbitone
48
By what routes can diazepam be given in the emergency treatment of status epilepticus and give the dose
- IV best, but difficult
- Per rectum
- Per osunreliable as an anti-convulsant
- 0.5-1mg/kg
49
How long does diazepam work as an anticonvulsant for and describe the dosing frequency?
- Lasts ~20 mins
- Repeat as necessary 3-4x
- CRI can be used
50
What is the first option for treatment of an ongoing seizure?
Diazepam
51
What is the second option for treatment of an ongoing seizure?
Phenobarbital
52
Describe the route, dose and time to effect for phenobarbital in the emergency treatment of status epilepticus
- Slow absorption PO, need to use IV
- IV 2-3mg/kg (same as PO dose) but can increase to 10mg/kg
- Can take 20 mins to take effect
53
What drugs can be added in the emergency treatment of status while phenobarbital takes effect?
Diazepam or propofol
54
Outline the dose and length of action of propofol in the emergency treatment of status
- IV titrated to effect, should be anto-convulsant prior to anaesthetic effect
- Lasts 20mins
55
What should be available quickly when using propofol as an emergency anticonvulsant?
ET tube and ventilation in case of accidental anaesthetic induction
56
Discuss the use of pentobarbitone as an emergency treatment for status
- Effective, up to 8 hours effect but not available as sterile preparation, cannot be legally defended
- BUT status carries poor prognosis so may need to consider euthanasia anyway
57
What factors, other than the seizure activity, need to be addressed in the emergency treatment of status epilepticus?
- Electrolytes
- Hypoglycaemia
- Temperature (hyperthermia due to seizure, use fans, wet towels, ice enemas etc.)
58
Outline the logical approach to emergency spinal trauma
- First: assessment: neuro and other problems e.g. haemorrhage
- Radiography but no anaesthesia due to risk of ischaemic episode, care with positioning to avoid exacerbating trauma
59
What are the options in the case of a spinal cord laceration following spinal trauma?
Poor prognosis, euthanasia likely, poor QOL
60
What are the options in a case of spinal trauma where deep pain sensation is present?
- Conservative management (1-2 weeks)
- Internal fixation
- Euthanasia
61
Outline a logical approach to emergency cranial trauma
- Eyes may look dramatically affected but may not be most important, consider fractures and trauma to brain
- Ocular damage may not be saved in many cases
- Need to consider the treatment for increased ICP in any cranial trauma case
- Can use the pupil size as indication of intracranial pressure and compression of the brain
- Need to give time
62
What is the main aim of treatment in emergency cranial trauma with regards to the intracranial pressure and how is this achieved?
Need to reduce brain swelling to reduce ICP, do this by increases cerebral circulation (ischaemia due to raised ICP leads to swelling, which increases the ischaemia present)
63
Following cranial trauma, the pupils are bilaterally constricted. What does this indicate and what is the prognosis?
Midbrain compression, guarded prognosis
64
Following cranial trauma, one pupil is enlarged and the other is normal. What does this indicate and what is the prognosis?
Unilateral III nucleus or nerve damage, guarded prognosis
65
Following cranial trauma, the pupils are bilaterally normal. What does this indicate and what is the prognosis?
Brain is "normal" and good prognosis
66
Following cranial trauma, the pupils are bilaterally blown and the PLR is lost. What does this indicate and what is the prognosis?
Bilateral III nucleus or nerve damage, grave prognosis
67
How can cerebral perfusion be maintained following cranial trauma?
Shock rate fluids (increase arterial blood pressure)
68
What is required in the emergency treatment of all cases of cranial trauma in general practice?
- maintain cerebral perfusion
- Increase oxygenation
- Maintain sufficient cerebral blood flow
69
Outline the requirement for increasing oxygenation and how this can be done in the emergency treatment of cranial trauma
- Need to not over do it
- Likely to have damage to thoracic and abdo cavity
- Thoracic cavity damage likely to lead to reduced oxygenation e.g. pneumo or haemothroax
- Oxygenation with oxygen tent or nasal oxygen
70
Discuss the use of anaesthesia in the emergency treatment of cranial trauma
Contraindicated - can reduce blood pressure further
71
Discuss the use of diuretics in the emergency treatment of cranial trauma
- Mannitol
| - Will drop blood pressure, but can balance this with fluids, give up to 5x maintenance
72
Outline the emergency treatment for cerebellar herniation
- Mannitol 1g/kg, give as fast as possible
- Care as cannot be given too often in a 24 hour period without causing kidney damage
- Steroids not recommended
- Frusemide
- CPR: if heart stopped due to cerebellar herniation, CPR will not recover the patient
73
Outline a logical approach to emergency disturbances of consicousness
- Glasgow Coma Score for dogs to asses neurological activity
- oculocephalic reflex: move head side to side and assess vestibular movements in eyes
- Gag response good to assess
- GCS good for assessment of improvement, no change or worsening
- Consider cause: seizure, trauma, vascular?
74
What are the options for acute onset paraparesis/plegia?
Treat, refer, kill
