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604 Cards in this Set

  • Front
  • Back
olfactory bulb targets
pyriform cortex
olfactory tubercle
amygdala
entorhinal cortex
olfactory targets project to:
entorhinal cortex --> hippocampal formation

all: thalamus, hypothalamus, orbitofrontal cortex
lesion of path from thalamus to orbitalfrontal cortex
unable to discriminate/perceive odors
scratch and sniff test for Alzheimer's
first sign of Alzheimer's is difficulty identifying common odors because of lesion between thalamus and orbitalfrontal cortex
lesion of path to amygdala and hypothalamus
emotional, motivational and visceral effects of odors -probs
visceral motor responses to smell/olfaction:
pleasant odors: salivation, increased GI motility, anticipation, fond memories
unpleasant/noxious: gagging, vomiting, aversive association and memories
autonomic and reproductive responses to olfaction
opposite gender attraction
perfumes and pheromones
hyperosmia
seizures
hysteria
iatrogenic
how many taste cells make a taste bud? where are they localized?
30-100
taste buds are localized to papillae in oral cavity
how is gustatory sense transduced?
ionic and 2nd messenger mediated gating of ion channels
-leads to depolarization and chemical transmission of receptor potential to gustatory afferent
*note that olfaction is only 2nd messenger G protein mediated
labeled lined code--neural code for taste definition:
taste cells and their afferent nerve fibers are specialists, responds to single taste ligands
prude prude prude
describe central gustatory pathway
CN7,9,10--> nucleus of solitary tract --> VPM of thalamus --> insula and frontal cortex --> amygdala
solitary tract also project to hypothalamus and amygdala
function of anterior insula and frontal operculum cortex
recognition
appreciation
subjective reaction
hypothalamus and amygdala function in taste:
appetite
satiety
emotional/motivational/visceral effects: salivation/pleasure/dislike/digestive actions/superior and inferior salivatory nuclei associated with CN7
what is trigeminal chemoreception?
polymodal nociceptors from CN 5, 9, 10 that convey GENERAL somatic sensory responses
activated by irritatns or toxins
input to SPINAL TRACT and NUCLEUS of CN 5
triggers pain and visceral effects like salivation, tearing, sweating, bronchoconstriction
concentration dependent
number of functionally unique genetically encoded human odorant receptors
350
can be highly selective (prude prude)
or slightly promiscuous (slut prude)
combined activity of odorant receptors discriminate how many odors?
10,000
olfactory tract is made up of: (2 branches) which is main one?
medial and lateral (main)
eye has inner layer consisting of a neural and nonneural portion. the non-neural anterior potion consists of:
iris and ciliary body
middle layer of eye = uvea consists of:
choroid
ciliary body
ciliary process
iris
steps to eye development
optic stalk from embryonic forebrain
invaginate to form optic vesicle --> cup becomes retina
vesicles induces ectoderm to form lens vesicle --> differentiate and overlying corneal epithelium
mesenchyme condenses to form vascular and connective tissue layers
layers of cornea
epithelium -stratified nonkeratinized squamous
bowman's membrane - acellular thick BM
substantia propria
Descemet's membrane
endothelium
faulty drainage of this will cause glaucoma
canal of schlemm
aqueous humor is drained into:
venous system
iris is
pigmented diaphragm w/ smooth mm
controls amount of light admitted via pupil
functions in accomodation
contains pigmented cells, loose connective tissue, vessels, separates anterior from posterior chamber
pupillary sphincter -nerve innerv
CNIII parasympathetics
pupillary dilator - nerve innerv
superior cervical ganglion
sympathetics
adhesion of pigment epithelium
from outer layer of optic cup
potential space from embryonic development, adhere strongly to choroid more than the rest of retina
function of pigment epithelium
absorbs scattered light rays
phagocytosis of worn out discs shed from rods
stores and releases VITAMIN A to photoreceptors
outer segments of rods made up of:
modified cilia, contain discs derived from outer PM of cilium vi
visual pigments of cones sensitive to what colors?
blue
green
red
external limiting membrane is:
specialized desmosome-like junctions btwn glial cells of retina nad photoreceptors
appears like line at LM level
signal transmission in phototransduction
receptor potentials (hyperpolarizing in light) by photoreceptors
slow grade potentials by bipolar cells
APs by ganglion cell layer
rhodopsin is made from
aldehyde of vit a
retinal + opsin
AMD
common cause of blindness in older individuals
human ear is most sensitive to what frequency range?
1200-4000 Hz
why decrease audibility with age?
lose auditory and vestibular hair cells
loss of ganglion cells
loss of hearing and balance esp high frequencies
20-30 db difference at 2000-4000 hz
function of outer hair cells
sharpen frequency
otoacoustical smissions
endolymph
perilymph
inside cell
voltage in mVs?
endolymph is 80 mV
perilymph is 0 mV
inside cell is -45 mV
how does tip links start signal transduction?
displace cells towards stria vascularis --> open cation selective channels --> depolarization
K+ influx from endolymph
Ca2+ entry
activates Ca-dependent K+ efflux
release of transmitter (glutamate_
8th nerve excitation/inhibition
receptor potentials are proportional to:
frequency of cilia shearing
frequency of BM vibration
frequency of soundwave
olivocochlear input mechanism
able to block out background noise
descending inhibition
near superior olivary nucleus
regulate flow of auditory input into CNS
terminates on hair cell/afferent fibers of IHC
cause OHC to contract --> auditory sensitivity/input responses
medial geniculate and auditory cortex send input to hair cells
intensity encoding depends on:
degree of movement of BM
intensity of hair movement
receptor potential
amount of transmitter released
firing rate and recruitment of 8th nerve
2 ways of pitch interpretation
one to one correlation
place theory
one on one correlation
low frequencies up to 3 kHz
volley theory: nerve cells fire in groups
the pattern of firing determines pitch
1 receptor potential --> 1 8th nerve fiber discharge
place theory
tonotopic organization
labeled line coding
each hair/neuron is tuned to a specific frequency
medial superior olive responsible for
interaural TIME DIFFERENCES
analyze difference in time to etermine where sound arises
lateral superior olive
interaural SOUND differences

**pontine vascular lesion and MS difficulty localizing sound
acoustic startle reflex
head sound, turn head
due to TECTOSPINAL TRACT
lateral meniscus connects superior olive of medulla to inferior colliculus of pons
brachium of inferior colliculus innervates
medial geniculate
in conduction deafness: AC and BC?
BC > AC
causes of unilateral hearing loss
EAC
cochlea
8th nerve
middle ear
cochlear nuclei
*once information enters brainstem info immediately crosses bilaterally at multiple levels
treat otosclerosis by:
microsurgery to make stapes mobile or replace stapes
tx Meniere's
antihypertensives and diuretics
-prevent rupture of membraneous labrynth
otosclerosis caused by
arthritis ossification of middle ear bones/neogenesis of labrynthine spongy bone
fixes stapes
parts of cochlear implant
microphone
speech processor
electrode array
use cochlear implant when:
pt is deaf with intact auditory nerve
neurofibromatosis type 2
tx by transect 8th nerve
must use brainstem inplant
what disease with these sx?
nausea vomiting vertigo tinnitus
meniere's
nystagmus
slow -opposite (vestibular)
fast - same (cortex)
post rotary nystagmus
slow - same side
fast - opposite side
spin 10x, stop suddenly
past pointing
in direction of head rotation
tendency to fall
in direction of head rotation
spontaneous nystagmus
pathology
lesion to labryinth, CN8, brainstem nuclei, flocconodular lobe of cerebellum
vertigo
opposite direction of original rotation
irritative lesion
slow-opposite
fast-same
destructive lesion
slow-same
fast return to opposite
what condition causes:
canalithiasis
prevalent in adults
caused by sudden changes in position
test using dix hall-pike positional test
benign paroxysmal position vertigo
canalithiasis
rocks in posterior and horizontal semicircular canal are LOOSE
how do you treat canalithiasis?
resposition loose canaliths CRPs
what autonomic effects does vestibular stimulations cause?
motion sickness
sweating pallor
nausea vomiting
caloric test - test for
vestibular function
brainstem integrity
caloric test - method
recline 60 degrees
horizontal canal is vertical
irrigate EAC with warm or cold water --> deflection of cupula/stimulate hair cells
irrigation perceived as profound unilateral stimulus
Caloric test-normal response
COWS
cold (Decrease firing) =fast to opposite
warm (increase firing)= fast to same
eyes move side to side if brainstem is intact
caloric test - abnormal
unequal response
good caloric - cortex prob
unilateral response = MLF lesion
no caloric response = brainstem prob
positional vertigo test (dix-hallpike)
vestibular dysfunction test
recline head face left or right
change position for max stimulation
positional vertigo test -normal
no nystagmus
no vertigo
positional vertigo test-abnormal
nystagmus with complaint of vertigo
peripheral vertigo
short onset delay with adaptation with repetition
Central vertigo
immediate
not adaptation
oculocephalic doll's eye
unconsciou patient
test vestibular function
passive movement of head side to side
oculocephalic -normal
eyes move oppositely to head
oculocephalic abnormal
eyes are fixed
brainstem/MLF prob
ear develop from what?
rhombencephalon (hindbrain)
what is the spiral bony extension from modiolus and site of Basilar membrane attachment?
spiral lamina
saccades
rapid ballistic movements of eyes that abruptly change point of fixation
cannot control velocity
voluntary, conjugate movements
commands originate in frontal cortex
smooth pursuit movements
much slower tracking movements of eyes designed to keep a moving stimulus on the fovea
under voluntary control, conjugate movement
originates in parietal-occipital cortex
optokinetic nystagmus
combination of smooth pursuit and saccadic correction
alternating slow and fast movement of eye in response to stimuli
normal reflexive response of eyes in response to large scale movements of visual scene and should not be confused with pathological nystagmus (Due to brain injury)
commands originate in occipital cortex
fixation on an object in visual field can suppress vestibulo-ocular reflex
requires an image on retina
reflex conjugate movements
commands originate in occipital cortex
fixation on object in visual field can suppress vestibulo-ocular reflex
vergence movements
align fovea of each eye with targets located at different distances from observer
linked with pupillary constriction and accomodation to keep image in focus (near triad)
conjugate eye movement
2 eyes move in same direction
disconjugate eye movement
vergence movements either convergence of divergence of lines of sight of each eye to see an object that is nearer or farther away
vestibulo-ocular movements
vestibular input keeps visual images fixed on retina during head movement
continuous input from semicircular canals
nystagmus resets eyes when reach limits of orbit
reflex conjugate movements
commands originate in vestibular nuclei
vestibular control
signals originating in semicircular canals drive vestibular input
directly input in abducens, trcholear, oculomotor not through gaze centers
What is required for conjugate gaze?
MLF
what participates in control of eye movement through vestibular neurons?
cerebellum
_______ is the horiontal or lateral gaze center
paramedian pontine reticular formation
lateral gaze venter is important for what?
control in saccade and pursuit for conjugate eye movements
stimulation of PPRF drives the eyes to the:
ipsilateral side
destruction of PPRF results in
paralysis of ipsilteral gaze
vertical gaze center
located in the rostral part of midbrain reticular formation
responsible for vertical movements
lesion of right abducens nerve
CN6 palsy
right eye cant move to right
lesion of right abducens nucleus
right lateral gaze palsy
both eyes cannot look right
lesion of PPRF
right lateral gaze palsy
both eyes cannot look right
lesion of left MLF
when looking right:
right eye nystagmus
left eye cannot look right
lesion of left MLF and left abducens nucleus
when looking right,
right eye nystagmus
left eye cannot look right
when looking left,
both eyes cannot look left
(left lateral gaze palsy)
strabismus
misalignment of eyes
strabismus has what symptoms??
diplopia due to
esotropia
exotropia
esotropia
weakness of lateral rectus causes eye to be pulled medially
exotropia
medial rectus is weak so lateral rectus is pressed laterally
amblyopia
constant diplopia
brain ignores input one eye and does not focus or orient the eye
paralysis of lateral gaze of the left eye with ptosis together with hemi paresis on riaght side of body would be consistent with a vascular lesion of:
the ventral midbrain
INO internuclea ophthalmoplegia
MLF lesion
the side of INO, is side of lesion
eye adduction on affected side is impaired with horizontal gaze but it often spared during convergence because inputs to oculomotor nucleus mediates convergence that arise from the pretectal region and does not travel in caudal MLF
may observe a slight lag in adduction of eye on affected side
common causes of MLF
MS plaques
also: pontine infarcts, neplasms
one and a half syndrome
MLF lesion on one eye
and abducens nucleus lesion on same side
frontal eye fields controls what in eye movement?
contralateral saccades via connections with contralateral PPRF
parieto-occipito-temporal area controls what in eye movement?
ipsilateral smooth pursuit via connections with vestibular nuclei, cerebellum, and PPRF
may make some contralateral eye movement contributions too
what descending control of eye movement heavily influences visual inputs?
primary visual cortex and visual association cortex
vertical gaze venter is impotant for control of:
saccades and pursuit conjugate eye movements
___________ organize vertical conjugate eye movements
mesencephalic reticular formation and pretectal area
vertical eye movements require activity on both side of midbrain with communication through what?
posterior commissure
convergence of eyes is produced by
medial recti
divergence of eyes is produced by
lateral recti
disconjugate eye movements are organized in:
midbrain, near oculomotor nucleus
based on retinal disparity
accomodation and pupillary constriction is accomplished through retinal input to:
optic tectum (superior colliculus) and Edinger-Westphal nucleus (parasympathetic)
Parinaud's syndrome
constellation of eye abnormalities usually seen with lesions compressing dorsal midbrain and pretectal area:
impaired vertical gaze especially upgaze
large irregular pupils, do not react to light
eyelid abnormalities
impaired convergence sometimes convergence-retraction nystagmus
what is responsible for pupillary dilation?
sympathetics
what is responsible for pupillary constriction?
parasympathetics
what sympathetics are involved in pupillary dilation?
superior cervical ganglion
carotid and ciliary ganglion
from T1-L2
what parasympathetics?
edinger-westpal
via oculomotor nerve to ciliary ganglion
pupillary light reflexes
direct/consensual reflexes to light in one eye
pupil size is determined by a balanced input of both sympathetic/parasympathetic systems
accomodation response
miosis
small pupil - loss of sympathetics
mydriasis
dilated pupil - loss of parasympathetics
anisocoria
pupillary asymmetry
Argyll-Robertson pupil
accommodating
will constrict on vergence
not responsive to light
result of tertiary syphilis, alcoholism, encephalitis
Horner's syndrome is caused by what kind of nervous damage?
sympathetics
a vascular infarct of what could cause horner's?
PICA - dorsal lateral medulla infarct
nonvascular causes of horner's
spinal cord injury usually trauma
sympathetic chain injury or trauma
T1 and T2 spinal roots, apical lung tumor
carotid plexus - carotid dissection
cavernous sinus - thrombosis, infection, tumors, aneurysms
orbit infection or neplasm
Cause of Parinaud's syndrome
tumor of pineal gland
hydrocephalus can increase pressure of optic tectum of midbrain(pushes down by dilation of 3rd ventricle)
parinaud's syndrome has paralysis of:
upward gaze (cannot elevate eye)
paralysis of convergence
common causes of visual loss
optical (refractive errors)
medial opacities (cataracts)
retinal disease (macular degeneration/diabetic retinopathy)
optic nerve diseases (glaucoma/optic neuritis)
CNS (ischemia-CVA)
visual acuity
ability to see detail
as measured on eye chart
dyschromatopsia
inability to distinguish colors
"color blindness"
scotoma
small (visual field defect)
anopsia
larger (visual field defect)
agnosia
inability to recognize, name objects
what is needed for good visual acuity?
1. proper focus of light rays on macula
2. clear media - cornea/lens/vitreous
3. healthy macula and optic nerve
refractive errors
light rays coming in from a distance
if not focused on retina, image will be blurred
myopia

what lenses to correct?
near sighted

minus power lenses needed
hyperopia
far sighted

plus power lenses needed
astigmatism
not a disease but a complicated optic error where there are multiple focal points because cornea is not perfectly spherical
poor focus near and far
need special cylinder lens
cataracts cause
loss of visual acuity
no specific visual fields loss
macula
contains fovea
allows for sharp and detailed vision
macular degeneration
loss of central acuity
still can have ambulatory vision
retinitis pigmentosa
loss of night vision
loss of peripheral vision
papilledema
optic nerve head (disc)
swelling due to high intracranial pressure
glaucoma
increased cupping of disc
loss of RIM OF NEURO-RETINAL TISSUE (ganglion cell axons)
comprise nerve tissue of optic nerve
optic neuritis
often caused by MS
optic atrophy
loss of axons
describe rods
higher sensitivity
low light levels
monochromatic
peripheral vision
describe cones
bright light
color
detailed central vision
color vision - cones have 3 types of pigment:
red
green
blue
dichromats
red or green deficiency most common
monochomats
see only one cone pigment or no cones just rods or even a cerebral deficit
hereditary dyschromatopsias
5-6% males have some color vision loss
usually red/green discrimination deficit
X-linked
acquired dyschromatopsias
can be red/green or blue/yellow
sign of macular disease or optic nerve disease
e.g. optic neuritis
projections of retinal ganglion to:
lateral geniculate nucleus
hypothalamus (suprchiasmatic nucleus)
superior colliculus (saccadic eye movements)
pretectum (pupillary eye reflex)
lateral geniculate involved in
vision
hypothalamus (suprachiasmatic nucleus) involved in
circadian rhythms
superior colliculus
coordination of head and eye movements
pretectum
pupillary eye movements
projections of retinal ganglion to:
lateral geniculate nucleus
hypothalamus (suprchiasmatic nucleus)
superior colliculus (saccadic eye movements)
pretectum (pupillary eye reflex)
main visual pathway
ganglion cells --> LGN --> occipital cortex
2 neuron pathway
lateral geniculate involved in
vision
optic radiations
2 parts
meyer's loop in temporal lobe (superior visual field)
fibers representing superior retinal quadrants (inferior visual field)
hypothalamus (suprachiasmatic nucleus) involved in
circadian rhythms
extra-striate visual areas
occipital lobe not dead end
dorsal pathway - parietal lobe
ventral pathway - temporal lobe
superior colliculus
coordination of head and eye movements
parietal lobe involved in:
spatial vision and movement processing
pretectum
pupillary eye movements
temporal lobe involved in:
object recognition
color appreciation
main visual pathway
ganglion cells --> LGN --> occipital cortex
2 neuron pathway
optic radiations
2 parts
meyer's loop in temporal lobe (superior visual field)
fibers representing superior retinal quadrants (inferior visual field)
extra-striate visual areas
occipital lobe not dead end
dorsal pathway - parietal lobe
ventral pathway - temporal lobe
parietal lobe involved in:
spatial vision and movement processing
temporal lobe involved in:
object recognition
color appreciation
projections of retinal ganglion to:
lateral geniculate nucleus
hypothalamus (suprchiasmatic nucleus)
superior colliculus (saccadic eye movements)
pretectum (pupillary eye reflex)
lateral geniculate involved in
vision
hypothalamus (suprachiasmatic nucleus) involved in
circadian rhythms
superior colliculus
coordination of head and eye movements
pretectum
pupillary eye movements
main visual pathway
ganglion cells --> LGN --> occipital cortex
2 neuron pathway
optic radiations
2 parts
meyer's loop in temporal lobe (superior visual field)
fibers representing superior retinal quadrants (inferior visual field)
extra-striate visual areas
occipital lobe not dead end
dorsal pathway - parietal lobe
ventral pathway - temporal lobe
parietal lobe involved in:
spatial vision and movement processing
temporal lobe involved in:
object recognition
color appreciation
projections of retinal ganglion to:
lateral geniculate nucleus
hypothalamus (suprchiasmatic nucleus)
superior colliculus (saccadic eye movements)
pretectum (pupillary eye reflex)
lateral geniculate involved in
vision
hypothalamus (suprachiasmatic nucleus) involved in
circadian rhythms
superior colliculus
coordination of head and eye movements
pretectum
pupillary eye movements
main visual pathway
ganglion cells --> LGN --> occipital cortex
2 neuron pathway
optic radiations
2 parts
meyer's loop in temporal lobe (superior visual field)
fibers representing superior retinal quadrants (inferior visual field)
extra-striate visual areas
occipital lobe not dead end
dorsal pathway - parietal lobe
ventral pathway - temporal lobe
parietal lobe involved in:
spatial vision and movement processing
temporal lobe involved in:
object recognition
color appreciation
what would cause a unilateral visual defect?
retinal disease
degenerative/ischemic
optic nerve disease: glaucoma, optic neuritis, ischemia
macular degeneration
central field loss
ophthalmoplegia can be caused by
internal: iris and ciliary body muecles

external: extraocular muscles
pupillary light reflex pathway
Optic Nerve
Optic Chiasm
Crossing Over Occurs
Pretectum
Crossing over occurs
Edinger-Westphal Nuclei
Joins IIIrd Cranial Nerve
Ciliary Ganglion
Pupillary Sphincter muscle
relative afferent pupillary defect (RAPD)
unilateral afferent dysfunction results in diminished efferent impulses traveling back to both pupils
anisocoria
damage to iris/pupil, surgery, glaucoma, trauma
pharmacologic
toxic
efferent pathway problem
Marcus Gunn pupil relative afferent pupil defect
several optic nerve diseases
optic neuritis
other optic nerve disease: tumor/ischemia/infarctions/optic atrophy
some retinal disease - ischemia
Central retinal artery occlusion
parasympathetics control:
pupil constriction
accomodation
3rd CN, ocular motility
eyelid retraction
sympathetics control
pupil dilation
lid elevation
sweating
horner's syndrome sx
ptosis
miosis
anhydrosis
CN3 controls these muscles
levator palpebrae
superior rectus
inferior rectus
inferior oblique
medial rectus
CN4
superior oblique
CN6
lateral rectus
fxn of superior oblique
primarily intorsion

some depression
fxn of inferior oblique
primarily extorsion

some elevation
ductions
single eye movements
adduction
abduction
infraduction
supraduction
excycloduction
incycloduction
versions
movement of both eyes
convergence/divergence
fixation
keeping eye steady on a visual target
maintaining image on fovea of a stationary target
VOR
maintain fixation with head movements
saccades
sudden rapid ballistic movements to refixate
-rapid eye movements to fixate on a stationary object of regard
smooth pursuit
maintain stable eye tracking of a slowly moving object
optokinetic (nystagmus)
stabilize retinal image during sustained head rotation
following fast moving objects
INO
lesion to MLF
producing ipsalateral adduction deficit
left gaze palsy
lesion in left PPRF or left 6th nerve nucleus
right gaze palsy
lesion in right PPRF or right 6th nerve nucleus
dorsal midbrain syndrome
cannot look up
compress rostral midbrain RF and pretectal area
study of brain waves during sound stimuli
BAER
what can cause unilateral hearing loss?
any disease affecting middle and inner ear apparatus or
cranial nerve 8
ex: otitis media, otosclerosis, Meniere's, presbyacusis, acoustic schwannoma
what neurological systems are necessary to maintain balance?
proprioception-vibration sysem (dorsal columns)
visual system
vestibular-midline cerebellum system
poor speech discrimination suggests where is lesion?
cochlear nerve or most rostral parts of auditory pathway
what would result in problems closing left eye tightly?
facial nerve lesion
corneal reflex -afferent/effent limb?
afferent is trigeminal ophthalmic division
efferent is facial nerve
well circumscribed enhancing lesion without surrounding edema extending from internal auditory canal into left cerebello-pontine angle
acoustic schwannoma
what would acoustic schwannoma cause in BAE?
wave I (auditory nerve) and wave II (cochlear nucleus in pns) would cause prolongation in interlatency difference between Wave I and II
due to disturbance of vestibular apparatus of inner ear
peripheral vertigo
due to CNS disturbance
central vertigo
• Slow onset of hearing loss in left ear
• Odd sensation of fullness in back of his head
• Unsteady when walking especially after a quick turn
• Mild balance and agility problems
• Hissing noise became progressively worse in left ear
• Stooping → dizziness and loss of balance

Neuro exam
• Definite hearing loss on left
• Poor speech discrimination and decreased perception of loud noises
• Weber lateralize to the right
• Depressed direct corneal reflex on left
• Depressed consensual reflex on right
• Facial sensation normal
• Left face mildly weaker than right
acoustic schwannoma
sensation of motion of self or surrounding
vertigo
mild
nystagmus is multidirectional
nonfatiguable
abrupt in onset
long duration
central vertigo
due to brainstem problem
perception of abnormal sounds in ear like buzzing, humming, whistling, roaring, clicking, hissing pulselike
tinnitus
nonvibratory tinnitus
only heard by patient
implies disease of middle ear, inner ear or 8th cranial nerve
vibratory tinnitus
conduction of sound from other structure of head and neck, vascular bruit, repetitive contraction of muscles of palate, ear popping
defect in amplification and conduction due to diseases process of outer/middle ear
conductive hearing loss
sensorineural loss
disease of cochlear and auditory nerve
why does lying on right side help vertigo?
allow to easily look toward affected side to decrease amount of subsequent nystagmus
suggesting left labryinth is probably effected
fast beating nystagmus suggests what?
slow phase (vestibular) to left
fast phase to right (cerebral cortex provides corrective saccade to opposite direction)
• Whistling in ear
• Hearing loss
• Room spinning
• Nausea and vomiting
• Climbed in bed, more comfortable on right side with eyes open
• Normal mental status
• Bilateral hearing loss with relative preservation of speech discrimination
• Whistling in ears
• Other CNs are normal
• Increased whistling
• Middle attack of spinning during physical exam
• Nystagmus was noted, fast beating to right
what is dx?
Meniere's
what CN would be affected with a large tumor in the cerebellar pontine angle?
5, 7, 8

6 is more ventral
39 yo is unconscious but responds to pain stimuli
cold calorics in both ears provokes no nystagmus
both eye moves slowly to side irrigated and remain there
these finding are indicative of damage limited to:
cortex drives fast phase
33 yo male suffers severe trauma to left side of his head that destroys the inner ear cochlea and labyrinth. During early stages of his recovery he is unsteady and has poor balance. 6 months later, no longer has deficits in balance
the right labyrinth compensates by decreasing its function
visual and proprioceptive systems increase function to compensate
under normal circumstances, irrigating a patient’s left external adutory meatus with warm water would elicit:
left beating nystagmus
fast phase of nystagmus is same as side of irrigation
cluster of nuclei in caudal pons is the first to receive binaural input and responsible for localization of sound:
superior olive
in an unconciscous patient caloric testing reveals:
cold water in right ear causes right eye to look right but left eye does not move.
cold water in left ear causes left eye to look left, right eye does not move where is the likely location of lesion?
MLF bilateral
Meniere's is also called
endolymphatic hydrops
4 yo presented with painful earache, fever, complained of right ear was touched
drum was red and inflamed suggesting infection and infection of middle ear
what do you expect to be the child’s condition
dysfunctional eustachian tube
53 yo man noticed that hearing in his right ear was deteriorating
could not hear a watch ticking on right
left side as normal
conduction deafness
most likely otosclerosis
45 yo man who went to see his family physician for a life insurance exam
he is a hunter. His pure tone right ear audiogram indicated peripheral abnormality
evidence of a sensorineural hearing loss
65 yo diabetic woman has aphasia secondary to stroke involving inferior division of left middle cerebral artery
hearing is intact
temporal lobe infarction will not produce complete deafness because
each cochlear nerve projects to BOTH temporal lobes
13 yo has a severe case of left sided mastoiditis
develops a fluent aphasia
aphasia is most likely the result of extension of the infection into the
temporal lobe
Wernicke's
52 yo man on multiple medication medications develops temporary hearing loss which agent?
aspirin
50 yo man is evaluated for tinnitus
worse on some days than others
which of the following may exacerbate tinnitus?
think auditory
aspirin quinine
aminoglycosides
21 yo right handed woman works at airport as a luggage handler
ear protection must be worn to protect against hearing loss and development of
tinnitus
what is dissociated sensory loss?
regional sensory loss that involves only one of 2 primary sensory modalities with sparing of the other
electric shocklike sensation spreading down body or into back or extremities when she flexes her neck is:
Lhermitte's sign
what causes Lhermitte's sign?
lesion of cervical spinal cord due to:
MS, tumor, herniated disc, body ridge indenting cord
what kind of lesion can cause Horner's?
caused by lesion to sympathetic nerve fibers that innervate face
-caused by ipsilateral lesion inhypothalamus, brain stem reticular formation, cervical and upper thoracic spincal cord, superior cervical ganglion, sympathetic fibers running along carotid artery and branches of cranial nerve V
what are all the possible levels of neuraxis at which a lesion can produce this triad?
lower cervical and upper thoracic spinal cord
what muscles elevate the eyelid?
levator palpebrae
superior tarsal muscle
levator palpebrae is innervated by
CN III (voluntary)
superior tarsal muscle
involuntary, sympathetic nervous system
left leg hyperreflexi and increased muscle tone suggests:
upper motor dysfunction due to ipsilateral lesion affecting left corticospinal tract in cervical and thoracic spinal cord
plantar response
superficial NOCICEPTIVE reflex elicited by stroking the lateral plantar surface of foot from heel toward the ball of foot
normal: plantar flexion of great toe
babinski's is abnormal, extension of groeat toe IMPLIES UPPER MOTOR NEURAL LESION involving corticospinal tract
abdominal reflexes
superficial NOCICEPTIVE reflexes obtained by stroking skin lightly on abdomen from umbilicus toward any abdominal quadrant
look for deviation of umbilicus toward the quadrant stroked
absence of abdominal reflexes on one side suggest UMN dysfunction and roughly equivalent to extensor plantar response
lesion in left cervical spinal cord can produce ipsilateral upper motor neuron dysfunction, ipsilateral dorsal column sensory dysfunction and contralateral spinothalamic sensory dysfunction
this is called
Brown sequard's syndrome
where does the dorsal columns pathway cross?
internal arcuate fibers of medulla
where does anterolateral pathway cross?
right when enter spinal cord and synapse at dorsal horn, anterior white commissure
lower motor neuron dysfunction is associated with
decreased muscle bulk
hypoactive muscle stretch reflexes
upper motor neuron dysfunction is associated with
hyperactive and plantar response to be extensor (babinski)
where can you get a single lesion that affects BOTH right and left anterolateral pathways
anterior white commissure
• Both hands lost muscle bulk
• Right neck pain that radiates down right arm and describes a burning in quality
• Burned right hand and forearm
• Decreased muscle bulk in intrinsic muscles bilaterally and left forearm
• Mild spastic catch in both legs
• Lower extremity strength is normal bilaterally
• Loss of thermal sense and pinprick over posterior neck and shoulders extending down both arms in “capelike” fashion
• Plantar response is extensor on right (Babinski) and flexor on left
• Gait is normal
due to central lesion in cervical spinal cord such as syrinx
list 3 regions that can produce a left hemibody sensory loss
right parietal cortex
right corona radiata
right thalamus
left-sided neglect is caused by
ability to attend to hemispatial field is a function of CONTRALATERAL PARIETAL LOBE
pronator drift is specific to what kind of dysfunction?
upper motor neuron
sensory drift
profound loss of sensation resulting in inability to localize in space
profound hemisensory lesions that split the midline are often seen where?
THALAMUS where the sensory inputs converge
can localize to right thalamus in lateral and medial division of VPL and VPM
sensory relay nuclei relay somatosensory/facial sensory information to primary sensory cortex
what supplies the thalamus?
thalamogeniculate branches of PCA (right lateral thalamus)
thalamic pain syndrome (Dejerine-Roussy)
involvement of VPL and VPM of thalamus
usually due to vascular lesion--> distressing spontaneous pain and discomfort on side of contralateral lesion
truncal sensory level
diminished sensation from all dermatomes below a particular dermatome on the trunk
tertiary syphilis can cause
deficits in fine touch vibratory proprioceptive sens
T4 vertebral fracture at what spinal level would these deficits in pain and thermal sense be greatest?
T6 and lower
anterolateral tract lesion distribute info rostrally
complete loss 2-3 segments below
Brown-sequard syndrome
results in dissociated sensory loss
DORSAL-VENTRAL hemisection of spinal cord
why can a spinal cord lesion produce horner's?
fibers from hypothalamus descend in spinal cord to control preganglionic sympathetic neurons
a patient revels deficits in sensation of vibration, fine touch, proprioception but NO EVIDENCE of CNS lesion
you suspect a peripheral neuropathy involving what kind of fibers?
A-beta fibers
Anterolateral tracts are primarily served by what class of peripheral nerve fibers?
group 3 and 4
A delta fibers convey
initial response, first pain that leads to STT, is fed by a-delta fibers to check the integrity of the anterolateral system
slow persistent pain is conveyed by
C fibers
A pt presents with hypoesthesia to thermal and nociceptive sensations in a capelike distribution across both shoulders and both arms?
anterior white commissure
syringomyelia
central cavitation of spinal cord
18 yo male present with dissociated segmental deficits in thermal/pain sensation across both arms hyperreflexia and spasticity with weakness and atrophy of arm and hand muscles
cervical syrinx has UMN AND LMN damage
herniated disk is ONLY LMN damage
what is the comorbidity to a cervical cord syrinx?
herniation of cerebellar tonsils (chiari malformation)
54 yo hypertensive and diabetic female complains of several recent episodes of paresthesias in right arm and shoulder
transient ischemic attacks
59 yo male suffers stroke resulting in complete LEFT side hemibody sensory loss of modalities but NO motor impairment. Based only on this info, what are possible sites of lesion
right posterior parietal cortex, right corona radiata/internal capsule/right thalamus/right dorsal pons
where do sensory tracts run together? Both the DC-ML and AL tracts run together in a VERY small region in the dorsal pons → thalamus → corona radiata/internal capsule → posterior pariteal cortex
same male stroke resulting in complete left side hemibody sensory loss of modalities but no motor impairment and no left-sided sensory neglect. What structure can you now eliminate from you list of possible sites?
Right parietal cortex – involved in space and spatial representation
Same guy suffers a stroke resulting in complete left side hemibody sensory loss of all modalities but NO motor impairment
The lack of motor signs allows to diminish which of the following potential lesion site
corona radiata and internal capsule
Same guy suffers a stroke resulting in complete left side hemiody sensory loss of all modalities but not motor impairment and NO cranial nerve deficits
right dorsal pons would cause CN deficits
must be thalamus
Stroke 9 mo ago and reports episodes of severe burning and stabbing on right side of his body where was stroke?
Especially shoulder arm and torso
left VPL nucleus of thalamus
thalamic pain syndrome
A stroke results in complete left side hemibody sensory loss of all modalities, no motor impairment and no cranial nerve deficits. Nine months later he develops thalamic pain syndrome
What arteries most likely compromised?
right thalamoperforator and thalamogeniculate
known risk factors for stroke
high blood cholesterol
high LDL
hypertension
diabetes
peripheral artery disease
coagulation disorder
medial medulla is supplied by
paramedian branches of vertebral and anterior spinal arteries
lateral medulla
verebral artery
or more commonly PICA
anatomical structures found in the medial medulla
pyramidal tract
medial lemniscus
hypoglossal nucleys and exiting CNXII fascicles
anatomical structures found in lateral medulla
inferior cerebellar peduncle
vestibular nuclei
trigeminal nucleus
spinothalamic tract
desceding sympathetic fibers
nucleus ambiguus
nucleus solitarius
medial medullary syndrome -symptoms
contralateral arm or leg weakness
contralateral decreased position and vibration sense
lateral medullary syndrome (Wallenberg's syndrome) symptoms
ipsilateral ataxia, vertigo, nystagmus nausea
ipsilateral facial decreased pain and temp
cnotralateral body decreased pain and temp
ipsilateral horner's
hoarseness dysphagia
ipsilateral decreased taste
lateral caudal pons supplied by
AICA
dorsolateral rostral pons supplied by
SCA
Weber's syndrome
branches of PCA and top of basilar artery infarct
causes oculomotor nerve ipsilateraly palsy
contralateral hemiparasis due to cerebral peduncle
midbrain tegmentum is supplied by
PCA and basilar
cause of Claude's syndrome
an infarct in PICA can cause what?
Lateral medullary syndrome or Wallenberg's
what are the symptoms?
ipsilateral ataxia vertigo nystagmus
ipsilateral facial decreased pain and temperature
contralateral body decreased pain and temperature sense
ipsilateral horner's syndrome
hoarseness and hysphagia
ipsilateral decreased taste
lesion of oculomotor nerve fascicles
ipsilateral third nerve palsy
lesion of vestibular nuclei causes
vertigo
nystagmus
trigeminal nucleus and tract lesion causes
ipsilateral facial decreased pain and temperature sensation
facial colliculus lesion causes
ipsilateral face weakness
ipsilateral horizontal gaze palsy
lesion of hypoglossal nucleus and its existing fascicles
ipsilateral tongue weakness
lesion of nucleus solitarius
ispilateral decreased taste
lesion of descending sympathetic fibers
Horners syndrome
radiculopathy
pain or neuro abnormality in a dermatome
absent ankle reflex caused by
S1
subjective weakness plantar flexion caused by
S1
slight numbness left posterolateral leg
L5, S1
main cause of back pain in 30 yo
musculoskeletal
herniated disc
40 yo cause of back pain
degeneration, infection, ovarian cancer, pancreatitis
over 50 yo cause of back pain
metastatic cancer
spinal stenosis
rheumatoid diseases
abdominal aneurysm
myeloma
does most back pain arise from herniated disc?
NO
3% of herniated discs require surgery
distinguish low back pain from radiculopathy
radiculopathy is defined as an abnormality involving a nerve root (pain in a dermatomal pattern)
back pain: pain arising from muscle or peripheral nerve entrapment (no radiating pain to limbs)
left S1 radiculopathy with pain radiating to the left posterolateral leg and lateral foot
numbness in a left S1 dermatomal pattern and absent Achilles reflex (S1)
sensory and motor changes
weakness if subtle
findings due to physical compression or irritation of nerve root by herniated disc
review tx options for radiculopathy
opioid based analgesic
hydrocodone
acetaminophen
stronger NSAID
physical therapy is optional
most common psychiatric disorders in patients with lower back pain
depression
generalized anxiety disorder
somatization disorder
personality disorder
paracentral disc herniation of left lateral L5-S1 will cause impingement of what nerve root?
S1 nerve root
is this acute or chronic?
low back pain with left S1 radiculopathy
left herniated disc at L5/S1
mild neurological findings
acute pain
Tx for persistent pain
epidural injection of steroids and local anesthetics may provide good pain relief
effect on DRG -irritating
anti-inflammatory mechanism most well-established
inflamed ganglion demonstrates upregulation of:
opiod receptors
sodium channels
NK1 receptors whe
when do you consider surgery for back pain?
disc is concordant with sx
pain is radicular
adequate time for healing has passed
risk factors for surgery are appropriate
back pain alone responds less well
gate control theory
activity on large diameter afferents can inhibit activity on small diameter pain transmission neurons
occurs in DH
requires inhibitory interneurons
what is the basis for counter irritatns to relieve pain?
gate control theory
what type of fibers have the lowest threshold
large fibers
PAG send output to monoaminergic nuclei in medulla to:
Raphe (serotonin)
locus coeruleus (NE)
monoaminergic fibers descend in dorsolateral region of SC to terminate on dorsal horn
similar projections to:
caudal spinal nucleus of CN5
2 ways to block pain transmission via NE/5-HT
1.excite interneurons --> release enkephalin --> inhibit pain transmission at synaptic junction where glutamate and substance P are released
2. may synapse directly on pain transmission fibers to inhibit impulse
stress induced analgesia
give examples
anticipatory, preparatory, emtional stress
physical exertion and exercise
acupuncture/acupressure
placebo
how does stress induced algesia work?
via hypothalamus and limbic system (amygdala)
opiates and non-opiate mechanisms are involved
PAG receives descending input from:
RF, STT, SRT, SMT
implanted electrodes
opiate drugs (morphine)
stress and anxiety (limbic system/endocannabinoids)
PAG send out descending projection to synapse at:
raphe magnus --> dorsolateral spinal cord/spinal nucleus of 5 --> dorsal horn --> serotonin to enkephalin interneurons --> inhibit pain transmission
locus coeruleus --> lateral spinal cord/spinal nucleus of CN5 --> dorsal horn --> NE to enkephalin interneurons --> inhibit pain transmission
what type of pain is NOT pathological
somatic superficial pain
yperalgesia
enhanced pain response to noxious stimuli after injury
primary at site of injury
2ndary at surrounding sit of injury due to spread of chemical mediators
allodynia
severe sensitization to extend that normal non-noxious stimuli are painful
what type of pain is slow, generally localized emotional, motivational
persisting: can be inflammatory vs. neuropathic
caused by inflammation
OR altered receptor, damaged nerve, facilitated CNS transmission
what type of pain persists beyond healing period
profoundly altered receptor, nerve or CNS pathways
abnormal/chronic
TRPV1
legitimate polymodal receptor
elicits intense burning pain sensation
concomitant exposure to 2 or more adequate stimuli --> hyperalgesia or allodynia
TRPV1 responds to:
capsaicin
low pH (H+)
heat
inflammatory pain (peripheral)
sensitized peripheral receptors
chemical mediators (cytokines and chemical that decrease threshold of nociceptors)
primary afferent cell surface receptors and receptive intracellular signaling
pharmacologic basis for analgesic (NSAIDS)
neuropatic pain (peripheral)
damage/demyelination
ectopic impulse generation via pseudoreceptors/short circuits
barrage of input from recurrent excitation in local circuit
transcriptionally altered primary afferents
C fibers express MORE nociceptors
large fibers begin to convey nociceptive input
Central desensitization
damage to peripheral nerves
Abeta fibers rearrange termination to make MORE synapses with nociceptive relay neurons
altered secondary relay neurons
new receptors are expressed for NTs of primary pain afferents: glutamate/substance P
altered electrophysiology
Reverberation (thalamic syndrome)
damage to descending inhibitory pathways
nonnociceptive central pathways take on role of conveying nociception
what is a key component of PERSISTENT NEUROPATHIC PAIN
central desensitization
CRPS1
complex regional pain syndrome
no identifiable nerve injury
how do you treat central sensitization
opiods dont work well
gabapentin, pregabalin, tricyclic antidepressants are effective
CRPS2
identifiable nerve trauma/disease --> neuropathic pain
what is the etiology of CRPS?
unknown etiology
NE activates and sensitives nociceptors
cytokine abnormality
autoimmune
visceral pain is conveyed by
anterolateral system
dorsal columns-ML
spinocervical -ML
referred visceral pain
poorly localized
convergence of 2 or more primary afferents
superficial receptive field onto visceral receptive field
spread via Lissauer's
conveyed by AL system
brain interpretes input as coming from a familiar region
referred pain
phantom limb
brain remembers missing limb in somatotopic map so SS cortex and map are rewired
what happens when nerves dev independently of peripheral input
phantom limb
what could cause tickle itch and sex?
carried by small diameter myelinated and unmyelinated fibers
STT, SRT, VTT
could be due to pattern vs population coding
or labeled line primary afferents selective for category of sensation
how does brain respond differently than other organs?
localization: site of lesion makes a big difference
confined to a fixed volume/space
BBB
selective vulnerability
autoregulation - brain can control its own blood flow in response to oxygen and glucose levels
no lymphatic drainage
glial - not fibrotic sars
-DOES NOT make fibrotic scars in response to lesions/undergoes glial proliferation
cause gliosis and involved in Alzheimer's type II change
astrocytes
proliferation of astrocytes in response to injury (nonspecific)
gliosis
Alzheimer's type II changes
change in astrocytes
has nothing to do with Alzheimer's disease
seen in metabolic issues like hepatic encephalopathy - toxic injury to brain
losing oligodendrocytes leads to
demyelination
rod cells, nodules, phagocytosis
microglia
definition of ICP
P > 200 mm water
complications of increased intracranial pressure
headache
confusion
papilledema
what can cause ICP?
cerebral edema
tumors
abscesses
hematoma
main adverse effect: herniation
noncommunicating hydrocephalus
obstruction of ventricular system

ex: pineal tumor
communicating
not due to obstruction of ventricular system
due to impaired reabsorption of CSF at arachnoid villi (scarring)
or meningeal scarring after meningitis --> subarachnoid hemorrhage
fibrosis occlude foramen of magendie
overproduction of CSF by choroid plexus is what kind of hydrocephalus
due to benign tumor choroid plexus that makes too much CSF
communicating
bulging tense soft spot on top of infants
large prominent veins in scalp
may not be able to look downward with white of eyes (setting sun sign)
irritability/lethargy
high pitched cry
seizures
vomiting
papilledema
hydrocephalus in babies
anterior horn of lateral ventricles rounded tip instead of sharp point
hydrocephalus
increased ICP with headache
signs of dementia, parkinsonian gait, memory loss,
hydrocephalus
brain pushing out during craniotomy
ventricular dilation due to cerebral atrophy
dilatation of ventricles bc brain is shrinking
hydrocephalus ex vacuo
ex of communicating hydrocephalus
anterior cerebral artery infarct
cingulated gyrus pushes under falx
subfalcine herniation
oculomotor compression
posterior cerebral artery infarct
midline midbrain/pontine (duret) hemorrhages
uncus gets pushed under tentorium
transtentorial herniation
compression of medulla/respiratory centers
tonsillar
1-5 per 1000 live births
replaced by area cerbrovasculosa
posterior fossa spared
frog babies
missing skull and brain
forebrain is replaced by tangled up mass of blood vessels and neuropil
anencephaly
forebrain replaced by tangled mass of blood vessels and neuropil
area cerebrovasculosa
opening in occipital or posterior fossa
encephalocele
meningocele and meningomyelocele are examples of
spina bifida
opening to meninges or to spinal cord
spina bifida
what is the least significant form of spina bifida?
spina bifida occulta
open from head to lower spain - worst neural tube defect
craniorachischesis
how do you test for neural tube defect?
look for elevated alpha-fetoprotein
prenatal folate deficiency increases risk of what?
having a baby with neural tube defect
small posterior fossa, cerebellar vermis displace down through foramen magnum, hydrocephalus, lumbar meningomyelocele
arnold-chiari malformation
posterior fossa is enlarged
4th ventricle is a cystic area
posterior vermis is not there (rudimentary)
dandy-walker malformation
hydromyelia
dilated central canal (patent and dilated, normally should be completely collapsed)
syringomyelia
cleftlike cavity of inner portion of cervical cord or brainstem
little cavities in cervical SC
usually due to a space occupying lesion, arnold-chiari malformation, trauma
incomplete midline separation, midline facial anomalies (cyclopia)
trisomy 13
arrhinencephaly
holoprosencephaly
what is arrhinencephaly
lack of olfactory apparatus
petau syndrome
trisomy 13
sometimes corpus callosum fails to form in agenesis
holoprosencephaly
spectrum of retardation (normal to severely mentally retarded)
• Premature babies often have
• Hemorrhage in the periventricular brain parenchyma, particularly in germinal matrix where neurons are growing before the move out the cortex
• Germinal matrix very prone to hemorrhage
• Right under ependymal cells so if it hemorrhages it is easy to break through into the CSF (reason neonatologists call intraventricular hemorrhage)
intraparenchymal hemorrhage
infarcts with mineralization, prematurity, extensive cases multicystic encephalopathy
• Also happens in premature babies
• Infarcts in brain that tend to calcify
• Sometimes there will be lots of these and they become cystic which results in multicystic encephalopathy
periventricular leukomalacia
- deep sulci in cortex (ulegyria), basal ganglia & thalamus aberrant myelination
• Brings us back to concept of selective vulnerability
• Some neurons are more susceptible to different kinds of injury, especially ischemia, than others
• Neurons on cerebral cortex surface are more resistant to ischemia than deep neurons
• Ulegyria
ischemic injury
– gyri look like a mushroom, at base of gyrus it looks shrunken up
ulegyria
elastic biconvex transparent
composed of living cells
highly modified epithelial cells from ectoderm
lens
lens is low in
water 66%
lens is high in
protein 33%
does the lens have blood supply?
no and low oxygen
what is important in lens?
glutathione
what does glutathione do?
lowers the O2 content
what is important in regenerating glutathione?
ascorbic acid
metabolism in the lens is by
anaerobic
glycolysis
zonules
attach lens to ciliary process for focusing
what pathway is important for using high glucose levels and recycling NADPH from HMP shunt?
sorbitol
what converts glucose to sorbitol?
aldose reductase
what maintains the low water content in lens?
Na+/K+ ATPase
what keeps protein from aggregation?
glutathione lower O2 content and keeps protein reduced
what is a molecular filter for light and reduces chromatic aberration?
lens
effect of sorbitol on lens
diabetic cataracts
what does aldose reductase convert galactose to?
Galactitol or Dulcitol
Can infants or adults metabolize galactose better?
adults
what enzyme do you need to break down galactose and is only found in trace amount in infant liver
UDP-Gal pyrophosphorylase
what are 4 kinds of protein found in the lens?
alpha-crystallin
beta-crystallin
gamma-crystallin
albuminoid
which is more potent? sorbitol or galactitol (dulcitol)
dulcitol bc it does not get neutralized to fructose
cataract formation causes what types of changes
change in permeability of membrane of lens cells
change in physical state of proteins
change in enzymatic properties of lens
how much oxygen does the retina have?
5x the oxygen content of any other tissue in the body
does the retina have a large blood supply?
yes
has more membrane than any other tissue
how does retina maintain fluidity of retinal membrane?
polyunsaturated fatty acids
lots of omega 3s
light breaks double bonds of lipids in membrane of retina in presence of O2 to form...
free radicals
2 superoxides + 2H+ forms
peroxide and oxygen
superoxide + hydrogen peroxide forms
peroxidation and cleavage of unsaturated fatty acids --> destroys eye with Iron (fe3+)
what can break down hydrogen peroxide?
catalase
hydrogen peroxide + 2GSH is catalyzed by what to form GSSG and water?
glutathione peroxidase
need selenium
lens protects against what wavelengths?
315-400 nm light
UV light is blocked by what in the eye?
cornea and lens
only wavelengths that gets to retina
400-1400 nm
what protects against 400-500 nm light in macule?
carotinoids
what helps protect against light damage?
pigment in the iris (not good to have blue eyes)
what absorbs almost all of damaging UV?
cornea
does retinal pigment epithelium protect against light damage?
no not much
probably used to block light scatter
what are the bodyguards tha help arrest harmful free radicals?
vit E, C, beta-carotene

others:
superoxide dismutase
glutathione, taurine
chromium
selenium
what kinds of cells in the eye are analogous to neuoglia of CNS?
Muller - have long cytoplasmic processes which embrace encircle retinal neurons
what type of metabolism does the retina use?
glycolysis
krebs cycle
what has 5x more glutamine synthetase?
retina in the muller cells

remember that glutamate is toxic to retina if not metabolized
what has a high requirement for protein and phospholipid for membrane synthesis?
retina
light converts 11-cis retinal to
all trans forms
inner segment of rod photoreceptors contain
prominent golgi apparatus and many mitochondria
outer segment contains
stack of flattened membrane discs, incorporate rhodopsin
membranous discs are continuously shed from end of rod
phagocytosed by pigmented epith cells
phototransduction-steps
light converts rhodopsin to a fom that activates transducin (GDP-GTP)
transducin activates phosphodiesterase (PDE) by Talpha subunit
PDE decreases cGMP
cGMP increases Na+ inflow in photoreceptor cell
this light is an off signal
ratio of proteins in eye
900 rhodopsin/ 1 PDE/ 2 cGMP
1 rhodopsin activates:
2000 PDE --> Hydrolyzes 2.5 million cGMP/sec

rhodopsin is embedded in disc membrane
does the lens last a lifetime?
yes
no turnover, but slow addition of cells at periphery
transplantable
anterior epithelium of lens is made up of
single layer of cuboidal cells
mature lens fibers are greatly elongated specialized epithelial cells, prism-shaped, los nuclei as they age and squeezed toward midline. new lens fibers form from lens cells at:
equator
compress central cells
what has a vascular core surrounded by double layer of pigmented epithelium?
ciliary processes
what does the ciliary processes secrete?
aqueous humor
what serves as the junction between ciliary body and choroid?
ora serrata
vascular and pigmented
helps provide nutrition to the retina and absorbs scattered light
choroid
what is derived from the outer layer of embryonic optic cup?
pigment epithelium
what are the functions of the pigment epithelium?
absorbs scattered light rays
phagocytosis of worn out discs
stores and releases vitamin A to photoreceptors
where are receptor potentials generated in the eye?
rods and cones
specialized desmosome-like junctions between glial cells of
retina (Muller cells) and photoreceptors. Appears like line at L.M. level.
external limiting membrane
what are horizontal cells?
association neurons (interneurons) involved in local processing of visual information in retina
what kind of cells are found in the outer plexiform layer?
bipolar and horizontal cells
what kind of cells are found in the inner nuclear layer?
bipolar neurons
what kind of potential do bipolar cells generate?
slow graded potential
what kinds of cells are found in the inner plexiform cells
amacrine, bipolar, ganglion
nerve fiber layer
unmyelinated axons of retinal ganglion cells that follow curvature of retina
become myelinated optic nerve outside retina after existing lamina cribosa
what do ganglion cells generate?
APs
expanded ends of muller glial cells and BM directly adjacent to vitreous
appears like line with light microscopy
internal limiting membrane
where is the blind spot in the eye?
optic disc
is cis stable or trans rhodopsin?
cis is more stable
trans is unstable and dissociates from opsin --> increase outward conduction in calcium --> reduce membrane permeability to Na --> hyperpolarization/generation of receptor potential which leads to production of further electrical signals to brain
Two transmitters of primary afferent fibers.
Glutamate
Substance P
olfactory sensation is processed virtually entirely by components of:
limbic system
Lesions of the trigeminal nuclei produce this laterality of facial sensory deficits.
ipsilateral
Level of brainstem rostral to which all sensations from the face are represented contralaterally?
mid pons
common cause of caloric testing reveals both L and R eyes cannot adduct
bilateral MLF
cause of this: MS
General (NOT TASTE!) somatic sensation from the oral & nasal cavities is carried by these CNs and this pontomedullary nucleus.
CN V, IX, X
Deficits, laterality and body region involved with a lesion of the anterior white commisure of the SC.
CAN be cape-like if it’s in the cervical cord.
Lesion lower→ bilateral band of loss of sensation 2-3 segments below.
Ear that will hear the loudest song if you plug your L ear & place a tuning fork on your forehead midline.
left ear
CN level to which CNS depression must descend (be present) if the Doll’s Eyes (oculocephalic reflex) is absent
a. CN VI or below
i. You have to get at least to VI bc you have to get to MLF. If you go further, it’s even worse…
ii. You have to get III & VI to get the eyes locked in the head
iii. Btw 3 and 6 would be equivalent to an MLF lesion.
Labyrinth pathology accounting for the following: slow phase of nystagmus (active, physiologically driven movement), past-pointing and a tendency to fall to the R:
irritative lesion on LEFT
destructive lesion on RIGHT
if my eyes are HYPOACTIVE on the R, i would look R
Descending inhibition of nociception utilizes these THREE transmitters @ a minimum:
NE
5-HT
opiods
most caudal location of a lesion producing decreased pain/ temperature sensation over the L face and decreased pain/ temperature sensation on the R side of the body, below the head.
left caudal medulla
aka lateral medullary syndrome
Infarct of this vessel can produce deficits in taste from the tongue, palate & epiglottis.
PICA and vertebral artery
where solitary nucleus is
nociception, thermal sense & perception of pain from the body are conveyed by this system that is comprised of these tracts:
AL: SMT, STT, SRT
Specific area of brainstem involved w sound localization through analyzing time differences.
superior olive
medial (time)
lateral (intensity)
Lesions of trigeminal nuclei produce this laterality of facial sensory deficits:
ipsilateral
CN V nuclei involved in relaying two-point discrim & vibr sense from the face
Chief or principal sensory
rostral spinal (2/3)
location of lesion causing CN deficits and deficits of sensory and / or motor modalities from the body: (where do long tracts cross CN nuclei)
brainstem (medulla and pons)
19. CN V sensory nucleus involved exclusively in proprioception and reflex control of chewing:
mesencephalic nucleus of V
Internal structures that amplify sounds by 30-40 db
ossicles
brainstem nucleus & thalamic nucleus responsible for conveying taste sensation
solitary nucleus of V
VPM
CNs responsible for conveying taste
7, 9, 10
possibly symptoms assoc with acoustic neuroma (schwannoma)
a. tinnitus,
b. ipsilateral deficits in corneal reflex,
c. spontaneous facial pain with sensory loss,
d. ipsilateral facial weakness and decreased taste,
e. deafness,
f. loss of equilib
dynamic function of vestibular function
VOR eye movements
tract utilized and effect exerted to maintain balance when pushed or shoved while studying
lateral vestibulospinal tract & facilitation of motor neurons of leg extensors (VSR)
main blood supply to pons at level of CN6 and 7
circumferential br of basilar
AICA
infarct of this vessel leads to alternating hemianesthesia
loss of pain and themal sense from one side of face and opposite side of body, vertigo, nystagmus, and ipsilateral Horner's syndrome
vertebral artery and PICA (lateral medullary syndrome)
main blood supply to all SS tracts at the level of the midbrain
PCA
condition and pathology that causes sensory loss in hands or feet in a glove or stocking pattern
diabetic neuropathy
lesion of CN VI nucleus and/or surrounding reticular formation produces this deficit
ipsilateral gaze paralysis
hyperalgesia to extent that non-noxious stimuli are painful
allodynia
lesion below R calcarine fissure results in visual field deficit
Left superior quadrantanopia
pie in the sky
visual field defect caused by lesion of R caudal part of temporal lobe
L superior quadrantanopia (meyer's loope)
object recognition will be lost
lesion of ascending MLF leads to this visual defect
INO internuclear ophthalmoplegia
injury-induced local mechanism leading to hyperalgesia originating at peripheral receptors
inflammation caused by release of local chemical mediators
lesion of this assocn cortical region can produce asterognosis & agraphesthesia
5 & 7 parietal cortex
right side bilterally is wiped out
R homonymous hemianopia
cause of the following: L eye rotated down and out at rest & dilated L pupil
lesion of CN3, including edinger-westphal
3 signs of horner's syndrome
ptosis
miosis
anhydrosis
41. lesion that causes loss of pain and temp sense from L body and loss of proprioception, fine touch and vibratory sense on the R body lacking face involvement (include laterality)
brown-sequard
recently discovered and cloned receptor family that fulfills criteria of a legit polymodal nociceptor at “Free nerve endings.”
TRP
possible mechanism contributing to central sensitization of the dorsal horn of the spinal cord:
a. rearranegement of A-β fibers to nocicceptive relay cells and/or transcriptionally altered secondary relay neurons (RE-WIRING)
pituitary tumor can produce this visual field defect
bitemporal hemianopsia
optic chiasm is squished
accommodation triad
convergence
pupillary constriction
ciliary muscle contraction
eye movement deficits seen with destruction of L cerebral hemisphere anterior to central sulcus
frontal fields, no saccadias
b. lessened ability to excute voluntary R saccades (conj gaze
lesion of this causes ipsilateral complete sensory (and motor) loss in one dermatome
DRG or spinal nerve lesion
site of lesion and vessels causing complete L facial paralysis and inability to abduct eye
MCA and AICA
tumor growing in this structure causes parinaud's syndrome
paralysis of upward vertical gaze
pineal gland tumor compresses on tectum
vessel supplying region of sensory and motor cortex that maps leg and foot
ACA
51. arteries supplying the ventral basal thalamus
thalamoperforator and thalamageniculate arteries of PCA
52. site of a focal lesion and vessels most likely involved that explains the following: complete R side deficits to all somatic sensation and upper motor neuron heiparesis on the entire R side, no visual deficits & no sensory neglect.
Posterior limb of the L internal capsule; lenticulostriate branches of the MCA and/or anterior choroidal artery
the lever system of ossicles causes
increase in force
decrease in amplitude
tensor tympani inserts into
malleus
innervated by mandibular division of V
stapedius inserts onto
stapes
innervated by facial
eustachian tube connects what to what?
middle ear to nasopharynx
to equalize pressure during yawning or swallowing
perilymph
high in Na+, low in K+ like CSF
endolymph
high in K+, low in Na+
hair cells -specialized neuroepithelial mechanoreceptors for audition and vestibular function, located in specialized regions of membranous labryrinth
invagination of ectoderm from hindbrain pinches off and forms what?
otocyst
otocyst becomes
membranous labyrinth to form bony labyrinth
what forms bony labyrinth?
mesoderm
tectorial membran is a stiff gelatinous structure attached to:
limbus - a connective tissue shelf extending from spiral lamina
pilar (tunnel) cells are
specialized support cells around tunnel of corti
tightly attached to BM
contain tonofibrils (large microtubules) that make rigif triangular structure which acts as a fulcrum of BM
a gelatinous mass (glycosaminoglycans) in which the stereocilia are embedded.
Cupola is tethered to roof of ampulla.
cupula
elevated ridge of highly specialized
epithelial tissue inside ampulla of membranous semicircular duct, is the sensory organ for
detection of rotational motion (angular acceleration).
crist ampullaris
role of melanin in choroid
revents light rays that have passed through the rods and cones from bouncing back onto these cells
retina receives its blood supply primarily from branches of
ophthalmic artery
which comes from internal carotid
strong electrical potential will record AP with what types of nerve fibers?
Abeta, delta, C
weak electrical AP in what fiber?
Abeta only
big nerve fibers have lowest threshold
tap, light pressure, movement
Abeta peak only
heavy pressure
Abeta and A delta
pinch prick
Abeta C
Hot, cold
A delta and C
Strong electrical with pressure cuff
Adelta and C
strong electrical with local anesthetic
Abeta peak only
fast conduction fibers
large diameter
heavily myelinated
Abeta
intermediate conduction fibers
smaller diameter
lightly myelinated fibers
slow conduction fibers
smallest diameter
unmyelinated C
ischemia preferentially blocks
large myelinated fibers
local anesthetics first block
unmyelinated fibers then lightly myelinated then heavily myelinated (myelination protects against anesthetic)
large diameter fibers subserve
reflex activities
fast discriminative sensations
well localized and characterized
high quality and fidelity
small diameter fibers subserve
slow and more diffuse sensation
can be poorly localized and characterized
lower quality and fidelity
free nerve endings include
thermal receptors
pain receptors
specialized cells that directly affect afferent nerve terminal:
touch receptors such as merkel's, meissner's pacinian
hair follicles
golgi tendon organ
exteroceptors
localized on external surface
sense ambient environment
proprioceptors
mainly in muscles, tendons, joints
signal position and movement of limbs by sensing muscle length
interoceptors
localized to internal organs and blood vessels
sense visceral and internal environment
mechanoreceptors
physical change or movement
fast and slow adapting
thermoreceptors
warm cold slowly adapting
nociceptors
mechanical nociceptors
thermal nociceptors
polymodal nociceptors
slowly adapting
ex of proprioceptors
muscle spindles
golgie tendon organs
joint receptors
rapidly adapting
generally out of realm of conscious awareness
can be perceived consciously
important modality to assess neurologic deficits
are receptor potentials grade?
yes
amplitude is proportional to stimulus strength
receptor potentials trigger what in afferent nerve if threshold is exceeded?
APs
frequency of action potential firing is proportional to what?
the magnitude of receptor potential
larger receptor potential
faster the neuron will fire
neural code
pattern, frequency, and duration of groups of APs
encodes intensity and duration
adequate stimulus
type of stimulus energy to reach lowest threshold
slow adapting
on response followed by sustained response
A delta and C fibers
signals location and continued presence of stimuli
nociceptors can show afterdischarge
continued generation of APs after cessation of nociceptive stimulus
receptor potential and frequency of firing is related how?
proportional
stronger stimuli excite more receptors and afferents = recruitment of sensory units
location coding depends on 3 principals
receptive fields of peripheral afferents
dermatomes
somatotopic organization of pathways
what is peripheral receptive field
area of body that contains receptor ending of a single afferent fiber and stimulated with adequate stimulus for receptor endings
activates afferent fiber
receptive fields-can be exitatory or inhibitory with respect to projection neurons?
yes
surround inhibition in CNS
sharpens contrast of stimulus signals for better intensity and location coding
sensory systems function as edge detectors and contrast comparators
change in neural activity pattern = increased contrast
do receptive fields differ in size at different parts of body?
yes
small on hands and face
large on back and legs and arms
spatial discrimination ability is best where
small receptive fields like hands
2 point discrimination
on hands/lips are small -mm
back and legs --cm
occlusive stroke caused by
thrombosis
atherosclerosis
hemorrhagic strokes caused by
hypertension
aneurysm
excitotoxicity elicits cell death by
binding inflammatory cytokines like TGF to receptors in neuronal membrane
loss of neuronal connections to a target and deprivation of trophic support --> cell death
necrosis
nonphysiological
disrupt homeostasis
characteristics of necrosis
disrupt cell membrane
influx of Ca2+ ions/water/ionic gradients
mitochondria swell/dysfunction
lysosomal enzymes activated
cell swells and lyses
denatured proteins, DNA --> local inflammatory response
apoptosis
programmed cell death is death with integrity
function in normal dev and homeostasis
features of apoptosis
req new RNA and protein synthesis
req activity of specific genes
involve endonucleolytic cleavage and cellular DNA fragmentation
membrane blebbing
intracellular compaction of nucleus and deposit electron dense chromatin
pinch off membrane bound apoptotic bodies
internal/external membranes are preserved
glial scarring is accompanied by increased secretion of:
TGF, FGF, TNFalpha, interleukins, interferon gamma, IGF1
excitotoxicity and apoptosis can be triggered by
perturbation of intracellular Ca homeostasis
dysregulation of free radical metabolism
Is there evidence showing ischemia can lead to excitotoxicity?
Conc’s of Glu and Aspartate (Asp) in the synaptic cleft around neurons increase during ischemia
Microinjection of Glu receptor antagonists in experimental animals protect neurons.
Presumably reduced supply of oxygen and glucose during ischemia elevates extracellular Glu levels by slowing the energy-dependent removal of Glu at synapses.
blocking glutamate should protect neurons, but it hasnt worked well in clinical trials. why?
substantial excitotoxic injury occurs quite soon after ischemia prior to typical treatment
excitotoxcity only one of several mechanisms by which ischemia damages neurons.