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NEU2 > Neurological diseases of small animals 4 > Flashcards

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

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2
Q

Give examples of drugs licensed for the treatment of osteoarthritis in the UK

A
  • Cimicoxib
  • Carprogen
  • Meloxicam
  • Firocoxib
  • Grapiprant
  • Robenacoxib
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3
Q

Give examples of drugs not licensed, but indicated, for the treatment of osteoarthritis in dogs in the UK

A
  • Derocoxib

- Etodolax

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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
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5
Q

Describe the histopathological apperance of chromatolysis

A
  • Swelling and loss of Nissl substance

- Nucleus pushed to side

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6
Q

Explain how chromatolysis of neurones occurs

A
  • Axonal damage or toxicity

- Neuronal degeneration

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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
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8
Q

Describe the appearance of necrotic neurones

A
  • Cells appear red
  • More condensed
  • Pyknotic neuclei
  • Irreversible
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9
Q

What may cause the histopathological appearance of swollen neurons?

A

Lysosomal storage diseases

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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
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11
Q

Describe the histopathological appearance of lysosomal storage diseases

A
  • Markedly enlarged neurons with some kind of inclusion

- White metabolite may be seen

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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)
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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)

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14
Q

Describe the inclusion bodies seen with distemper

A

Large eosinophilic inclusion bodies in the neuron nucleus

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15
Q

What conditions may cause the cytoplasmic vacuolation of neurones?

A

Spongiform encephalopathies - pathognomic

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16
Q

What causes the vacuolation of white matter tracts?

A

Trauma to spinal cord leading to the degeneration of white matter tract

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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)
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18
Q

What causes gliosis on histopathology?

A

Acute or ongoing liver failure e.g. hepatic encephalic syndrome in horses

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19
Q

Describe the apperance gliosis on histopathology

A

Alzheimer type 2 cells

- Upset astrocytes, round cells with vacuolation (activation and proliferation)

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20
Q

What are Gitter cells?

A

Microglia cells that become enlarged

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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

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22
Q

Describe the histopathological appearance of demyelination

A
  • White matter phagocytosed by gitter cells
  • Strands visible (remnants of axons)
  • WM completely gone
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23
Q

Give an example of a disease that causes a demyelination histopathological appearance

A

Distemper (causes death of oligocytes)

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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
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25
Q

What conditions may cause the hypomyelination apperance on histopathology?

A

In utero infection with BVDV or Border disease

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26
Q

Describe the histopathological appearance of cerebral oedema

A
  • Increased extracellular fluid

- Seen as white spaces in tissue

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27
Q

Describe the histopathological appearance of cytotoxic oedema

A

Increased intracellular fluid

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28
Q

What conditions may cause cytotoxic oedema of neural tissue?

A
  • Vascular leakage e.g. vasculitis, blood thinning, toxic agent
  • Low ATP, low oxygen affecting cellular pumps
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29
Q

Where and why does brain herniation usually occur in the dog?

A
  • Oedematous fluid in brain due to lack of space

- Foramen magnum

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30
Q

Describe the gross pathological apperance of congenital hydrocephalus

A
  • Expansion of ventricles

- Loss of CNS tissue (pressure atrophy, necrosis, hypoplasia)

31
Q

Explain the ways in which congenital hydrocephalus can develop

A
  • 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
Q

What is congenital lissencephaly? Clinical signs?

A

Smooth brain, may have no clinical signs even with little to no neocortex left esp. if only neocortex affected

33
Q

What causes congenital lissencephaly?

A

Disturbance of neuronal migration and proliferation during development, common in Lhasa Apso

34
Q

List the potential causes of cerebellar hypoplasia

A
  • In utero BVDV
  • congeital malformation
  • Parvovirus in dogs possible cause (rare)
35
Q

What is myelomalacia? Aetiology?

A
  • Necrosis of the spinal cord

- Potential aetiology: FCE

36
Q

Describe the histopathological appearance of myelomalacia

A

Pale cartilaginous emboli in haemorrhagic spinal cord segment

37
Q

Describe the histopathological appearance of listeriosis

A
  • Caudal brainstem: suppurative foci with numerous neutrophils, some macrophages infiltrating the neuroparenchyma (aka microabscesses)
  • Pons affected most
38
Q

How do viral neuro infections often manifest histopathologically?

A

Non-suppurative (meningo)-encephalo(myel)itis, with or without viral inclusion bodies

  • Pure lymphocytic glial disease
  • Perivascular accumulations of lymphocytes common
39
Q

Describe the histopathological appearance of Aujesky’s disease

A
  • Characterised by perivascular cuffing and intense focal liosis and inflammatory infiltration within neocortex
  • Some neutrophils present in the infiltrate
40
Q

Describe the pathological appearance of cerebral cortical necrosis

A
  • 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
Q

Name the primary neoplasias of the CNS

A
  • Meningioma
  • Astrocytoma and oligodendroglioma
  • Ependymoma/choroid plexus tumour
  • Neuroblastomas/medulloblastoma (PNET)
42
Q

Briefly describe meningiomas

A
  • Slow growing, surgery often curative

- Common in cats, 9 different subtypes

43
Q

Briefly describe astrocytomas and oligodendrogliomas

A
  • 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
Q

Briefly describe ependymomas/choroid plexus tumours

A
  • Ventricular tumours
  • If large can obstruct CSF flow
  • Leads to acquired hydrocephalus, herniation, severely ill/dead animal
45
Q

How do metastasis in CNS tissue occur?

A

Haematogenous spread only

46
Q

What are the treatment goals in emergency status epilepticus treatment?

A
  • Terminate seizure activity

- Identify and treat cause for seizures

47
Q

List the emergency treatment options for status epilepticus

A
  • Diazepam
  • Phenobarbital
  • Propofol
  • Midazolam
  • Pentobarbitone
48
Q

By what routes can diazepam be given in the emergency treatment of status epilepticus and give the dose

A
  • IV best, but difficult
  • Per rectum
  • Per osunreliable as an anti-convulsant
  • 0.5-1mg/kg
49
Q

How long does diazepam work as an anticonvulsant for and describe the dosing frequency?

A
  • Lasts ~20 mins
  • Repeat as necessary 3-4x
  • CRI can be used
50
Q

What is the first option for treatment of an ongoing seizure?

A

Diazepam

51
Q

What is the second option for treatment of an ongoing seizure?

A

Phenobarbital

52
Q

Describe the route, dose and time to effect for phenobarbital in the emergency treatment of status epilepticus

A
  • 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
Q

What drugs can be added in the emergency treatment of status while phenobarbital takes effect?

A

Diazepam or propofol

54
Q

Outline the dose and length of action of propofol in the emergency treatment of status

A
  • IV titrated to effect, should be anto-convulsant prior to anaesthetic effect
  • Lasts 20mins
55
Q

What should be available quickly when using propofol as an emergency anticonvulsant?

A

ET tube and ventilation in case of accidental anaesthetic induction

56
Q

Discuss the use of pentobarbitone as an emergency treatment for status

A
  • 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
Q

What factors, other than the seizure activity, need to be addressed in the emergency treatment of status epilepticus?

A
  • Electrolytes
  • Hypoglycaemia
  • Temperature (hyperthermia due to seizure, use fans, wet towels, ice enemas etc.)
58
Q

Outline the logical approach to emergency spinal trauma

A
  • 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
Q

What are the options in the case of a spinal cord laceration following spinal trauma?

A

Poor prognosis, euthanasia likely, poor QOL

60
Q

What are the options in a case of spinal trauma where deep pain sensation is present?

A
  • Conservative management (1-2 weeks)
  • Internal fixation
  • Euthanasia
61
Q

Outline a logical approach to emergency cranial trauma

A
  • 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
Q

What is the main aim of treatment in emergency cranial trauma with regards to the intracranial pressure and how is this achieved?

A

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
Q

Following cranial trauma, the pupils are bilaterally constricted. What does this indicate and what is the prognosis?

A

Midbrain compression, guarded prognosis

64
Q

Following cranial trauma, one pupil is enlarged and the other is normal. What does this indicate and what is the prognosis?

A

Unilateral III nucleus or nerve damage, guarded prognosis

65
Q

Following cranial trauma, the pupils are bilaterally normal. What does this indicate and what is the prognosis?

A

Brain is “normal” and good prognosis

66
Q

Following cranial trauma, the pupils are bilaterally blown and the PLR is lost. What does this indicate and what is the prognosis?

A

Bilateral III nucleus or nerve damage, grave prognosis

67
Q

How can cerebral perfusion be maintained following cranial trauma?

A

Shock rate fluids (increase arterial blood pressure)

68
Q

What is required in the emergency treatment of all cases of cranial trauma in general practice?

A
  • maintain cerebral perfusion
  • Increase oxygenation
  • Maintain sufficient cerebral blood flow
69
Q

Outline the requirement for increasing oxygenation and how this can be done in the emergency treatment of cranial trauma

A
  • 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
Q

Discuss the use of anaesthesia in the emergency treatment of cranial trauma

A

Contraindicated - can reduce blood pressure further

71
Q

Discuss the use of diuretics in the emergency treatment of cranial trauma

A
  • Mannitol

- Will drop blood pressure, but can balance this with fluids, give up to 5x maintenance

72
Q

Outline the emergency treatment for cerebellar herniation

A
  • 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
Q

Outline a logical approach to emergency disturbances of consicousness

A
  • 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
Q

What are the options for acute onset paraparesis/plegia?

A

Treat, refer, kill

NEU2 (23 decks)

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