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126 Cards in this Set

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  • Back
what are the fluids contained in the internal ear? what are their compositions?
the bony labyrinth: PERIlymph (low K+, high Na+). typical.

the osseus labyrinth: ENDOlymph (high K+, low Na+). unique.
how many bony canals make up the cochlea? what is it spiralled AROUND?
the cochlea is a single bony canal, wound 2 1/2 times around the modiolus (central bony core) with a limbus projecting from it.
how many spaces are within the cochlea? how are they divided?
BTWN membranes: cochlear duct, aka scala media

it's roof: vestibular (Reissner's) membrane.

it's floor: basilar membrane (attached centrally to the limbus).

scala vestibuli: btwn vestibular mem. & bony wall

scala tympani: btwn basilar mem. & bony wall

s.vestibuli and tympani are connected at the APEX of the cochlea.
both hearing and balance are based on hair cells bathed in ____?
what is the organ of corti? which hair cells contact the tectorial membrane?
the organ of corti is a spiral strip of specialized mechanoRECEPTOR hair cells and SUPPORTING cells resting on the basilar membrane at its central side, and covered by the tectorial membrane.

OUTER hair cells contact the tectorial membrane.
what is the position of the auditory hair cells? how is sound transduced from the outer ear to the basilar membrane?
auditory hair cells are btwn the basilar membrane at their base and the tectorial membrane at the tips of the stereocilia.

pressure waves in PERIlymh originate from the footplate of the stapes at the oval window of the vestibule.

those pressure waves cause the basilar membrane to move up and down.
what type of force is created when the basilar membrane vibrates? where?
SHEAR forces are generated between the tectorial membrane and the stereocilia when the basilar membrane vibrates.
why are the auditory hair cells considered mechanoreceptors?
basilar membrane UP:
stereocilia bent AWAY from limbus = DEPOLARIZATION

basilar membrane DOWN:
stereocilia bent TOWARDS limbus = HYPERPOLARIZATION
how do loud sounds damage hearing?
loud sounds cause extreme vibration which may shear the hairs off the hair cells (or otherwise damage the o of c) producing hearing loss OF THOSE FREQUENCIES.
what is the spiral ganglion? how is it involved in sound transduction?
the spiral ganglion is a grouping of the bipolar cell bodies of the peripheral processes of the organ of corti.

a depolarized hair cell transmits impulse to peripheral process(dendrite) of spiral ganglion. *excitatory*
the vast majority of peripheral processes innervate ______ and almost all auditory info passing centrally comes from these.
INNER hair cells!
what is tonotopy? how is it distributed?
tonotopy = pitch localization (aka orderly relationship btwn frequency and location)

HIGH pitch (short wave): proximal (basilar base)

LOW pitch (longer wave):
distally (basilar apex)
what is the afferent nerve distribution with respect to inner and outer hair cells?
ONE inner hair cell produces MANY afferent nerve fibers.

MANY outer hair cells produce ONE afferent nerve fiber.
where is the cochlear spiral ganglion located?
within the modiolus.
how is the cochlear nerve formed? describe it's path as the vestibulocochlear nerve
central processes of the spiral ganglion cells project through channels in the modiolus to converge at the distal end of the internal acoustic meatus (IAM): cochlear nerve!

c + v = VIII (shares IAM with CN VII and labyrinthine artery of AICA)

VIII crosses subarachnoid space to brainstem where it enters at the cerebellopontine angle.

VIII bifurcates to dorsal and ventral cochlear nuclei.
where do the primary cochlear afferents synapse? where are the locations?
auditory axons in the 8th cranial nerve synapse on the ipsilateral cochlear nuclei!

dorsal and ventral cochlear nuclei are located superficially in the ROSTRAL medulla lateral to the base of the INFERIOR cerebellar peduncle.
what are the auditory nuclei? how many cochlear nuclei are there?
the auditory nuclei:
relay (ascending order):
superior olivary
lateral lemniscus
inferior colliculus
medial geniculate

there are THREE cochlear nuclei:
what are possible causes of unilateral deafness?
unilateral lesion of any of the structures from o of c thru cochlear nuclei:

shearing of stereocilia (high amp sound)

neuroma of IAM

occlusion of AICA
what are the pathways of the afferent auditory fibers after synapsing on the cochlear nuclei?
dorsal: decussate & ascend to inferior colliculus

ventral: project bilaterally to superior olivary in caudal pons (TRAPEZOID of ventral tegmentum in caudal pons, btwn and ventral to ML)
what forms the lateral lemniscus (LL)?
lateral lemniscus is formed from ASCENDING fibers from superior olivary and dorsal cochlear nuclei.

LL ascends thru the pons to caudal midbrain, synapse on inferior colliculus.

PONS: LL is lateral to ALS which is lateral to ML. nuerons along the way = nucleus of LL.
lemniscal fibers MAY synapse here.
projection fibers from LLnucleus may decussate to CL LLnucleus.
what types of fibers does the lateral lemniscus carry?
2nd order and HIGHER axons
what is the major auditory relay nucleus in the caudal midbrain tectum? what synapses here?
inferior colliculus is the major relay center in the caudal midbrain tectum.

most lateral lemniscus fibers synapse here, including:

1.IL & CL s. olivary axons (unsynapsed) fibers from CL dorsal cochlear nuclei
3.IL and CL LLnuclei axons
what is the path of neurons after synapsing on the inferior colliculus?
they project bilaterally, decussation occurs thru the commisure of the inferior colliculi.

fibers project thru the brachium of the inferior colliculus to the medial geniculate nucleus.
what is the medial geniculate nucleus? what is the pathway of it's neurons?
m.geniculate nucleus is a thalamic SENSORY relay nucleus on the ventral thalamus.

fibers project thru the sublenticular (lower)part of the posterior IC to form the AUDITORY RADIATION (AR)in the temporal lobe.

AR ends on superior surface of temporal lobe (primary auditory cortex).
which auditory pathway is bilateral (binaural) and polysynaptic? what does this mean clinically?
the central ascending auditory pathway is bilateral, it can extract features of sound and compute it's source.

a uni lesion to the tracts/relay nuclei SUPERIOR to the cochlear nuclei DOES NOT produce uni deafness b/c supply is bilateral. (there WILL be deficits though.)
which nuclei projects to Heschl's gyri? what BA is located there?
medial geniculate nucleus projects IL to transverse temporal gyri (heschl's).

this is BA 41(42), in the floor of the lateral sulcus.
what is the tonotopy of the primary auditory cortex?
HIGH f: posteromedial
LOW f: anterolateral
what allows the CNS to modify it's input? how is sensitivity regulated?
descending (centrifugal) pathways allow the CNS to have "selective hearing".

olivocochlear fibers regulate sensitivity. (olivocochlear bundle is part of VIII)
a lesion of ____ produces loss of speech recognition.

explain this area's location.
WERNICKE'S area (via MCA)

wernicke's is the posterior part of BA22, which surrounds the primary auditory cortex (41) along with BA42. lateral surface of superior temporal gyrus.
what gyri are involved with speech recognition?
wernicke's area
how can the secondary auditory association cortexes be differentiated?
LEFT: larger
RIGHT: emotional aspects of speech (tone)
which pathway is involved with "what" is making the sound? "where"?
what: frontal lobe
where: parietal lobe
what structure interconnects the auditory cortices?
the corpus callosum.
an acoustic neuromma may cause ipsilateral deafness. where do they often occur? what other symptoms are present?
acoustic neurommas often occur along the VIII nerve from the CP angle to the IAM.

symptoms may also include facial paralysis.
what is the arterial supply to the pontine lateral lemniscus? inferior colliculus? medial geniculate nucleus? primary and secondary auditory cortices?
LLnucleus: bbrs of the basilar artery.

inferior colliculus: superior cerebellar artery

medial geniculate nucleus: posterior cerebral artery.

auditory cortices: MCA
where is the inner ear located? what is the vestibular system?
inner ear is located in the petrous part of the temporal bone btwn middle ear (tympanic cavity) laterally and IAM medially.

vestibular system:

receptors of semicircular canals and vestibular canals acting in concert.
what do the receptors of the vestibular system detect? how do the receptors differ?
receptors detect head motion (acceleration) and head position (relative to gravity).

utricle and saccule fxn via inertia and gravity. STATIC.

SCCs fxn via fluid movement. DYNAMIC.
what is a macula? where is it located?
a macula is a receptor organ located within the utricle and saccule, found in the bony labyrinth.

it is a field of hair cells whose apical surfaces have an array of stereocilia and ONE kinocilium
how are the hair cells in the bony labyrinth and the membranous labyrinth different?
both the membranous and bony hair cells have stereocilia and one kinocilium, but the bony cilia are embedded in otolithic membrane, crystallized for stability.

the cilia of the membranous labyrinth projects into gelatinous cupula, no stones.
why does the otolithic membrane have calcium carbonate?
b/c the utricle and saccule operate via static movement. the added weight increases the inertial and gravitational mass.
how is cellular bending utilized in the vestibular system?


**dynamic is SAME plus:
endolymph towards utricle = depolarization

endolymph away from utricle = hyperpolarization
how is the brain constantly provided with information about head position?
macular orientation:

utricular are horizontal, saccular are sagittal. the hair cell fields are divided in half and utricular cells point towards e/o, saccular away from e/o.
what is scarpa's ganglion?
peripheral processes of bipolar neurons from each ampullae, utricle and saccule converging at the lateral IAM.
where do vestibular and cochlear fibers diverge to different nuclei? what types of fibers are they?
v and c diverge at the brainstem. the are both SSA fibers.
where are the vestibular nuclei located? how many components are there to this nucleus?
they are located laterally, next to the inferior cerebellar peduncle in the dorsolateral tegmentum of rostral (open) medulla.

FOUR components: superior, inferior, medial and lateral vestibular nuclei.
what are the two pathways of the vestibular primary afferents?
1.synapse in vestibular nuclei, then to flocculonodular cortex and BACK to vestibular nuclei.

2.synapse in flocculonodular lobe of cerebellum (vestibulocerebellar path).

cerebellum is used to fine-tune motor reflex output! ICP is utilized for the parallel circuit.
what is vestibular information used to accomplish? what tracts are used for these tasks?
vestibular information:
1.maintain stable image on retina during head movements
2.maintain balance/posture

rostrally: MLF bilaterally
caudally: vestibulospinal IL
why do vestibular nuclei project thru the MLF?
vestibular nuclei project bilaterally to the MLF to access to nuclei of IV, VI and III to coordinate EYE movmement with HEAD position.
what are the various pathways of the vestibular nuclei caudally?
MEDIAL vestibulospinal tract:

BI-laterally in anterior funiculus (may be considered a MLF component) in CERVICAL and UPPER THORACIC LEVELS.

LATERAL vestibulospinal:

IL in ventral lateral funiculus at ALL LEVELS OF SPINAL CORD.
what does loss of macular fxn cause? where might this occur?
loss of macular fxn may cause the pt to fall to SIDE OF LESION b/c of EXTENSOR loss.

vestibulospinal neurons synapse on interneurons in the ventral horn; they inhibit proximal flexor mm grps and excite proximal extensor grps.
how do vestibular fibers prevent vertigo?
the utricular maculae projects fibers to the MLF which synapse with III, IV and VI nuclei to cause rolling of the eyes OPPOSITE to direction of head tilt.
(eye mm nuclei all located in dorsal medial tegmentum)

NS attempts to maintain a stable visual image on the retina.
describe the position of the 3 semicircular canals (SCC).
horizontal (lateral): bulges LATERALLY into medial wall of middle ear cavity.

anterior & posterior: ABOVE horizontal, they all meet at 90 degree angle.

**anterior of one side is in the same plane of the posterior on the opposite side**

SCC's representing same plane fxn as COMPLIMENTARY PAIRS.
name the important aspects of the SCC's and their fxns.
each SCC has an enlargement near it's utricle: ampulla with receptor organ, crista ampullaris.
where does the crista ampullaris project? what does it contain?
the crista ampullaris projects into the lumen of the SSC. it has stereocilia and one kinocilium which project into the cupula.
how is sound transduced in the SCCs?
currents in the endolymph bend the cupula which bends the hair cells.

hair cells are all oriented same direction:
endolymph towards utricle (utriculopetal), stereo towards kino = DEPOL.

endolymph away from utricle (utriculofugal), stereo away from kino = HYPER
what occurs when the head turns left, with regards to the SCCs?
left bony canal moves P, so fluid moves A = hair cells bent TOWARD utricle.

right bony canal moves A, fluid P = hair cells AWAY from utricle.
how are the eye mm involved with horizontal head motion?
VI and III are involved:

LEFT turn:
R lr and L mr contract.
R mr and L lr relax.

accomplished via bilateral projections of vestibular nuclei.
what is optokinetic nystagmus? how is nystagmus defined?
optokinetic nystagmus is the fast and slow alternating movement brought about by spinning the head.

nystagmus is defined by FAST phase direction.

*abnormal nystagmus = peripheral or brainstem dz*
what positioning needs to be considered when doing caloric testing of the vestibular pathways?
the endolymph of the horizontal canal can be affected by irrigation of ex.auditory meatus.
pt head must be tilted BACK 60 degrees to reach vertical.
(ampulla of horizontal canal is now superior)

warming = rise of endolymph to ampulla (utriculopetal)

cooling = sink of endolymph away from ampulla (utriculofugal).
what are higher auditory components?
what other systems does the auditory project to? why?
superior colliculus (visual), III, IV and VI: reflex turning of head & eyes towards loud sound.

VII and V motor nuclei: stapedius and tensor tympani to dampen amplitude of ear drum and ossicle vibration.

VII motor nucleus: orbiculars oculi, wink at loud sounds.
what are some features of the external auditory canal?
outer cartilaginous part + inner osseus canal.

cartilaginous: skin attached to perichondrium. epidermis has papillae, hair follicles, sebaceous and apocrine sweat glands.

cerumen: impervious lipid and acid cloak for the skin with anti-bac and anti-fungal action.
what are normal flora of the external ear?
same as oily skin:

staph epi
what are the gram negative diseases of the external ear?
1.acute diffuse external otitis (p.aeruginosa, proteus vulgaris & fungi)

2.bullous external otitis (hemorrhagic) (p.aeruginosa)

3.granular external otitis (proteus & p.aeruginosa)

4.necrotizing external otitis (p.aeruginosa)
what is one of the most common types of ear infections?
acute diffuse external otitis (p.aeruginosa or proteus vulgaris and fungi as secondary) humid weather
2.itching, pain, fullness discharge, redness culture
what type of ear infection causes a bloody discharge but is NOT a middle ear infection? how can it be differentiated from a middle ear infection?
bullous external otitis has bloody discharge via rupture of bullae on OSSEUS canal walls.

no prior respiratory infection indicates it is NOT a middle ear infection.
what can diffuse otitis externa lead to? what are the tell-tale symptoms?
skin of meatus is raw, scanty pus and granulations on osseus meatus. DO CULTURE

necrosis on floor of external auditory canal at junction of osseus and cartilage canals. can cause osteomyelitis and meningitis.
what are infections of the outer ear caused by gram POSITIVE bactteria?
1.furuncle and carbuncle (staph aureus via acute LOCALIZED otitis externa)

2.abscess (s.aureus)

3.cellulitis (strep or staph)

4.erysipelas (grp A beta hemolytic strep)

5.ecthyma (grp A beta-hem strep, some s.aureus as secondary)

6.impetigo contagiosum (" ")

7.infectious eczematoid dermatitis (via PERFORATED otitis media) (s.aureus)
what outer ear infections are caused by fungi?
1.acute otomycosis
2.chronic otomycosis

BOTH caused by aspergillus and mucor. chronic conditions may also be the result of dermatophytes, yeastlike fungi, misc fungi and actinomycetes.

1.candida ostomycosis
2.typical skin parasites, ie malassezia furfur & dermatophytes
what is symptomatic of a fungi-outer ear infection? weather
2.antibiotic/steriod ear drops
4.velvet gray pseudomembrane lines skin of meatus & tympanic membrane.
5.wet mount: fungi, neutrophil & epithelial cells.
what is candida otomycosis?
a pathogenic outer ear fungal ear infection.

2.immunological compromise
4.redness, edema, pus
5.hyperkeratosis & hyperplasia
what are viral outer ear infections?
1.herpes simplex
2.herpes zoster
3.verrucae (warts via papovavirus)
4.molluscum contagiosum (poxvirus)
name the outer ear infections caused by arthropod parasites.
SKIN PROBLEMS, scabies in children/infants.

(ie: wheals, vesicles, bullae)
what outer ear diseases are caused by hypersensitivity?
1.eczematoid external otitis (delayed, hairspray)

2.photoallergic dermatitis (delayed, soap/sunscreen)

3.atopic dermatitis
describe the middle ear.
1.simple squamous epithelium
2.communicates with nasopharynx via eustacian
3.lateral: tympanic membrane
4.medial: oval & round windows
why are children's ears easier to infect?
children's eustacian tubes (ET) enter the nasopharynx 10 degrees above horizontal, making it easier for infections to enter (adults 45). adult eustacian tubes are also LONGER.
eustachian tube is ____ and open near the middle ear; it is _____ near the nasopharynx and the walls are in ______ except when we swallow or yawn.
what normal flora is found in the middle ear?
NONE. but bacteria & viruses may enter via nasopharynx to eustachian tube (lined with lymphoid tissue at this junction).
what are the diseases of the middle ear?
1.acute suppurative otitis media (> 6wks) (strep pneumonia, h.influenzae, moraxella catarrhalis, grp A strep, s.aureus, some g-rods. maybe nothing!)

2.acute suppurative otitis media NEWBORNS (same as #1, but some neonatal sepsis organisms - staph, chlamydia).

3.chronic otitis media with effusion (OME)
(allergy, virus. bacteria present 1/3 of time, same that cause acute otitis media)
what are the major predisposing factors for acute suppurative otitis media?
1.previous otitis media
2.URI (dec-march)
3.deviation of ET
4.allergy, day care
5.inverse to breast feeding up to 1 yr old.
what is the pathogenesis of acute suppurative otitis media?
1.viral URI closes ET
2.negative middle ear pressure = aspired organisms
3.increased middle ear pressure = bulge typmanic membrane.
4.inflammation, lack of drain
5.abnormal patency of ET
what are the signs of acute suppurative otitis media? how is it diagnosed and treated?
1.ABRUPT pain, fever (not all)
2.unilateral tympanic membrane
4.moderate leukocytosis
5.spontaneous perforation 24-48 hrs
6.usually do not aspirate fluid, test pressure:
pneumatic otoscope
acoustic reflectometry
7.tylenol, antibiotics
8.myringotomy if needed
what sequelae is associated with acute suppurative otitis media?
1.fluid in middle ear for wks
2.recurrence, chronic
3.meningitis (rare)
when is culture of the otitis media necessary? what are the predisposing factors in this case?
acute suppurative otitis media of the newborn requires culture.

predisposing factors:
3.septic infants born to mothers with prematurely ruptured membranes
what type of otitis media infection utilizes 'watchful waiting'? what is it's etiology?
chronic otitis media with effusion utilizes watchful waiting. it can be caused by allergy, virus or previous ASOM.
complete obstruction of the ET predisposes one to this infection.

other tx:
tympanostomy tubes

rare sequelae: GLUE EAR
how is recurrent otitis media defined?
more than 3 acute episodes in 6 months.

same etiology as acute otitis media, but s.aureus too (esp w rupture of tympanic membrane).
what ear infection requires surgery? what are it's symptoms?
chronic otitis media requires surgery. it is caused by anatomic changes in the middle ear cavity that persist even without fluid.

almost always associated with central or anterior perforation and mastoid infection.

skin of ex.auditory canal and surface squamous epi of tympanic membrane may grow thru aperture and invade middle ear.

pus & cholesteatomatous material. usually gram NEGATIVE.
what is a disease of the tympanic membrane?
bullous myringitis:

inflammation of the lateral surface of the tympanic membrane.

blebs with blood/serous fluid.

etiology: mycoplasma pneumoniae.
what types of cells are present in the retina? what do they do?
rods - detect amt of light, night vision.
cones - detect 3 wavelengths, color.

horizontal cells
bipolar cells
amacrine cells

3.ganglion cells (collect image info and send to CNS)
where does retinal detachment most commonly occur?
retinal detachment can occur between the photoreceptor dendrites and the cytoplasmic processes of the pigment epithelium. fluid can accumulate here.
what is macular degeneration?
macular degeneration is a pathological change which leads to loss of visual acuity in the central part of the field.
at the optic chiasm _____ decussate while _____ remain ipsilateral.
nasal retinal (decussate)

temporal retinal (ipsilateral)
what information does the optic tract carry? the optic nerve?
optic tract: HALF image (IL temporal retina + CL nasal retina, aka both left halves or both right halves).

optic nerve: WHOLE image (IL)
where do the majority of optic tract fibers project to? minority?
majority: (IL)lateral geniculate nucleus

minority: superior colliculus & pretectum
what is the lateral geniculate nucleus?
1.thalamic relay nucleus for vision.

2.principal target for ganglionic axons from retina.

3.body bulges on ventral diencephalon (below posterior pulvinar nucleus), aka LGB.

4.receives input from visual field corresponding to optic tract.
how is the LGN organized?
SIX layers from optic tract:

three uncrossed, three crossed. numbered ventral to dorsal.
what is the optic radiation? what is it's arterial supply?
optic radiation:
the fibers traveling from the diencephalon (LGB) to medial occipital lobe (primary visual cortex). the fibers go thru "c" of lateral ventricle (rostral/inferior horn; caudal/occipital horn).

anterior: MCA (ant.choroidal)
posterior: PCA
how is the visual field separated in the geniculocalacrine tract? where is this tract going?

superior visual field travels in meyer's loop (rostral). travels to INFERIOR calacrine cortex.

inferior visual field travels in the caudal optic radiation.
travels to SUPERIOR calacrine cortex.
which part of the visual field does the left cortex recieve?
the RIGHT visual field (inverted!)
how is peripheral and macular vision distributed on the cortex?
peripheral: anterior (rostral)

macular: posterior (caudal)

**cortical macular area is proportionately larger than retinal macular**
what is BA 17 known as?
BA 17 is the primary visual cortex, AKA the striate cortex.

striate: line of gennari, a thickened layer of cortex with mostly myelinated fibers. visible to naked eye!
what may cause an optic nerve lesion? what is the effect?
1.trauma in orbit
2.increase CSF pressure
3.i carotid, opthalmic a., central retinal a.
4.complete blindness IL
what may cause an optic chiasm lesion? what is the effect?
2.midline pituitary tumor
3.tiny bbr of i.carotid a.
4.CENTRAL: bitemporal hemianopia
5.LATERAL: (via bilateral i.carotid dz) binasal heteronymous hemianopia
what may cause an optic tract lesion? what is the effect?
what else can cause this effect?
1.ischemia via compression/infarction.
2.PCA, PcommA, ant.choroidal
3.R/L homonymous hemianopia

**lateral geniculate lesion causes the SAME effect**
what can cause an optic radiation lesion? what are the symptoms?
1.vascular compromise
3.ROSTRAL: R&L upper quadrantanopia
4.CAUDAL: R&L lower quadrantanopia
5.lesion of entire optic radiation: hemianopia
what artery is mainly involved with visual cortex lesions? what is the effect of an entire cortex lesion (IL)?
PCA supplies the visual cortex. lesion to 1/2 the visual cortex causes R/L homonymous hemianopia.
what is macular sparing?
macular sparing occurs in some patients suffering cortical blindness. a small central area of acute vision is spared due perhaps to MCA supply or anastamoses of the MCA to the PCA at the occipital pole.

*macular area is projected to the most posterior part of occipital cortex*
what would result if BOTH upper/lower banks of the calacrine sulcus were lesioned? what might cause this?
upper: lower altitudinopia
lower: upper altitudinopia

*with or w/o macular sparing*

CAUSE: falcine tumor growing laterally to give bilateral effect.
what can produce a 'central scotoma'?
fall/blow to back of head at occipital pole affects macular vision selectively.

*scotoma: blindness in limited part of retina which is surrounded by normal vision area*
what are the autonomic mm of the eye?
sympathetic: RADIAL dilator pupillae mm. (radially)

parasympathetic: SPHINCTER pupillae mm. & CILIARY mm (both circularly)
when does pupillary dilation occur? how does it happen? light thru optic nerve

2.cortical visual areas output to hypothalamus for dilation (more light let in).

3.sympathetic efferents from hypothalamus descend to upper thoracic, synapsing on pre-g in intermediolateral cell column.

5.descending sympathetics (hypothalamo-spinal) course in LATERAL brainstem tegmentum and LATERAL funiculus of spinal cord.
how does contraction of the pupil occur?
MIOTIC reaction:
1.afferent limb of reflex includes IL optic nerve, BOTH optic tracts and nuclei.

2.ganglion cells carrying info about light intensity bypass the LGN and synapse on pretectal nuclei in brainstem.

3.pretectal nuclei decussate thru AWC to EW nuclei

4.EW paras run with CNIII to ciliary ganglion

5.postg course thru short ciliary nn to sphincter pupillae.
what is lesioned in the case of 'marcus gunn' pupil? what causes this?
the AFFERENT limb of the reflex (IL optic nerve, BOTH optic tracts and midbrain nuclei) is lesioned in marcus gunn pupil.

caused by either neuritis or MS.
what pupillary reflex lesion is often the result of syphilis?
argyll-robertson is often the result of syphilis. location of injury is unknown; tell-tale signs are intact convergence-accomodation & LOSS of pupillary light reflex (no miotic rxn).

why? EW nuclei pathway for miosis is different from the visual c-a pathway.
what occurs when focusing on a NEAR object?
1.eyes CONVERGE (m.rectus, CNIII)

2.lens THICKENS (ciliary m, ↑ refractive power, EW nucleus + CNIII).

3.pupil CONSTRICTS (sphincter pupillae mm contracts, smaller aperture allows for ↑ depth of focus & field. EW via CNIII).
where is the pretectum located? the EW nucleus?
pretectum is immediately rostral to the superior colliculus. it projects IL to EW which is just rostral to III nucleus in the superior colliculus.
where does the oculomotor nerve exit the brainstem?
CNIII exits the brainstem between the cerebral peduncles.
name the three ocular mm nuclei and their locations.
1.oculomotor: superior colliculus of rostral midbrain. near midline just inferior to periaqueductal gray.

2.trochlear: CAUDAL midbrain, caudal to CNIII nucleus. **decussates**

3.abducens: CAUDAL tectum of pons (floor of 4th ventricle).
what are 'vergence' movements? how are they regulated?
'vergence' movements are when both eyes move in opposite directions.

vergence center is in rostral midbrain (nuclei + assoc. circuits). BA19, occipital eye field.

convergence: center projects to the two CNIII nuclei controlling abduction.

divergence: relaxation of m.rectus (unopposed l.rectus)
what can cause vergence paralysis?
vergence paralysis may result from a pineal tumor pressing on the rostral midbrain.

*loss of adduction/convergence = diplopia**
where are the horizontal gaze centers?
horizontal gaze centers are in the paramedian pontine reticular formation (PPRF).

coordinates conjugate horizontal gaze to SAME side.

PPRF projects to IL CNVI (l.rectus) and CL CNIII (m.rectus; via MLF). PPRF rcvs instruction from 'frontal eye field' (posterior middle frontal gyrus).

contract lr on side looking towards, and mr on opposite side.
what is another name for internuclear ophthalmoplegia? what is the cause and effect?
MLF syndrome:

1.unilateral lesion

2.can't adduct IL eye when trying to GAZE opposite. CAN adduct during convergence.

3.bilateral MLF syndrome = MS
where are the nuclei controlling the vertical conjugate movements? what mm are controlled?
vertical gaze center is in the periaqueductal gray matter of the rostral midbrain.

i.oblique, i.rectus(CNIII)
s.oblique (CNIV)
what can cause vertical gaze paralysis?
PINEAL TUMOR pressing on rostral midbrain. gaze upwards goes FIRST b/c of pressure on tectum.

*parinaud's syndrome: lesion of dorsal midbrain & pretectal area.
upward gaze lost FIRST b/c that part of the vertical gaze center is compressed first.
EW also effected - large pupils.
what types of reflexes help keep the eyes fixed on a visual target when the head moves?
vestibulo-ocular reflexes. they regulate the conjugate eye movements.
how many vestibular nuclei are there? where are they located?
superior - caudal pons
lateral, medial and inferior - rostral medulla