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
Are the clinical signs of bacterial meningitis acute or chronic? Do they progress?
Acute/peracute | Progress rapidly
26
What are the clinical signs of bacterial meningitis?
Pyrexia CNS signs and CN deficits Neck pain in some cases
27
What would you expect to see on a CSF of a patient with bacterial meningitis?
Pleocytosis Increased protein (may be able to culture bacteria from blood/protein)
28
What is the treatment for bacterial meningitis?
Antibiotics +/- surgical drainage | Guarded Px
29
Do intoxications have acute or chronic onset of symptoms?
Acute - <24 hrs
30
What are the clinical signs of intoxications?
Status epilepticus (5+ min seizure) Muscle tremors/fasciculations GI, CV, respiratory signs
31
Head trauma involves primary injury and sometimes secondary injury. What is primary and secondary injury?
``` Primary = physical damage to brain parenchyma Secondary = release of inflammatory mediators and continued haemorrhage ```
32
What score is used to measure head trauma?
Modified Glasgow coma scale | higher score = better prognosis
33
What 2 drugs can be given to manage increased intracranial pressure with head trauma?
Mannitol | Hypertonic saline
34
Hypertonic saline can be given to manage intracranial pressure seen with head trauma. When is it contraindicated?
Hyponatraemia | Cardiac/respiratory disease
35
Why should you be cautious when administering morphine for head trauma?
May cause vomiting (which increases intracranial pressure)
36
Why should the head be kept elevated at 30 degrees after head trauma?
Avoids jugular compressions | Prevents increased intracranial pressure
37
How often should an immobilised patient be turned to avoid pressure sores?
Every 4-6 hours
38
How often should the bladder be emptied in an immobilised patient (if a maintained catheter is not in place)?
Every 6 hours
39
In what circumstances may head trauma require surgical intervention?
Severely raised intracranial pressure Haematomas Fractures compressing brain parenchyma or contaminated fragments
40
Can steroids be used in head trauma? Why?
NO Associated with hyperglycaemia, production of lactic acid (causes cell death), higher risk of infection, alters metabolism
41
What is hydrocephalus?
Abnormal dilation of ventricular system within the cranium | Due to increased CSF
42
What type of dogs are usually affected by congenital hydrocephalus?
Young, toy breeds | Associated with congenital head shape
43
What can cause hydrocephalus in older dogs?
Space occupying lesion
44
What rare the clinical signs of hydrocephalus?
``` Domed shaped head Persistent fontanelle (suture lines between cranium) Abnormal behaviour Obtundation Seizures Vestibular signs ```
45
Hydranencephaly and porencephaly are communications between the subarachnoid space and/or lateral ventricles. What are the clinical signs?
Circling, abnormal behaviour (1st few months of life) | Seizures (up to years later)
46
What is a hepatic encephalopathy?
Neurological signs secondary to acute or chronic liver failure (Usually acute hepatic or end stage liver failure)
47
Are hepatic encephalopathies permanent or reversible?
Reversible
48
What is the pathogenesis of hepatic encephalopathies?
Hyperammonaemia Neuroinflammation Cerebral oedema Derange neurotransmission
49
What are the clinical signs of hepatic encephalopathies?
Vague signs -weight loss, PUPD, GI signs | Forebrain- behaviour changes, blindness, pacing, seizures
50
Hepatic encephalopathies may cause neurological signs to develop particularly after which surgery?
Portosystemic shunt surgery | Post-attenuation syndrome - 50% fully recover
51
How are hepatic encephalopathies diagnosed?
Bile acid stimulation test Fasting ammonia Ultrasound/CT Angiography
52
How are hepatic encephalopathies treated?
Lactulose Antibiotics Diet restricted in protein (results in decreased ammonia) Seizure control
53
Why is lactulose used to treat hepatic encephalopathies?
Traps ammonia | Decreases aborsption of ammonia in intestines
54
Why are antibiotics used to treat hepatic encephalopathies?
To reduce the ammonia-producing bacteria in the GIT
55
What are some of the underlying causes of hypoglycaemia?
``` Insulinoma Insulin overdose in diabetic patients Liver disease Glycogen storage disease Juvenile hypoglycaemia ```
56
What are the clinical signs of hypoglycaemia?
``` Lethargy Ravenous appetite Anxiety, depression Weakness Tremors Reduced vision Seizures ```
57
What are clinical signs of sodium derangements?
``` Altered mentation Blindness Seizures Coma Death ```
58
How does hypocalcaemia cause muscle contraction and tetany?
Decreased calcium Increased neuronal permeability to sodium Excitability and spontaneous discharging of nerve fibres Causes muscle contraction and tetany
59
Give examples of primary neoplasias of the brain
Intra-axial - gliomas | Extra-axial - meningiomas, choroid plexus tumours
60
What are the clinical signs of hypocalcaemia?
``` Muscle spasm/cramping Muscle twitching, trembling, stiffness Tonic-clonic spasms Episodic rigidity Tetraparesis Seizures ```
61
Give examples of secondary neoplasias of the brain
Metastases e.g. haemangiosarcoma | Direct extension of neoplasia outside of brain e.g. nasal tumours
62
Brain tumours are more common in what age and size of dogs?
Older dogs | Large breeds
63
What are the clinical signs of brain tumours?
``` If supratentorial (above tentorium cerebelli) - seizures If subtentorial - central vestibular dysfunction ```
64
How are brain neoplasias treated conservatively?
Less sedative AEDs Anti-inflm doses of prednisolone Analgesia - paracetamol, gabapentin
65
What is the pathogenesis/cause of changes in behaviour/memory/learning ability seen with degenerative cognitive dysfunction?
Accumulation of beta amyloid Senile plaque formation Neurofibrillary tangles
66
What are the clinical signs of degenerative cognitive dysfunction?
``` Soiling/lack of house training Disturbances in sleep Staring into space Getting stuck in corners Vocalising/pacing at night New behaviour problems ```
67
How can degenerative cognitive dysfunction be treated?
Selegeline - Parkinson's meds Nutritional supplementation (anti-oxidants, brain protectants) Behaviour modification and environmental enrichment