Vision and auditory

Question 1

Which embryological layers form the eyeball structures?

Answer 1

1) neuroectoderm (retina),
2) surface ectoderm (lens and cornea),
3) mesoderm-neural crest (cornea, sclera, and uvea).

Question 2

Which structure does the optic vesicle bulge from?

Answer 2

prosencephalon

Question 3

The optic stalk connects with the optic vesicle. Which structure does the optic stalk form from?

Answer 3

diencephalon

Question 4

Name the layers of the pars optica retinae

Answer 4

1) pigment epithelium
2) photosensitive layer (rods, cones)
3) external limiting membrane
4) external nuclear layer (cell bodies of rods and cones)
5) external plexiform layer
6) internal nuclear layer (cell bodies of bipolar neurons)
7) internal plexiform layer
8) ganglion layer
9) nerve fiber layer
10) internal limiting membrane

Question 5

Which visual pigments are contained within the rods and cones?

Answer 5

Cones - iodopsin (day vision, colour vision)

Rods - rhodopsin (night vision, more abundant in nocturnal animals) - more abundant

Question 6

The rod to cone ratio in the dog?

Answer 6

18:1

Question 7

Which structures are contained within the external plexiform layer?

Answer 7

1) axons and telodendria of the photoreceptor neurons
2) axons and dendritic zones of bipolar neurons
3) horizontal cells (interneurons)

Question 8

Which structures are contained within the external plexiform layer?

Answer 8

1) Axons and telodendria of the bipolar neurons
2) Axons and dendritic zones of the ganglionic neurons
3) Amacrine interneurons

Question 9

Which structures are contained within the nerve fiber layer?

Answer 9

1) axons of the ganglionic neurons (unmyelinated)
2) stellate astrocytes

Question 10

Name the structures

Answer 10

Microscopic section of the pars optica retina of a dog’s eye. The pigment at the top is in the inner (vitreal) portion of the choroid. Beneath this portion, in order,
1) The tapetum lucidum of the choroid (1),
2) the pigment epithelium of the retina (without pigment), the external segments of the photosensitive layer (densely stained), the internal segments of the photosensitive layer (2), 3) the external nuclear layer (nuclei of rods and cones) (3),
4) outer plexiform layer (4),
5) inner nuclear layer (primarily nuclei of bipolar cells) (5),
6) inner plexiform layer (6),
7) ganglion cell layer (single layer of large neurons) (7),
8) nerve fiber layer (8).
9) The vitreous is at the bottom.

Question 11

Which domestic animal may have a central area (spot/macula/fovea) seen in humans, used for the most distinct vision?

Answer 11

cats (dorsolateral to optic disc)
- cone rich area

Question 12

Which domestic species has the most and which the least myelinated optic disc?

Answer 12

Most - dogs
Least - cattle

Question 13

Which domestic animal does this fundus belong to?

Answer 13

Medium sized dog

Note the abundant myelination of the optic disc, which is at the inferior border of the choroidal tapetum lucidum. Note the veins located in the center of the optic disc.

Question 14

Which domestic animal does this fundus belong to?

Answer 14

Cat

The optic disc positioned over the area of the choroidal tapetum lucidum. Note that the optic disc is small, and all the blood vessels are at the margin of the optic disc.

Question 15

Which domestic animal does this fundus belong to?

Answer 15

Cow

the optic disc at the inferior border of the choroidal tapetum lucidum with the large tortuous blood vessels and the minimal myelination.

Question 16

Which domestic animal does this fundus belong to?

Answer 16

Horse

Note the prominent optic disc just below the inferior border of the choroidal tapetum lucidum (nontapetal nigrum area). Note the very small blood vessels only located at the margin of the optic disc.

Question 17

Degree of crossing of the optic nerve axons at the optic chiasm for different animal species?

Answer 17

Fish and birds - 100%

Primates: ca 50%
Cat: 65%
Dogs: 75%
Horse/farm animals: 80-90%

The axons that cross in the optic chiasm come from ganglionic neurons in the medial (nasal) aspect of the retina.
Axons from ganglionic neurons in the lateral (temporal) aspect of the retina remain ipsilateral in their course through the central visual pathway.

Question 18

Which occipital gyri form the visual cortex?

Answer 18

caudal part of the marginal, ectomarginal (laterally), occipital (caudally), and the splenial (medially) gyri

Question 19

When should the menace response be present in different animal species?

Answer 19

in foals and calves by 1 to 2 weeks of age and

by 10 to 12 weeks of age in puppies and kittens

Question 20

Lesion of which parts of the cerebellum may cause a loss of menace response?

Answer 20

Diffuse lesions, especially if the lateral or interposital nuclei are affected (ipsilateral)

Question 21

Chromatographic testing in dogs with SARDS: explain the findings

Answer 21

Dogs with blindness caused by SARDS only responded to high-intensity blue and not red
wavelength light compared with healthy patients that had a normal pupillary light reflex with very low light intensities using blue and red wavelength light.

These findings imply the loss of rod-cone–mediated pupillary light reflex with preservation of ganglion cell–mediated pupillary light reflex.

Question 22

Which anomalies can be caused in kittens when the queen receives griseofulvin during gestation?

Answer 22

Microphthalmia
Meningomyelocele
Cyclopia

Question 23

Which disease can cause an optic nerve hypoplasia in calves

Answer 23

Infection with BVDV in utero (about 25% of calves develop o.nerve hypoplasia in adition to cerebellar hypoplasia and atrophy)

Question 24

Deficiency of which vitamin may cause blindness and why?

Answer 24

Vitamin A

1) Night blindness results from the loss of rod photoreceptor function because of the inability to produce rhodopsin.

2) complete blindness is caused by compression and degeneration of the optic nerves where they course through the optic canals. Stenosis occurs at this location because of a thickening of the dura and a failure of the optic canals to enlarge as the calves grow (this also causes elevated ICP due to arachnoid vili fibrosis - can be visible as optic disc oedema on fundic examinatioon)

Question 25

Which muscles are involved in maintaining the palpebral fissure?
DDs for ptosis and a wide palpebral fissure

Answer 25

Size of palpebral fissure:
Levator palpebrae superioris (CN III); levator anguli oculi medialis (CN VII) in the horse and farm animals; orbitalis (sympathetic)

Narrow:
1) Ptosis (sagging or drooping of the superior eyelid):
Oculomotor nerve paralysis with strabismus and mydriasis
Sympathetic nerve paralysis (Horner syndrome)
Facial paralysis in the horse and farm animals
2) Narrowed fissure without ptosis:
Chronic atrophy secondary to facial nerve paralysis
Hemifacial tetany

Wide: Facial paralysis in small animals occasionally

Question 26

DDs for protrusion of the 3rd eyelid

Answer 26

Sympathetic nerve paralysis (Horner syndrome)
Tetanus when stimulated
Facial paralysis when menaced
Severe depression in cats
Hyperplasia of the gland of the third eyelid
Secondary to enophthalmos that occurs with atrophy (denervation or from a myopathy) of the temporal and pterygoid muscles
Retrobulbar mass (located ventral to the globe)

Question 27

DDs for strabism

Answer 27

Oculomotor nerve paralysis, ventrolateral, constant
Abducent nerve paralysis, medial, constant
Trochlear nerve paralysis, dorsal deviation of the medial angle (ruminants), constant;
lateral deviation of the dorsal angle (cats), constant
Vestibular system dysfunction, ventrolateral in some head positions

Question 28

DDs for myosis and mydriasis

Answer 28

Mydriasis:
Oculomotor nerve paralysis with ptosis and strabismus
Retinal or optic nerve disease with blindness
Glaucoma
Iris atrophy
Spastic pupil syndrome associated with feline leukemia virus infection
Sympathetic stimulation (Pourfour du petit syndrome)

Miosis:
Sympathetic nerve paralysis (Horner syndrome)
Acute prosencephalic disease, release of oculomotor neurons
Ocular discomfort: oculopupillary reflex
Iritis

Question 29

DDs for polioencephalomalacia (cerebrocortical necrosis) in ruminants

Answer 29

thiamin deficiency,
sulfur toxicity,
lead toxicity,
osmolar imbalance (salt or water toxicity),
cerebral anoxia
Copper deficiency (in lambs)

Question 30

Which areas of the brain are most sensitive to hypoxia/thiamin deficiency?

Answer 30

neocortex, lateral geniculate nuclei, and the caudal colliculi
- populations of neurons that are the most sensitive to anything that interferes with their aerobic metabolism
- The earliest recognizable histologic lesions are a cytotoxic edema of cerebrocortical astrocytes and then adjacent neurons.

Question 31

Clinical signs of thiamin deficiency in cattle?

Answer 31

an acute onset of depression, mild ataxia, blindness, and occasionally tremors followed by rapid progression to recumbency (nonambulatory tetraparesis) with opisthotonus, abnormal positional nystagmus, semicoma (stupor), extremely miotic pupils with dorsal deviation of the medial aspect of both pupils (dorsomedial strabismus), and occasional seizures.
As patients respond to treatment, the blindness is usually the last deficit to resolve and the one that occasionally persists.

Question 32

Thiamin deficiency neuro signs in small animals

Answer 32

Cats:
The initial neurologic signs usually consist of a cerebellovestibular ataxia followed by dilation of the pupils that respond poorly to light and blindness.
Seizures, head and neck flexion, coma, and death follow.
Seizures are sometimes elicited by handling the cat, which induces a severe flexion of the entire neck and trunk. The cat will act as if it were trying to roll itself into a ball.

Dogs:
Dogs with thiamin deficiency usually show an initial depression and spastic paraparesis and pelvic limb ataxia that progress to vestibular ataxia, circling, and recumbency. Wide head excursions may reflect the bilateral vestibular nuclear lesions. Seizures usually occur after the dog is recumbent.

In both species the menace response may be absent because of the thalamic nuclear or the neocortical lesions.

Question 33

Cause of equine hypoxic ischemic myelopathy?

Answer 33

Equine hypoxic ischemic encephalopathy (neonatal encephalopathy), a form of maladjustment syndrome, occurs in newborn foals that are normal at birth.

The cause of the hypoxia is unknown but may occur before or during birth, and the delay in observation of the clinical signs may reflect the maturation period, as previously described.

From 1 to 14 days postnatally, these foals rapidly develop diffuse neurologic signs but predominantly prosencephalic with lethargy, inability to nurse, blindness, and seizures. Their lesions consist of cerebrocortical necrosis and brainstem nuclear degeneration similar to those observed after hypoxia (Fig. 14.81).

Question 34

What is Nervous Ketosis?

Answer 34

Nervous ketosis is the term used for the occasional occurrence of the encephalopathic form of the metabolic disorder ketosis. The encephalopathy is presumed to be the result of the ketoacidosis and hypoglycemia that interfere with the aerobic metabolism that is critical for normal neuronal function. Nervous ketosis may occur at any time during the first 8 weeks of lactation. These encephalopathic cattle are occasionally blind with normal pupillary size and pupillary light reflexes. They more commonly exhibit bizarre behavior that may include constant licking of one or more sites on their body or inanimate objects in their environment, biting and even breaking off the water cups from the water pipes, and propulsively pushing into their stanchion. If these cattle are loose, they may wander aimlessly or press their head against the fence or wall that confines them. They may act obtunded and demented or be very aggressive. The diagnosis is readily made by determining the presence of ketonuria or ketonemia. These clinical signs usually resolve with appropriate intravenous therapy with dextrose. However, blindness with responsive pupils may persist in a severely affected patient as a result of permanent lesions in the visual neocortex.

Question 35

Which toxin causes equine leukoencephalomalacia?

Answer 35

Fusarium verticillioides (formerly Fusarium moniliforme) or Fusarium proliferatum. This fungus produces a trichothecene toxin known as fumonisin B1

Question 36

What is the modiolus?

Answer 36

The portion of the bone that forms the center, or axis, of the coiled cochlea

Question 37

What is the helicotrema?

Answer 37

the connection of scala tympani and scala vestibuli

Question 38

What is the spiral organ (the organ of Corti)?

Answer 38

the specialized sensory neuroepithelium that is located on this basilar membrane.
This spiral organ is composed of hair cells and several types of supporting cells. The hair cells have modified microvilli on their luminal surfaces known as stereocilia. The tips of these stereocilia are embedded in a proteinaceous membrane, the tectorial membrane, which covers the hair cells and is attached medially along the apex of the cochlear duct. The hair cells are associated with various types of supporting cells located on the basilar membrane. The dendritic zones of the neurons in the cochlear portion of cranial nerve VIII are in synaptic relationship with the bases of the hair cells.

Question 39

Time from birth to perception of sound in domestic animals?

Answer 39

10 to 11 days of age in puppies. In normal dogs, it may take as long as 2 weeks for the external acoustic meatus to open completely.34 Audiometry studies first detect sound perception at 5 days of age in kittens and 14 days in puppies. Normal hearing of environmental sounds in dogs usually develops by 4 to 5 weeks of age. For that reason, as well as the practicality in handling puppies at this age, it is best to delay electrophysiologic tests for hearing until at least 6 to 8 weeks of age.

Question 40

Origin of the waves in BEAR testing

Answer 40

Wave I - CN VIII.

The origin of waves II through V is less precise.

Wave II - cochlear nuclei,
Wave III - dorsal nucleus of the trapezoid body,
Wave IV - lateral lemniscus and its nucleus,
Wave V - caudal colliculus,
Wave VI - medial geniculate nucleus.

Normal animals have four to six recognizable waveforms.

Question 41

Which waveforms would be expected to be absent in a comatose patient with absent brainstem function?

Answer 41

II-VI

Question 42

Two main forms of deafness

Answer 42

1) conduction
- obstacles include the air pathway in the external acoustic meatus, the tympanum and bony pathway of the ossicles through the middle ear, and the fluid medium of the perilymph in the cochlea
- causes: agenesis of external acoustic meatus (reported in a colony of GSD), inflammatory or neoplastic lesion of above mentioned structures

2) sensorinerual
- congenital (albinotic and abiotrophic formes)
-acquired

Question 43

Pathogenesis of the albinotic form of congential sensorineural deafness

Answer 43

Lack of melanocytes in the stria vascularis - inhibited function of production of endolymph (which is usually K+ ritch due to secretion of K+ from stria vascularis) –> abnormal endocochlear potential –> degeneration of hair cells of the spiral organ

• occurs in partially or completely albinotic animals

Question 44

Breeds of dogs and cats with the albinotic form of congential sensorineural deafness

Answer 44

Blue eyed white cats - 50% chance (white scotish fold, white devon rex, european white, white persian, white manx, white exotic …)

Dogs: reported
Dalmatians - 30% (autosomal dominant w/ incomplete penetrance)
Bull terriers - 1% (coloured) - 20% (white)
English setter (8%)
English cocker spaniel (7%)
Australian cattle dog (14.5%)

Question 45

Pathogenesis of abiotrophic form of sensorineural deafness?

Answer 45

Abiotrophy of the hair cells of the spiral organ - the endolymph potentials are normal.
Autosomal recessive.
Usually apparent after a few weeks of age, but can be late onset (Cavalier King Charles spaniel)

Question 46

Causes of acquired sensorineural deafness

Answer 46

1) inflammation of middle to inner ear (with vestibular signs)
2) temporal bone neoplasia
3) ototoxicity (aminoglycosides, some chemoterapeutics, some otic drugs if given thru perforated tympanum)
4) presbycusis (age related degeneration of hair cells)

Question 47

DDs for hepatic encephalopathy in horses

Answer 47

• Serum (antitetanus) causing hepatic necrosis
• PSS in foals
• pyrrolizidine alkaloid hepatopathy from ingesting plants (Senecio and Crotalaria spp.) that contain this toxin
• hyperammonemia-hyperornithinemia-hyperhomocitrullinuria in Morgan foals