Brain disease

Question 1

Where can the brain herniate in ICP?

Answer 1

forebrain herniates underneath the tentorium cerebelli or cerebellum herniates through the foramen magnum

Question 2

What are the signs of raised ICP?

Answer 2

• POOR mental status - ARAS
• Cushing’s reflex
• pupil size and PLR
• vestibular eye movement - MLF
• abnormal postures
 decerebrate
 decerebellate

Question 3

Outline the cushings reflex

Answer 3

• bradycardia & hypertension
• ICP increases above MAP resulting in cerebral ischaemia
• α-1-adrenergic sympathetic activation → systemic
vasoconstriction → hypertension
• carotid artery baroreceptors detect hypertension → vagal activation → bradycardia

Question 4

Outline pupil size as ICP increases

Answer 4

anisocoria to
bilateral pinpoint to
bilateral dilated not responsive to light.

N.B loss of physiological nystagmus = early sign of raised ICP

Question 5

Why does decerebellate positioning often occur?

Answer 5

Often d/t herniation of the cerebellum

Can be positional

Question 6

What are the main brain diseases based on VITAMIN D?

Answer 6

 V – CVA - ischaemic or hemorrhagic strokes
 I – MUOs, “White shakers”, bacterial ME, protozoal MEs (Toxoplasma, Neospora), viral MEs (CDV, FIP, FIV), fungal MEs
 T – head trauma, many toxins
 A – hydrocephalus, lissencephaly, hydranencephaly and porencephaly, CCA
 M – hepatic encephalopathy, hypoglycaemia, electrolyte imbalances
 I
 N – meningiomas, gliomas, pituitary tumours, lymphoma, metastases, MPNST
 D – lysosomal storage diseases, cognitive dysfunction, many degenerative GM and WM disorders

Question 7

What is white shakers?

Answer 7

• mostly young small breed dogs of any colour
• fine tremor – rapid, low amplitude, worse with stress/excitement, +/- other deficits:
• head tilt, reduced menace response, ataxia, opsiclonus
• Diagnosis:
• CSF – very mildly inflammatory
• +/- MRI to rule out other problems
• Treatment:
• corticosteroids for 4-6m
• +/- other immunosuppressive drugs
• diazepam initially
• fair to good px, can relapse
immune mediated dz

Question 8

Outline bacterial meningitis

Answer 8

• 3 main routes of infection:
• haematogenous
• direct invasion (ear, eyes, nose, bone, bite wounds)
• CSF
• usually acute CNS signs (obtundation and CN deficits most common)
• neck pain (~30%)
• pyrexia and neutrophilia in about 50%
• CSF
• increased protein concentration and pleocytosis
• phagocytosed organisms in CSF rare
• CSF/blood culture (positive ~15-30%) – inside abscess or in small amounts
• antibiotics +/- surgical drainage
• guarded prognosis

Question 9

What are the types of injury in head trauma?

Answer 9

Primary - • physical disruption of parenchyma
• concussion
• contusion
• laceration
• no intervention possible

Secondary -  release of inflammatory mediators
 continued haemorrhage
 leads to ↑ ICP (oedema, haemorrhage)
 the aim of our intervention

Question 10

How can you use the modified Glasgow coma scale?

Answer 10

 useful for serial monitoring

 ↑ score → better prognosis

Question 11

What are the aims of IVFT?

Answer 11

 restore intravascular volume to ensure adequate CPP
 hypotension significantly increases mortality
 resuscitation then maintenance
 avoid glucose containing fluids as hyperglycaemia is associated with a poorer outcome

Question 12

Outline the use of mannitol with raised ICP

Answer 12

 ↓ blood viscosity, ↑ CBF and oxygen delivery, free radical scavenger, osmotic effect
 0.5-1g/kg slow bolus over 20m
 follow with crystalloid therapy to prevent dehydration
 contraindicated in hypovolemia

Question 13

Outline the use of 7.5% saline in raised ICP

Answer 13

• hyperosmotic agent, free radical scavenger
• 4 ml/kg of 7.5% as slow bolus
• contraindicated:
• hyponatraemia
• cardiac or respiratory disease
 reverses shock
• decreases ICP
• increases CBF and oxygen delivery

Question 14

What are some considerations with pain in raised ICP

Answer 14

 pain increases blood pressure and therefore ICP

 caution as morphine may cause emesis and result in increased ICP

Question 15

Outline general care in head trauma patients

Answer 15

 keep head elevated (~30°)
 avoid jugular compression
 turn q4-6h
Cathterise and get feeding tube in some way

Question 16

Outline hydrocephalus

Answer 16

• abnormal dilation of ventricular system within cranium
• toy breeds, young age
• domed shaped head, persistent fontanelle, abnormal
behaviour, cognitive dysfunction, obtundation, circling,
pacing, seizures (?), vestibular signs
• treatment:
• medical (corticosteroids, furosemide, AEDs)
• surgical (VP shunt)

Question 17

What is lissencephaly?

Answer 17

 cerebrum has smooth surface without development of gyri and sulci
 seizures, behaviour changes
 Lhasa Apso, Korat cat

Question 18

What is hydrancephaly/ porencephaly

Answer 18

 presence of cerebral cavities, usually communicating with subarachnoid space and/or lateral ventricles
 signs in 1st few months (circling, abnormal behaviour) or up to few years (seizures)

Question 19

Outline brain neoplasia

Answer 19

more common in older and larger breed dogs
• most common clinical signs
• seizures in supratentorial tumours
• central vestibular dysfunction in infratentorial tumours
• median survival time 69 days
• infratentorial tumours 28 days
• supratentorial tumours 178 days
• treatment
• less sedative AEDs
• anti-inflammatory doses of prednisolone
• analgaesia (paracetamol, gabapentin)
• surgery +/- RT

Question 20

Outline hepatic encephalopathy

Answer 20

• reversible neurological manifestations secondary to any aetiology of acute or chronic liver failure (generally PSS)
• pathogenesis is multifactorial, complex and poorly understood
• hyperammonemia + neuroinflammation + cerebral oedema + deranged neurotransmission
• vague signs - failure to thrive, weight loss, PU/PD, GI signs
• forebrain signs: behaviour changes, blindness, seizures, etc
• rare brainstem or cerebellar signs reported in older dogs
• diagnosis relies on bile acid stimulation test, fasting ammonia, ultrasound or CT angiography

Question 21

How do you treat hepatic encephalopathy

Answer 21

lactulose
• traps ammonia as non-diffusible ammonium in intestinal lumen, decreases absorption of ammonia through cathartic effect and inhibits uptake of glutamine by intestinal wall
antibiotics
• reduce ammonia-producing bacteria in the gut
• diet
• aim to reduce gut derived blood ammonia
• restricted protein content, aromatic amino acids and short chain fatty acids
minimising contributing factors that:
• increase ammonia production (constipation, GI bleeding, azotemia, infection, hypokalemia)
• reduce clearance of toxins (dehydration, hypotension, anaemia)
• affect neurotransmission (benzodiazepines)
• seizure control (levetiracetam, KBr, PB, propofol)

Question 22

How does low BG affect the brain?

Answer 22

• glucose is major carbohydrate substrate of brain
• glucose oxidation is primary source of energy
• brain consumes ~25% of total blood glucose
• brain has 3x metabolic rate of peripheral tissues but 10-30% less extracellular glucose
• lack of glycogen stores in the CNS
• insulinomas, juvenile hypoglycaemia, hepatic dysfunction
• Clinical signs:
• anxiety, lethargy, depression
• ravenous appetite, exercise intolerance
• tremors, visual deficits, seizures, coma

Question 23

Outline low sodium causing brain signs

Answer 23

major extracellular ion in the body
• blood levels reflect ratio of sodium to water in extracellular fluid and account for most of the osmotically active particles in serum
• signs of forebrain dysfunction (altered mentation, blindness, seizures, coma)
• slow correction is essential
• oral administration safer when possible
• acute onset - 1mEq/l per hour
• chronic onset - 0.5 mEq/l per hour

Question 24

What are the degenerative brain diseases

Answer 24

• storage diseases - defect of a lysosomal enzyme
• accumulation and storage of substrate(s) within the
cytoplasm of neurons, as well as in cells in other
organs
• early onset
• diffuse neurological dysfunction
• progressive course, leading to death
• abiotrophies, axonopathies, leukodystrophies, etc…
• other late-onset degenerative disorders such as
Lafora disease

Question 25

Outline cognitive dysfunction of the brain

Answer 25

• pathological deterioration of the brain
• changes in behavior, memory, and learning ability:
• disturbances in sleeping, staring into space, getting
stuck in corners, loss of toilet training, pacing or
vocalising at night, newly developed behaviour problems
• accumulation of beta-amyloid, with senile plaque
formation and neurofibrillary tangles
Often oedema of the white matter
• Tx with selegiline, nutritional supplementation with
antioxidants and other brain protective compounds
and behavior modification

Question 26

What is the definition of hydroecephalus?

Answer 26

as an active distension of the ventricular system of the brain related to inadequate passage of cerebrospinal fluid (CSF) from its point of production within the ventricular system to its point of absorption into the systemic circulation

Question 27

Which breeds are pre-disposed to hydrocephalus?

Answer 27

Maltese, Yorkshire terrier, English bulldog, Chihuahua, Lhasa apso, Pomeranian, Toy poodle, Cairn terrier, Boston terrier, Pug, and Pekinges

Question 28

What is the prognosis of hydrocephalus?

Answer 28

Neurologic deficits can progress over time, remain static, or even improve after 1 to 2 years of age. Affected patients are often fragile and can worsen later in life coincident with other diseases or minor head trauma.

Question 29

What does hydrocephalus appear on U/S

Answer 29

Normal-sized ventricles appear as paired, slit like anechoic structures, just ventral to the longitudinal fissure, on either side of the midline. Enlarged ventricles are easily seen as paired anechoic regions. With marked ventricular enlargement, the septum pellucidum that normally separates the lateral ventricles is absent and the ventricles appear as a single, large anechoic structure.

Question 30

What is the mainstay of medical treatment for hydrocephalus?

Answer 30

Acetazolamide, alone or in combination with furosemide, is the most commonly used drug therapy. Acetazolamide is a carbonic anhydrase inhibitor that decreases CSF production. The loop diuretic furosemide inhibits CSF formation to a lesser degree by partial inhibition of carbonic anhydrase
Furosemide is added at 1 mg/kg orally once daily. The dose is tapered based on clinical effect. Electrolytes and hydration are monitored. Although these drugs can provide temporary relief, diuretic therapy does not provide long-term benefit in human patients and is associated with potential side effects, such as electrolyte abnormalities.
affected animals often improve with steroid therapy, at least temporarily. One protocol is prednisone at 0.25 to 0.5 mg/kg twice daily until signs improve, then reduce the dose at weekly intervals until 0.1 mg/kg every other day.