eye and ear

Question 1

Outer hair cells are damaged by what medication?

Answer 1

aminoglycosides

Question 2

What is the pathway of hearing?

Answer 2

inner hair cells synapses on spiral ganglion in the modialus -> axons of the spiral ganglion cells form the auditory nerve of CN VIII -> enter brainstem at cerebellopontine angle -> terminate in ipsilateral coclear nuclei in the inferior cerebellar peduncles in the medulla -> project to ipsilateral and contralateral superior olivary complexes -> lateral lemniscus -> inferior colliculus -> medial geniculate nucleus in thalamus -> heschl’s gyri (not via the internal capsule)

Question 3

What organ senses linear acceleration? What organ senses angular acceleration?

Answer 3

linear - otolith organs

vertical linear acceleration - saccule

horizontal linear acceleration - utricle

angular - semicircular canals

Question 4

What is the crista amupllaris?

Answer 4

Sensory epithelium of the semicircular canals containing hair cells and supporting cells

Question 5

Where are the hair cells in the semicircular canals? Where are the hair cells in the cochlea? Where are the hair cells in the otolith organs

Answer 5

semicircular canals - gelatinous cupula

cochlea - tectorial membrane

otolith organs - otoconia (calcium carbonate crystals imbedded in gelatinous matrix)

Question 6

How does acceleration get transmitted into electrical signals traveling in the vestibular portion of CN VIII?

Answer 6

Vestibular pathway - The stereocilia of hair cells in the semicircular canals are lodged in a gelatinous cupula. Angular head accelerations cause endolymph fluid movement that moves the cupula, thereby exerting a shear force on the stereocilia. If the stereocilia are displaced toward the kinocilium, the membrane of the hair cell depolarizes. If the stereocilia are displaced away from the kinocilium, the membrane hyperpolarizes.

Question 7

Where is the horizontal component of sound analyzed? Where is the vertical component of sound analyzed?

Answer 7

horizontal - superior olivary complex

vertical - pinna of outer ear

Question 8

What is the cocktail party effect?

Answer 8

outer hair cells change height to make certain frequencies less stimulatory so you can focus on certain sounds and ignore other sounds

Question 9

what are otoacoustic emissions?

Answer 9

noises that the outer hair cells make while changing height. Is used as part of auditory screening in newborns to test for deafness

Question 10

What does the vestibulo-thalamo-cortical pathway mediate? What is the pathway?

Answer 10

Conscious perception of equilibrium and head orientation in space

hair cells of the semicircular canals -> vestibular portion of CN VIII -> vestibular nuclei in medulla-> decussate and ascend to -> contralateral ventral posterior nucleus of the thalamus -> primary vestibular cortex (located just posterior to the face area of the postcentral gyrus)

Question 11

What does the vestibulo-ocular reflex mediate? What is the pathway of the VOR?

Answer 11

Mediates compensatory eye movements to maintain visual fixation on a stationary object while the head is moving.

Afferent arc: afferent fibers in CN VIII -> synapse on the medial vestibular nucleus -> projects to the

• contralateral abducens nucleus -> inhibiting one pair of medial and lateral rectus muscles
• ipsilateral abducens nucleus -> exciting the other pair of medial and lateral rectus muscles

Question 12

What reflex does the vestibulo-spinal pathway mediate? What is the pathway?

Answer 12

maintains postural equilibrium by activating anti-gravity muscles

Lateral vestibular nucleus -> descends ipsilateral through the lateral vestibulospinal tract -> motor neurons at all levels of the spinal cord

Question 13

What reflex does the vestibulo-colic pathway mediate?

Answer 13

Maintains head stability during body movement

Medial vestibular nucleus -> descends through the medial longitudinal fasciculus (MLF) -> cervical spinal nerves

Question 14

What reflex does the vestibulo-sympathetic pathway mediate?

Answer 14

Adjustments in blood pressure, heart rate, respiration and digestion during changes in position and posture

otolith organs -> vestibular nuclei -> brainstem parasympathetic control centers -> converges with baroreflex

Question 15

What is the pathway of the pupillary light reflex?

Answer 15

Afferent arc - CN II -> synapse in ipsilateral pretectal nucleus -> sends axons to ipsilateral and contralateral Edinger-Westphal nuclei -> sends parasympathetics to both eyes -> both pupils constrict

Question 16

When fixation is shifted from far to near, what three things happen? What nerve are they controled by?

Answer 16

1) accommodation - ciliary muscles change lens shape to increase refraction of light
2) convergence: both medial rectus muscles activate to direct both eyes inward towards the nose
3) pupillary constriction via the pupillary sphincter muscles

All three muscles (ciliary, medial recuts and pupillary spincter) are controlled by CN III

Question 17

What is the visual pathway of neurons?

Answer 17

Rods/cones -> bipolar cells -> ganglion cells -> axons of ganglion cells for the optic nerve -> decussation of nasal retinal fibers (temporal visual fields) at the optic chiasm -> optic tract -> lateral geniculate nucleus -> superior visual field fibers go into Meyer’s loop and inferior visual field fibers go into parietal radiations -> visual cortex -> “where” pathway to parietal lobe or “what” pathway ro temporal lobe

Question 18

What is the pathway of conjugate (saccade) eye movement?

Answer 18

“Burst” neurons in the paramedian pontine reticular formation (PPRF) synapse on motor neurons and interneurons in the abducens nucleus

• > motor neurons from the abducens nucleus cause the lateral rectus to contract
• > interneurons in the abducens nucleus travel through the medial longitudinal fasciculus (MLF) to synapse on the contralateral oculomotor nucleus and causes contraction of the medial rectus

Question 19

What lesion causes internuclear ophthalmoplegia? How does it present?

Answer 19

INO lesion is a unilateral lesion in the medial longitudinal fasciculus (MLF).

Presents as impaired conjugate gaze. The ipsilateral eye cannot adduct and the contralateral eye has nystagmus when abducting.

Vergence is intact.

Question 20

Where is the lesion in lateral (horizontal) gaze palsy? How does it present?

Answer 20

Unilateral lesion of the paramedian pontine reticular formation.

Impaired conjugate gaze in both eyes towards the side of the lesion. Conjugate gaze in both eyes away from the side of the lesion is normal.

Question 21

Where is the lesion in one-and-a-half syndrome? What causes this syndrome? How does it present?

Answer 21

Lesion of one paramedian pontine reticular formation and ipsilateral medial longitudinal fasciculus. Can be due to a stroke in the dorsal pons or multiple sclerosis.

Presents as a combination of ipsilateral horizontal gaze palsy (can’t move eyes to the side of the lesion) AND ipsilateral INO (ipsilateral eye can’t adduct and contralateral eye has nystagmus)

Question 22

What are the pupil abnormalities?

Answer 22

CN III palsy, Horner’s syndrome, Tonic pupil, Argyll-Robertson pupils, Marcus Gunn pupil

Question 23

What are the two muscles of the middle ear? What do they do? What nerve innervates them?

Answer 23

Tensor tympani - stretches the tympanic membrane to facilitate high frequency vibrations. Innervated by CN V

Stapedius muscle - pulls the stapes off the oval window, attenuating the impact of loud sounds (acoustic reflex). Innervated by CN VII

Question 24

Why can loop diuretics result in hearing loss?

Answer 24

There is a potential difference between the endolymph and the perilymph that maintain acoustic thresholds. Loop diuretics that block the Na+/K+/2Cl- transporter decrease the potential difference between the two fluids

Question 25

What is the purpose of inner hair cells? What is the purpose of outer hair cells? What areas of hte brain control outer hair cells?

Answer 25

Inner hair cells transduce sound and contribute to the auditory nerve

Outer hair cells change their height to either increase low frequency sound or sharpen frequency resolution (shorter) or protect inner hair cells from loud noises (taller).

Outer hair cells are controlled by the superior olivary complex

Question 26

What are the differences between central vertigo and peripheral vertigo?

Answer 26

Symptoms:

central - severe imbalance/ataxia; no hearing loss nor tinnitus; non auditory symptoms including diplopia and dysarthria

Peripheral - less severe imbalance/ataxia; hearing loss and tinnitus can be present; no non-auditory symptoms

Course:

central - more persistent than peripheral vertigo

peripheral - acute onset that tends to improve in days to weeks

Nystagmus:

Central - NOT inhibited by fixation of eyes; changes directions with gaze

peripheral - can be suppressed by fixation of eyes; only occurs away from the side of the lesion

Question 27

What are the four possible etiologies of a dizzy patient?

Answer 27

Vertigo - false sense of motion

imbalance - sensory disturbance of vestibular, visual or proprioceptive systems

disequilibrium - patient feels like things are off balance or that he is drunk

lightheadedness - patient feels like he will faint

Question 28

What is the pathogenesis of Meniere’s disease? What are its symptoms?

Answer 28

Overabundance of endolymph fluid (endolymphatic hydrops) cause distension of the membranes of the vestibular canals. When membrane ruptures, the vestibular canals cannot function properly. Once the pressure stabilizes, things go back to normal. Symptoms include episodic vertigo that is spontaneous and lasts for a coule of hours, nausea/vomiting, unilateral hearing loss

Question 29

What is the etiology of benign positional paroxysmal vertigo? What maneuver is used to diagnose this disorder? What are its symptoms?

Answer 29

Otoconia crystals dislodge and float in the endolymph. When the affected side is angled down, the crystals can drift into a semicircular canal and continually stimulate the canal, giving the patient the feeling of vertigo.

Can use the Dix-Hallpike maneuver.

Symptoms: positional vertigo brought on by head position change (eg rolling over in bed). Nystagmus starts 5-10 seconds after the vertigo. Repeated stimulation, including via Dix-Hallpike maneuvers, cause the nystagmus to fatigue or disappear temporarily. Nystagmus is suppressed by visual fixation.

Question 30

Where is the lesion in a CN III palsy? What are the common causes? What are the symptoms?

Answer 30

Lesion is in the CN III. Causes include a posterior communication artery aneurysm. Symptoms are mydriasis (due to unopposed sympathetics) and ptosis due to deficit in the levator palpebrae muscle

Question 31

What is the pathogenesis of Horner’s syndrome? What are its symptoms?

Answer 31

Horner’s syndrome is when there is a lesion in the sympathetic nerves to the head. Can be due to a dessection of the carotid artery. Symptoms include mild ptosis (due to deficit in the superior tarsal muscle), anhidrosis and miosis (due to unopposed parasympathetics)

Question 32

What causes Argyll-Robertson pupils? What are the symptoms?

Answer 32

Caused by tertiary neurosyphilis, diabetes

Pupils accommodate but don’t react to light (absent light reflex but preserved near reflex)

Question 33

Where is the lesion in Tonic pupil? What are its symptoms?

Answer 33

In a tonic pupil, there is a lesion in the ciliary ganglion leading to mydriasis. Pupils accomodate but don’t react to light (absent pupillary light reflex but preserved pupillary near reflex)

Question 34

What is the pathogenesis of Marcus Gunn pupil (relative afferent pupillary defect - RAPD)?

Answer 34

A lesion in the optic nerve caused by optic neuropathy or optic neuritis.

Moving a bright light from the unaffected eye to the affected eye would cause both eyes to dilate, because the ability to perceive the bright light is diminished. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, but reduced.

Question 35

What is the olfactory pathway?

Answer 35

Odorants in the air are detected by the cilia of olfactory receptor neurons -> axons of olfactory receptor neurons make up olfactory nerves -> transverse the cribiform plate -> synapse on ipsilateral olfactory bulb neurons (mitral cells) through glomeruli -> mitral cells in the bulb form the olfactory tract -> piriform cortex

• > hypothalamus -> feeding behavior and autonomic responses
• > dorsomedial thalamic nucleus -> orbitofrontal cortex -> conscious appreciation of odorants, association of odors with other environmental stimuli and olfactory guided memory
• > Insular and orbital cortex -> discrimination and identification of odors, taste integration
• > hippocampus -> olfactory guided memory

Question 36

In what ways is the olfactory system unique from the other sensory systems?

Answer 36

1) cell bodies of primary afferents are in the epithelium itself - there is no ganglia
2) olfactory neurons undergo continuous regeneration by basal stem cells
3) no thalamic relay before the cortex
4) pathway is entirely ipsilateral

Question 37

What is the pathway of taste?

Answer 37

primary afferents from taste buds of anterior 2/3 of tongue (CN VII), posterior 1/3 of tongue (CN IX) and epiglottis/esophagus (CN X) -> rostral regions of the solitary nucleus/tract in the medulla -> ventral posterior medial (VPM) nucleus in the thalamus -> insula, operculum of frontal lobe and orbitofrontal cortex

Exclusively ipsilateral

Question 38

What are the three pharmacological approaches to decreasing intraocular pressure in glaucoma? What drug classes fit each approach?

Answer 38

1) Decreasing aqueous humor production - β blockers, α2 receptor agonists, carbonic anhydrase inhibitors
2) increasing aqueous humor outflow through the Canal of Schlemm - cholinergic agonists
3) increasing aqueous humor outflow through the uveoscleral pathway - prostaglandin agonists

Question 39

What symptoms would you expect if there was a lesion in CN III? What types of things can cause a lesion in CN III?

Answer 39

Mydriasis (blown pupil)

complete ptosis

eye is in “down and out” position

pupil is non-reactive to light

Often caused by an aneurysm in the posterior communicating artery

Question 40

What is a Hutchinson pupil?

Answer 40

A sign of herniation of the temporal lobe uncus through the foramen magnum

CN III is being compressed by the hernation so the pupil becomes dilated and non-reactive to light

Question 41

What clinical symptoms would you expect if there was a lesion in the trochlear nerve/trochlear nerve dysfunction?

Answer 41

elevation of the affected eye

vertical diplopia

Question 42

What clinical symptoms would you expect if there was a lesion/dysfunction of the abducens nerve?

Answer 42

impaired ipsilateral abduction of the eye

inward deviation of the ipsilateral eye (esotropia)

Question 43

What is the horizontal gaze center that controls horizontal saccades? What is the vertical gaze center that controls vertical saccades? What is the pathway from the cortex to these control centers?

Answer 43

Horizontal - PPRF (paramedian pontine reticular formation)

Vertical - riMLF (rostral interstitial nucleus of the median longitudinal fasciculus)

Information from the cortex -> superior colliculus -> PPRF or riMLF