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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
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lens is low in
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water 66%
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lens is high in
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protein 33%
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does the lens have blood supply?
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no and low oxygen
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what is important in lens?
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glutathione
|
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what does glutathione do?
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lowers the O2 content
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what is important in regenerating glutathione?
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ascorbic acid
|
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metabolism in the lens is by
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anaerobic
glycolysis |
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zonules
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attach lens to ciliary process for focusing
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what pathway is important for using high glucose levels and recycling NADPH from HMP shunt?
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sorbitol
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what converts glucose to sorbitol?
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aldose reductase
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what maintains the low water content in lens?
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Na+/K+ ATPase
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what keeps protein from aggregation?
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glutathione lower O2 content and keeps protein reduced
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what is a molecular filter for light and reduces chromatic aberration?
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lens
|
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effect of sorbitol on lens
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diabetic cataracts
|
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what does aldose reductase convert galactose to?
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Galactitol or Dulcitol
|
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Can infants or adults metabolize galactose better?
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adults
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what enzyme do you need to break down galactose and is only found in trace amount in infant liver
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UDP-Gal pyrophosphorylase
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what are 4 kinds of protein found in the lens?
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alpha-crystallin
beta-crystallin gamma-crystallin albuminoid |
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which is more potent? sorbitol or galactitol (dulcitol)
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dulcitol bc it does not get neutralized to fructose
|
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cataract formation causes what types of changes
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change in permeability of membrane of lens cells
change in physical state of proteins change in enzymatic properties of lens |
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how much oxygen does the retina have?
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5x the oxygen content of any other tissue in the body
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does the retina have a large blood supply?
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yes
has more membrane than any other tissue |
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how does retina maintain fluidity of retinal membrane?
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polyunsaturated fatty acids
lots of omega 3s |
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light breaks double bonds of lipids in membrane of retina in presence of O2 to form...
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free radicals
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2 superoxides + 2H+ forms
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peroxide and oxygen
|
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superoxide + hydrogen peroxide forms
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peroxidation and cleavage of unsaturated fatty acids --> destroys eye with Iron (fe3+)
|
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what can break down hydrogen peroxide?
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catalase
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hydrogen peroxide + 2GSH is catalyzed by what to form GSSG and water?
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glutathione peroxidase
need selenium |
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lens protects against what wavelengths?
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315-400 nm light
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UV light is blocked by what in the eye?
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cornea and lens
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only wavelengths that gets to retina
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400-1400 nm
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what protects against 400-500 nm light in macule?
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carotinoids
|
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what helps protect against light damage?
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pigment in the iris (not good to have blue eyes)
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what absorbs almost all of damaging UV?
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cornea
|
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does retinal pigment epithelium protect against light damage?
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no not much
probably used to block light scatter |
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what are the bodyguards tha help arrest harmful free radicals?
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vit E, C, beta-carotene
others: superoxide dismutase glutathione, taurine chromium selenium |
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what kinds of cells in the eye are analogous to neuoglia of CNS?
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Muller - have long cytoplasmic processes which embrace encircle retinal neurons
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what type of metabolism does the retina use?
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glycolysis
krebs cycle |
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what has 5x more glutamine synthetase?
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retina in the muller cells
remember that glutamate is toxic to retina if not metabolized |
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what has a high requirement for protein and phospholipid for membrane synthesis?
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retina
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light converts 11-cis retinal to
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all trans forms
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inner segment of rod photoreceptors contain
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prominent golgi apparatus and many mitochondria
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outer segment contains
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stack of flattened membrane discs, incorporate rhodopsin
membranous discs are continuously shed from end of rod phagocytosed by pigmented epith cells |
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phototransduction-steps
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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 |
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ratio of proteins in eye
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900 rhodopsin/ 1 PDE/ 2 cGMP
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1 rhodopsin activates:
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2000 PDE --> Hydrolyzes 2.5 million cGMP/sec
rhodopsin is embedded in disc membrane |
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does the lens last a lifetime?
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yes
no turnover, but slow addition of cells at periphery transplantable |
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anterior epithelium of lens is made up of
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single layer of cuboidal cells
|
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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:
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equator
compress central cells |
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what has a vascular core surrounded by double layer of pigmented epithelium?
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ciliary processes
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what does the ciliary processes secrete?
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aqueous humor
|
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what serves as the junction between ciliary body and choroid?
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ora serrata
|
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vascular and pigmented
helps provide nutrition to the retina and absorbs scattered light |
choroid
|
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what is derived from the outer layer of embryonic optic cup?
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pigment epithelium
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what are the functions of the pigment epithelium?
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absorbs scattered light rays
phagocytosis of worn out discs stores and releases vitamin A to photoreceptors |
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where are receptor potentials generated in the eye?
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rods and cones
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specialized desmosome-like junctions between glial cells of
retina (Muller cells) and photoreceptors. Appears like line at L.M. level. |
external limiting membrane
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what are horizontal cells?
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association neurons (interneurons) involved in local processing of visual information in retina
|
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what kind of cells are found in the outer plexiform layer?
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bipolar and horizontal cells
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what kind of cells are found in the inner nuclear layer?
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bipolar neurons
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what kind of potential do bipolar cells generate?
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slow graded potential
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what kinds of cells are found in the inner plexiform cells
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amacrine, bipolar, ganglion
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nerve fiber layer
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unmyelinated axons of retinal ganglion cells that follow curvature of retina
become myelinated optic nerve outside retina after existing lamina cribosa |
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what do ganglion cells generate?
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APs
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expanded ends of muller glial cells and BM directly adjacent to vitreous
appears like line with light microscopy |
internal limiting membrane
|
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where is the blind spot in the eye?
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optic disc
|
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is cis stable or trans rhodopsin?
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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 |
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Two transmitters of primary afferent fibers.
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Glutamate
Substance P |
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olfactory sensation is processed virtually entirely by components of:
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limbic system
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Lesions of the trigeminal nuclei produce this laterality of facial sensory deficits.
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ipsilateral
|
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Level of brainstem rostral to which all sensations from the face are represented contralaterally?
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mid pons
|
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common cause of caloric testing reveals both L and R eyes cannot adduct
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bilateral MLF
cause of this: MS |
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General (NOT TASTE!) somatic sensation from the oral & nasal cavities is carried by these CNs and this pontomedullary nucleus.
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CN V, IX, X
|
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Deficits, laterality and body region involved with a lesion of the anterior white commisure of the SC.
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CAN be cape-like if it’s in the cervical cord.
Lesion lower→ bilateral band of loss of sensation 2-3 segments below. |
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Ear that will hear the loudest song if you plug your L ear & place a tuning fork on your forehead midline.
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left ear
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CN level to which CNS depression must descend (be present) if the Doll’s Eyes (oculocephalic reflex) is absent
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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. |
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Labyrinth pathology accounting for the following: slow phase of nystagmus (active, physiologically driven movement), past-pointing and a tendency to fall to the R:
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irritative lesion on LEFT
destructive lesion on RIGHT if my eyes are HYPOACTIVE on the R, i would look R |
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Descending inhibition of nociception utilizes these THREE transmitters @ a minimum:
|
NE
5-HT opiods |
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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.
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left caudal medulla
aka lateral medullary syndrome |
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Infarct of this vessel can produce deficits in taste from the tongue, palate & epiglottis.
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PICA and vertebral artery
where solitary nucleus is |
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nociception, thermal sense & perception of pain from the body are conveyed by this system that is comprised of these tracts:
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AL: SMT, STT, SRT
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Specific area of brainstem involved w sound localization through analyzing time differences.
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superior olive
medial (time) lateral (intensity) |
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Lesions of trigeminal nuclei produce this laterality of facial sensory deficits:
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ipsilateral
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CN V nuclei involved in relaying two-point discrim & vibr sense from the face
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Chief or principal sensory
rostral spinal (2/3) |
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location of lesion causing CN deficits and deficits of sensory and / or motor modalities from the body: (where do long tracts cross CN nuclei)
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brainstem (medulla and pons)
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19. CN V sensory nucleus involved exclusively in proprioception and reflex control of chewing:
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mesencephalic nucleus of V
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Internal structures that amplify sounds by 30-40 db
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ossicles
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brainstem nucleus & thalamic nucleus responsible for conveying taste sensation
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solitary nucleus of V
VPM |
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CNs responsible for conveying taste
|
7, 9, 10
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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 |
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dynamic function of vestibular function
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VOR eye movements
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tract utilized and effect exerted to maintain balance when pushed or shoved while studying
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lateral vestibulospinal tract & facilitation of motor neurons of leg extensors (VSR)
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main blood supply to pons at level of CN6 and 7
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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)
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main blood supply to all SS tracts at the level of the midbrain
|
PCA
|
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condition and pathology that causes sensory loss in hands or feet in a glove or stocking pattern
|
diabetic neuropathy
|
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lesion of CN VI nucleus and/or surrounding reticular formation produces this deficit
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ipsilateral gaze paralysis
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hyperalgesia to extent that non-noxious stimuli are painful
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allodynia
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lesion below R calcarine fissure results in visual field deficit
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Left superior quadrantanopia
pie in the sky |
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visual field defect caused by lesion of R caudal part of temporal lobe
|
L superior quadrantanopia (meyer's loope)
object recognition will be lost |
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lesion of ascending MLF leads to this visual defect
|
INO internuclear ophthalmoplegia
|
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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
|
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right side bilterally is wiped out
|
R homonymous hemianopia
|
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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
|
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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
|
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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. |