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Neurology (SA) > Brain disease > Flashcards

Brain disease Flashcards

1
Q

What 3 main diagnostic investigations are used to investigate brain disease?

A

Bloods - rule out metabolic disease
Imaging - MRI, CT for trauma
CSF analysis

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2
Q

Focal and lateralised brain disease usually indicates what cause (VIT D)?

A

Neoplasia
Vascular
(Inflammatory, infectious, trauma, anomalous)

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3
Q

Mutlifocal brain disease usually indicates what cause (VIT D)?

A

Inflammatory
Infectious
(Neoplasia, vascular, trauma, degenerative)

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4
Q

Diffuse and symmetrical brain disease usually indicates what VIT D cause?

A

Metabolic
Toxic
(Degenerative, inflammatory, infectious, trauma)

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5
Q

Why is brain disease particularly problematic (in terms of anatomy)?

A

Most diseases cause swelling

Limited brain expansion- causes intracranial pressure

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6
Q

What is one compensatory mechanism for increased intracranial pressure?

A

Compliance
If one component increases in size, other has to decrease to maintain pressure
(e.g. increased brain tissue causes decreased amount of CSF)

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7
Q

What can happen as a result of decompensation (cannot compensate with compliance) with increased intracranial pressure?

A

Brain herniation

Forebrain herniates under tentorium or cerebellum herniates through foramen magnum

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8
Q

What are the symptoms of raised intracranial pressure?

A

Altered mental state - dull/quiet, obtunded, stupor, coma
Bradycardia (Cushing’s reflex)
Altered pupil size and PLR
Nystagmus
Abnormal postures (decerebrate, decerebellate)

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9
Q

What is a decerebrate posture?

A

All 4 limbs extended

With opisthotonus

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10
Q

What is a decerebellate posture?

A

Only forelimbs extended

Hindlimbs flexed

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11
Q

What is aniscoria?

A

Unequal pupil size

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12
Q

What is the word for constricted pupils?

A

Miosis

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13
Q

What is the word for dilated pupils?

A

Mydriasis

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14
Q

What are the 4 subcategories of meningioencephalomyelitis of unknown origin (MUOs)?

A

Granulomatous ME
Eosinophilic ME
Necrotising ME
Necrotising LE (leukoencephalitis)

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15
Q

What breeds are predisposed to meningioencephalomyelitis of unknown origin (MUOs)?

A

Pug

French bulldog

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16
Q

MUOs often show pleocytosis on CSF analysis. What is this?

A

Pleocytosis = increased number of WBCs in CSF

Lymphocytic, neutrophilic or mixed

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17
Q

What findings would you expect to see on CSF analysis of MUOs?

A

Pleocytosis - increased WBCs

Increased protein

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18
Q

What findings would you expect to see on an MRI of a brain with MUO?

A

Multifocal, irregular changes

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19
Q

How are MUOs treated?

A

Immunosuppressants (e.g. prednisolone, ciclosporin)

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20
Q

Idiopathic tremor syndrome is usually seen in what dogs?

A

Young, small breeds

Especially white colour

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21
Q

What are the clinical signs of idiopathic tremor syndrome?

A

Fine tremor - worse with stress/excitement
Head tilt
Reduced menace response
Ataxia

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22
Q

What would you expect to see on CSF analysis of a dog with idiopathic tremor syndrome?

A

Very mild inflammation

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23
Q

What is the treatment for idiopathic tremor syndrome?

A

Corticosteroids (4-6 months)
+/- immunosuppression
Diazepam

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24
Q

What are the 3 main routes of bacterial meningitis infection?

A

Haematogenous
Direct invasion
CSF

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25
Q

Are the clinical signs of bacterial meningitis acute or chronic? Do they progress?

A

Acute/peracute

Progress rapidly

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26
Q

What are the clinical signs of bacterial meningitis?

A

Pyrexia
CNS signs and CN deficits
Neck pain in some cases

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27
Q

What would you expect to see on a CSF of a patient with bacterial meningitis?

A

Pleocytosis
Increased protein
(may be able to culture bacteria from blood/protein)

28
Q

What is the treatment for bacterial meningitis?

A

Antibiotics +/- surgical drainage

Guarded Px

29
Q

Do intoxications have acute or chronic onset of symptoms?

A

Acute - <24 hrs

30
Q

What are the clinical signs of intoxications?

A

Status epilepticus (5+ min seizure)
Muscle tremors/fasciculations
GI, CV, respiratory signs

31
Q

Head trauma involves primary injury and sometimes secondary injury. What is primary and secondary injury?

A 
Primary = physical damage to brain parenchyma
Secondary = release of inflammatory mediators and continued haemorrhage
32
Q

What score is used to measure head trauma?

A

Modified Glasgow coma scale

higher score = better prognosis

33
Q

What 2 drugs can be given to manage increased intracranial pressure with head trauma?

A

Mannitol

Hypertonic saline

34
Q

Hypertonic saline can be given to manage intracranial pressure seen with head trauma. When is it contraindicated?

A

Hyponatraemia

Cardiac/respiratory disease

35
Q

Why should you be cautious when administering morphine for head trauma?

A

May cause vomiting (which increases intracranial pressure)

36
Q

Why should the head be kept elevated at 30 degrees after head trauma?

A

Avoids jugular compressions

Prevents increased intracranial pressure

37
Q

How often should an immobilised patient be turned to avoid pressure sores?

A

Every 4-6 hours

38
Q

How often should the bladder be emptied in an immobilised patient (if a maintained catheter is not in place)?

A

Every 6 hours

39
Q

In what circumstances may head trauma require surgical intervention?

A

Severely raised intracranial pressure
Haematomas
Fractures compressing brain parenchyma or contaminated fragments

40
Q

Can steroids be used in head trauma? Why?

A

NO
Associated with hyperglycaemia, production of lactic acid (causes cell death), higher risk of infection, alters metabolism

41
Q

What is hydrocephalus?

A

Abnormal dilation of ventricular system within the cranium

Due to increased CSF

42
Q

What type of dogs are usually affected by congenital hydrocephalus?

A

Young, toy breeds

Associated with congenital head shape

43
Q

What can cause hydrocephalus in older dogs?

A

Space occupying lesion

44
Q

What rare the clinical signs of hydrocephalus?

A 
Domed shaped head
Persistent fontanelle (suture lines between cranium)
Abnormal behaviour
Obtundation
Seizures
Vestibular signs
45
Q

Hydranencephaly and porencephaly are communications between the subarachnoid space and/or lateral ventricles. What are the clinical signs?

A

Circling, abnormal behaviour (1st few months of life)

Seizures (up to years later)

46
Q

What is a hepatic encephalopathy?

A

Neurological signs secondary to acute or chronic liver failure
(Usually acute hepatic or end stage liver failure)

47
Q

Are hepatic encephalopathies permanent or reversible?

A

Reversible

48
Q

What is the pathogenesis of hepatic encephalopathies?

A

Hyperammonaemia
Neuroinflammation
Cerebral oedema
Derange neurotransmission

49
Q

What are the clinical signs of hepatic encephalopathies?

A

Vague signs -weight loss, PUPD, GI signs

Forebrain- behaviour changes, blindness, pacing, seizures

50
Q

Hepatic encephalopathies may cause neurological signs to develop particularly after which surgery?

A

Portosystemic shunt surgery

Post-attenuation syndrome - 50% fully recover

51
Q

How are hepatic encephalopathies diagnosed?

A

Bile acid stimulation test
Fasting ammonia
Ultrasound/CT
Angiography

52
Q

How are hepatic encephalopathies treated?

A

Lactulose
Antibiotics
Diet restricted in protein (results in decreased ammonia)
Seizure control

53
Q

Why is lactulose used to treat hepatic encephalopathies?

A

Traps ammonia

Decreases aborsption of ammonia in intestines

54
Q

Why are antibiotics used to treat hepatic encephalopathies?

A

To reduce the ammonia-producing bacteria in the GIT

55
Q

What are some of the underlying causes of hypoglycaemia?

A 
Insulinoma
Insulin overdose in diabetic patients
Liver disease
Glycogen storage disease
Juvenile hypoglycaemia
56
Q

What are the clinical signs of hypoglycaemia?

A 
Lethargy
Ravenous appetite
Anxiety, depression
Weakness
Tremors
Reduced vision
Seizures
57
Q

What are clinical signs of sodium derangements?

A 
Altered mentation
Blindness
Seizures
Coma 
Death
58
Q

How does hypocalcaemia cause muscle contraction and tetany?

A

Decreased calcium
Increased neuronal permeability to sodium
Excitability and spontaneous discharging of nerve fibres
Causes muscle contraction and tetany

59
Q

Give examples of primary neoplasias of the brain

A

Intra-axial - gliomas

Extra-axial - meningiomas, choroid plexus tumours

60
Q

What are the clinical signs of hypocalcaemia?

A 
Muscle spasm/cramping
Muscle twitching, trembling, stiffness
Tonic-clonic spasms
Episodic rigidity
Tetraparesis
Seizures
61
Q

Give examples of secondary neoplasias of the brain

A

Metastases e.g. haemangiosarcoma

Direct extension of neoplasia outside of brain e.g. nasal tumours

62
Q

Brain tumours are more common in what age and size of dogs?

A

Older dogs

Large breeds

63
Q

What are the clinical signs of brain tumours?

A 
If supratentorial (above tentorium cerebelli) - seizures
If subtentorial - central vestibular dysfunction
64
Q

How are brain neoplasias treated conservatively?

A

Less sedative AEDs
Anti-inflm doses of prednisolone
Analgesia - paracetamol, gabapentin

65
Q

What is the pathogenesis/cause of changes in behaviour/memory/learning ability seen with degenerative cognitive dysfunction?

A

Accumulation of beta amyloid
Senile plaque formation
Neurofibrillary tangles

66
Q

What are the clinical signs of degenerative cognitive dysfunction?

A 
Soiling/lack of house training
Disturbances in sleep
Staring into space
Getting stuck in corners
Vocalising/pacing at night
New behaviour problems
67
Q

How can degenerative cognitive dysfunction be treated?

A

Selegeline - Parkinson’s meds
Nutritional supplementation (anti-oxidants, brain protectants)
Behaviour modification and environmental enrichment

Neurology (SA) (8 decks)

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