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Y4 - Small Animals > Brain Disease > Flashcards

Brain Disease Flashcards

1
Q

Where can you localise brain lesions to?

A
  • Brain =
    -forebrain
    -brainstem
    -cerebellar
    -vestibular (peripheral vs central)
  • Spinal =
    -C1-C5, C6-T2, T3-L3, L4-S3
  • Neuromuscular system
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2
Q

What are your guides regarding location?

A
  • Neoplasia and Vascular are focal and lateralized
  • Infect / inflamm are asymmetric / multifocal
  • Degen / anom / nutritional are symmetrical
  • Extra-cranial diseases are symmetrical and diffuse
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3
Q

What is seen with forebrain lesions?

A
  • Change in behaviour - disorientated / depressed
  • Circling / head turn - towards lesion
  • Contralateral menace, blindness
  • Contralateral proprioception deficits
  • Seizures
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4
Q

What is seen with brainstem lesions?

A
  • Depressed, stupor
  • Tetraparetic / ataxia, head tilt
  • Ipsilateral cranial nerve deficit
  • Ipsilateral proprioception deficit
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5
Q

What is seen in cerebellar lesions?

A
  • Normal mentation
  • Hypermetric ataxia, head tilt
  • Ipsilateral menace deficit - not blind
  • Normal / delayed / hypermetric proprioception
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6
Q

What are your VITAMIN D differentials for brain disease?

A
  • Vascular = ischaemic / haemorrhagic - ‘strokes’
  • Inflammatory = MUO (meningo-encephalo-myelitis of unknown origin)
  • Infectious = Protozoal (toxo/neospora), viral (CDV/FIP), bacterial/fungal
  • Trauma
  • Toxic
  • Anomalous = hydrocephalus
  • Metabolic = HE, hypoglycaemia, electrolyte imbalances, sodium shifts
  • Idiopathic = idiopathic epilepsy / vestibular
  • Neoplasia = primary (meningioma, glioma), pituitary, nasal, metastatic
  • Degenerative = cognitive dysfunction
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7
Q

With vascular disease, what is its progression?

A
  • Peracute (minutes)
  • Instataneous
  • <24hrs
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8
Q

What are main causes of bacterial meningoencephalitis?
What is seen in the CSF?

A
  • Direct invasion =
    -otogenic intracranial infection
    -nasal
    -dog bite
  • Haematogenous
  • CSF = severe neutrophilic pleocytosis
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9
Q

What are protozoal meningoencephalitis?

A
  • Neopsora caninum
    -dogs only
    -CEREBELLUM in adults
    -causes necrotizing cerebellitis + cerebellar atrophy
  • Toxoplasma gondii = cats»>dogs
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10
Q

What are causes of viral meningoencephalitis?

A
  • Canine distemper virus (CDV)
    -dogs only = REsp, GI, derm, neurologic
  • Feline infectious peritonitis (FIP)
    -Cats = Dry form = brain +/or eye
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11
Q

What are peracute / acute brain diseases?

A
  • Vascular
  • Inflammatory / infection
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12
Q

What are the difference between primary + secondary brain tumours?

A
  • Primary = meningioma (cats + long nosed dogs), glioma (brachy dogs)
    -often focal + asymmetrical (lateralized), often forebrain
  • Secondary = haematogenous (haemangiosarc, lymphoma, round cell…)
    -direct extension of nasal / skull …
    -pituitary tumours = cushings (dogs), acromegaly (cats)
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13
Q

What is treatment of primary brain tumours?

A
  • Symptomatic = prednisolone (2months)
  • Surgery alone = meningioma (cures cats +/- dogs)
  • Radiation alone
  • Combination
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14
Q

What is hydrocephalus? + other anomalous diseases?

A
  • Ventricles too large
  • Toy breed (dome-headed) = chihuahua, yorkie
  • Abnormal at birth
  • forebrain mainly affected = vocalise, house-training
  • Porencephaly = focal defect in brain tissue
    *Hydranencephaly = absence of cerebral hemispheres
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15
Q

What are genetic / degenerative diseases that act in early age?

A
  • Lysosomal storage disease = accumulation + storage of substrates within cytoplasm of neurons - cerebellar then whole brain
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16
Q

What are old age degenerative diseases? Tx?

A
  • Canine cognitive dysfunction
    -changes in behaviour, memory + learning
    -disturbances in sleeping (sleep in day + awake at night), staring, getting stuck in corners, loss of house-training
    -accumulation of beta-amyloid w senile plaque formation + neurofibrillary tangles
  • Tx = selegiline
  • Lafora disease = muscle twitch + seizures, eventually blind + ataxic
17
Q

Traumas are easily to diagnose, how are they managed?

A
  • Reduce intracranial pressure
  • Address secondary injury
18
Q

What are primary / secondary injuries of traumatic brain injuries?

A
  • Primary = damage already been done = no intervention
    -contusion
    -concussion
    -laceration
  • Secondary =
    -release of inflammatory mediators
    -continued haemorrhage, oedema = increased ICP
19
Q

How is cerebral perfusion pressure calculated?

A
  • MAP - ICP = CPP
  • 100mmHG - 10mmHG = 90mmHG = blood can enter brain
  • 60mmHG - 60mmHG = 0mmHG = blood not entering brain
19
Q

What is cushings reflex? When does this occur?

A
  • Severe hypertension (>160mmHG) with severe bradycardia (HR<60)
  • Happens late in ICP raises
  • Happens to try increase cerebral perfusion pressure
20
Q

What occurs with cerebellar herniation?

A
  • Cerebellum moves back into foramen magnum where brainstem sits
  • Brainstem gets squashed =
    -opisthotonus
    -decerebellate rigidity
    -coma
    -resp depression
    -death
21
Q

What should be done if ICP?

A
  • Resolve hypotension
  • Increase osmolarity of circulating blood to “suck” fluid out of the brain
  • Resuscitation then maintenance
  • Hypertonic saline if hypovolemic
  • Hyperglycemia worsens prognosis so avoid glucose-containing fluids
22
Q

Whats the difference between mannitol and hypertonic saline?

A
  • Mannitol – osmotic diuretic
    -↓ blood viscosity, ↑ cerebral blood flow and oxygen delivery, free radical scavenger, osmotic effect
    -Follow with crystalloid therapy to prevent dehydration
    -Contraindicated in hypovolemia
  • Hypertonic saline – plasma volume expander
    -Hyperosmotic agent, free radical scavenger
    -Contraindicated / care in congestive heart failure
    -Excellent for hypovolemic, raised ICP patients
23
Q

What is one of the last brain reflexes to go with ICP + pressure on the brainstem?

A
  • Oculocephalic reflex
    -if both pupils completely dilated = grave prognosis
24
Q

Why would you not use steroids for ICP?

A
  • Cause hyperglycaemia = worse prognosis
25
Q

How is hepatic encephalopathy treated?

A
  • Lactulose = traps ammonia
  • AB = reduce ammonia producing bacteria
  • Diet = restrict protein
  • Minimise contributing factors
  • Seizure control
26
Q

What does hypoglycaemia cause? What can cause low enough glucose to seizure?

A
  • Brain consumes 25% of total blood glucose
  • Low glucose = seizure, changes in mentation, weakness, flaccid tetraparesis, tremors
  • Glucose <3mmol/l
  • Low enough to seizure = insulinoma, insulin overdose, juvenile hypoglycaemia
27
Q
A

Y4 - Small Animals (105 decks)

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