Neuro and special senses

Question 1

Which structures do peripheral vestibular disease involve?

Answer 1

CN 8 - vestibulocochlear
or semicrcular canal

Question 2

Which structures do central vestibular disease involve?

Answer 2

• vestibular nuclei of brainstem
• flocculonodular lobe of cerebellum
• caudal cerebellar peduncle

Question 3

Describe the neurological involvement of the menace response

Answer 3

Response because it requires recognition + processing in the cerebral cortex

Afferent:
Tests vision CNII (generally ipsilateral)
And cerebral function, occipital cortex, thalamus (integration – contralateral)

Efferent:
Motor cortex (contralateral), cerebellum (ipsilateral)
Motor response – CNVII (ipsilateral)

Question 4

Describe the neurological involvement of the PLR:

Answer 4

Midbrain
Afferent: CN II
Efferent: PNS component of CN III.

Question 5

Describe the innervation for corneal reflex:

Answer 5

Pons:
Afferent: CN V ophthalmic branch (sensation)
Efferent: CN VI function (globe retraction), CN VII (blink)

Question 6

Describe the innervations for trigeminofacial reflex

Answer 6

Pons
Afferent: sensation CN V
Efferent: CN VII

Question 7

Describe the innervations for gag reflex:

Answer 7

Medulla
Afferent: CN IX and X
Efferent: CN IX, X, XII

Question 8

Describe the innervations for physiologic nystagmus:

Answer 8

Pons, midbrain
Afferent: CN VIII
Efferent: CN III, IV, VI

Question 9

3 mandatory findings of irreversible cessation of brain function:

Answer 9

1) Coma
2) Absence of brainstem reflexes
3) Apnoea

Question 10

Indications for anticonvulsant therapy:

Answer 10

1. identified structural lesion or history of brain disease or injury
2. Acute repetitive seizures or status epilepticus
   a. seizure lasting 5min or more
   b. 3 or more generalised seizures within 24h period
3. 2 or more seizures in a 6 months period
4. Prolonged, severe or unusual postictal periods

Question 11

3 components of the brain:

Answer 11

Brain parenchyma, CSF, blood flow

Question 12

The Monroe-Kellie Doctrine:

Answer 12

Increase in the volume of one component requires a compensatory decrease in one or more of the other components if ICP is to remain unchanged (volume buffering)

Question 13

3 mechanisms to maintain ICP within a functional range

Answer 13

1) volume buffering: Monroe-Kellie doctrine (blood & CSF pushed extracranially)
2) autoregulatory mechanisms
i) pressure: cerebral arterioles response to changes in transmural pressure (operates with CPP 50-150mmHg)
ii) chemical: PaCO2, PaO2, cerebral metabolic rate (H+ ions)
3) Cushing response : catecholamine release as response to cerebral ischemia -> systemic vasoconstriction and increased CO. Baroreceptors cause reflex bradycardia.

Question 14

Proposed MoA of mannitol:

Answer 14

1) Immediate (minutes) plasma expanding effect: reduce blood viscosity, increasing CBF and O2 delivery
2) osmotic effect (15-30min), gradients are established between plasma and cells to reduce brain water content

Question 15

3 classes of traumatic neuropathies, based on severity (least to most):

Answer 15

1. Neurpraxia: loss of nerve conduction without structural change
2. Axonotmesis: axonal damage without loss of supporting structures (axon repair 1mm/day)
3. Neurotmesis: complete severance of the nerve

Question 16

Mechanism of paralysis for tick paralysis:

Answer 16

Holocyclotoxins
- impairs ACh release at the NMJ by blocking Ca2+ influx at the axon terminal
- impairs ACh at autonomic synapses -> sympathetic overdrive

Question 17

Mechanism of paralysis in botulism

Answer 17

Botulinum neurotoxin irreversibly binds the neuronal surface receptors on nerve terminals + prevent synpatic release at NMJ
Inhibits autonomic synapses (mild autonomic dysfunction)

Question 18

Mechanism of paralysis for myasthenia gravis:

Answer 18

autoantibodies are formed against nicotinic ACh receptors on the post-synaptic membrane of NMJ

Question 19

What are 6 differential diagnoses for canine generalized lower motor neuropathy with megaesophagus in North America?

Answer 19

• myasthenia gravis
• botulinum
• organophosphate toxicity
• hypothyroid polyneuropathy
• coral snake envenomation
• protozoa infection, polymyositis (Neospora)

Question 20

Possible reasons for seronegative MG:

Answer 20

1) damage to antigenic epitope during solubilisation process
2) majority of autoantibodies bound in skeletal muscle
3) autoantibodies directed against other components of post-synaptic NMJ (e.g. MUSK, muscle specific kinase)

Question 21

What are the exotoxins excreted by tetanus bacillus (2):

Answer 21

1. Tetanolysin: damage to local tissue, optimises enviro for bacterial multiplication
2. Tetanospasmin: acts on pre-synaptic nerve terminals to prevent neurotransmitter release. Mainly affects inhibitory interneurons.

Question 22

Indications for CSF (5)

Answer 22

1. Suspect infectious or inflammatory CNS disease
2. Suspect neoplastic disease (lymphoma exfoliates well)
3. Cluster or continuous seizure activity in which underlying infectious/inflam/neoplastic disease is likely
4. Acute, ascending LMN signs. CSF may help differentiate acute polyradic vs inflammatory disease vs infectious vs neoplasia
5. Monitoring (rare), short term response to tx in heavily sedated or MV patients