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BSAVA ECC > Neurology Module 2 > Flashcards

Neurology Module 2 Flashcards

1
Q

What is the primary and secondary injury related to traumatic brain injury?

A

Primary injury: high impact and results in mechanical disruption to brain tissue - this can not be stopped
Secondary injury: caused by swelling, haemorrhage, Increased ICP, ischaemia that results - can try to prevent and manage

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2
Q

What scores are good at lending prognosis for brain injury?

A

Modified GCS, ATT

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3
Q

What is the treatment for raised ICP and what are the goals?

A

Goals: Maintain cerebral perufsion, control ICP and hypotension BP 100-120mmHg
1. Elevate head - 30
2. Avoid jugular compression - decreased cerebral drainage - sample from peripherals
3. turn q4-6hrs
4. Avoid anything that will further increase ICP - vomiting/sneezing/coughing/urinating /seizures
5. Fluid therapy - maintain normovolaemic to hypervolaemic state - hypertonic saline or colloids followed with isotonic
6. Pain relief
7. Temperature - avoid hypo and hyper (increased O2 demand)
8. Enteral nutrition
9. Oxygenation and ventilation
10. urination management
11. Osmotic diuretic - mannitol - better for deteriorating patients
12. Steroids - only if underlying inflam cause to ICP
13. Control seizures

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4
Q

How is acute brain disease categorised?

A
  1. Diffuse or symmetrical lesions: metabolic, anomolous conditions, inflammatory/infectious, degenerative
  2. Focal or lateralised intracranial lesions: unilateral, blindness/proprioceptive deficits, circling, vestibular - neoplastic, inflam/infectious, vascular (ishaemia/strokes)
  3. Multifocal : infectious/inflamm, vascular, trauma, neoplastic, degenerative
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5
Q

What are the two types of stroke?

A

Ischaemic - caused by arterial or venous obstruction
Haemorrhagic: caused by rupture of intracranial vessels

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6
Q

What is the onset of action of a ischaemic stroke v. haemorrhagic stroke?

A

Typically acute and are non-progressive after the intial 24 hours. If less than 24hours of clinical signs = transient ischaemic attack, haem is more variable

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7
Q

What are concurrent metabolic problems with strokes

A

Mostly cats
- CKD
- Hypertension
- Protein losing disease
- Cushings
- Neoplasia
- Angiostronglyus
- DM
- HypoT4
- Cardiac disease

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8
Q

What is the normal presentation of inflammatory disease?

A

Can be infectious or non-infectious in origin
Can be acute or subacute in onset with variable progression
Often multifocal and asymmetric

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9
Q

What are infectious causes of inflammatory disease?

A

Distemper
Toxo, neospora - progressie cerebellar ataxia over weeks, cerebellar atrophy on MRI - clindamycin/TMPS
FIP - 30% cats have CNS involvement, immune mediated vasculitis, uveitis, insidious signs - most commonly tetraparesis, ataxia, nystagmus, and occasionally spinal cord disease

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10
Q

What breeds are commonly affected with MUO

A

Young to middle aged, small and toy breed dogs - 3-8yrs

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11
Q

What are the three forms of granulomatous meningo-encephalitis?

A

Disseminated: multifocal
Focal
Ocular: dilated, non-responsive pupils with edematous optic discs

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12
Q

What breeds are affected by necrotising meningitis?

A

Pugs/maltese/chihuahua/yorkie/boston T
acute onset
rapidly progressive (often forebrain) - seizures
causes necrosis of tissue

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13
Q

What diagnostics would you use to diagnose MUO?

A

Bloods: metabolic causes
Serology for infectious disease + culture
CSF analysis

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14
Q

What is the treatment of inflammatory brain diseases?

A

Antimicrobials if secondary to protozoal or bacteria disease
Immunosuppressive meds if immune mediated
AEDs if seizuring - levitir/phenobarb - pheno better for necrotising

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15
Q

Idiopathic Tremor syndrome: CS, Dx, Tx

A

Mostly young dogs
CS: fine tremor - rapid, low amplitude and worse with stress/excitement +/- head tilt, ataxia, decreased menace
Dx: CSF/MRI - rule out other
Tx: corticosteroids 4-6mths +/- other immunosup

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16
Q

Eosinophilic ME: CS, Dx, Tx

A

CS: large breed dogs, obtundation, vision impairment, ataxia, seizures
Dx: MRI/CSF - cortical atrophy on MRI

17
Q

Pachymeningitis: CS, Dx, Tx

A

Causes multiple CN deficits, abnormal mental status, visual deficits - sighthounds - thickened dura matter

18
Q

What percentage of seizures are caused by toxins?

A

40%
Common cause of status epilepticus - tends to need infusions (propofol)

19
Q

Toxins that can cause seizures

A

Metronidazole - diazepam outcompetes metro
Mycotoxin
Grapes
Cannibus
Metadehyde (blue GI content)

20
Q

Metabolic causes of seizures?

A

-Toxins
- Hypoglycaemia
- Hepatic encephalopathy
- Sodium derangements

21
Q

How does hypoglycaemia cause seizures?

A

Glucose is the major nutritive carbohydrate substrate of the brain. Can not store it effectively, needs to oxidise it and is brains primary source of E.
- Glucose less than 3mmol/L
- underlying diseases: juvenile hypogly, insulinoma, insulin overdose, liver disease, glycogen storage disease

22
Q

Treatment of hepatic encephalopathy?

A
  1. Lactulose: traps ammonia as non-diffusible in intestinal lumen, and decreases uptake
  2. Abs: decreased ammonia producing baceria
  3. Diet: aim is to decrease gut derived blood ammoia, restricted protein content, aromatic aminoacids and short chain fatty acids
  4. AEDs for seizures control
23
Q

How do sodium derrangements result in seizures?

A

Hypernatraemia: cell shrinkage - excess H2O loss - DM, D+, osmotic diuresis, cushings, salt poisoning
Hyponatraemia: cell swelling - hypovolaemia (renal, GI disease, cutaenous loss, 3rd space disease), hypervolaemia (CHf, liver failure, nephrotic syndrome)
Normovolaemia (primary polydipsia, waer intox, hypot4)

24
Q

What is the management of neoplasia causing seizures?

A
  1. AEDs - levitiracetam
  2. Anti-inflam preds
  3. Analgesia - paracetamol
25
Q

Optic Neuropathy: CS, Dx, Tx

A

CS: acute blindness, absent PLRs, uni or bilateral, swollen optic discs,
Dx: MRI inflam of nerve heads, CSF
Ddx: MUO, microbial infections, trauma, orbital inflam, toxins, neoplasia
Tx: ais

26
Q

Trigeminal neuritis: CS, Dx, Tx

A

Most common cause of dropped jaw in dogs - idiopathic condition with benign course and resolution in 3-4 weeks
- Muscle to help eat, supportive care, feeding tube
Underlying neoplasia/inflam/infection

27
Q

Facial nerve paralysis/paresis CS, Dx, Tx

A

Most commonly idiopathic - esp if bilateral
DDX: middle ear disease, polyneuropathies, brainstem lesions, Hypot4
Dx: Bloods, MRI/CT, CSF
- Most cases improve over 6-8 weeks some have permenant deficits
TX: avoid KCC

28
Q

What are the structures passing through the middle ear?

A

CNV5, CNV8, Sympathetic supply to the eye

29
Q

Clinical signs of otitis media?

A

Common in CKCS
mucus initially produced in TM and draining through the auditory tube to nasopharynx
Hearing loss, peripheral vestibular disease, facial paralysis
Dx: otoscopy, CT/MRI

BSAVA ECC (31 decks)

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