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417 Cards in this Set

  • Front
  • Back
Spinal cord arterial supply
Anterior and posterior spinal arteries (from vertebral arteries); radicular arteries (from segmental vessels)
Spinal cord length
Extends from medulla at foramen magnum to lower border of first lumbar vert
Spinal cord enlargements
cervical (upper extremity innervation) and lumbar ( lower extremity innervation)
conus medullaris
conical termination of the sacral spinal cord, btw L1 and L2
filum terminale
a condensation of pia mater from the conus medullaris to the coccygeal ligament
cauda equina
large number of lumbosacral roots surrounding filum terminale
Spinal nerves
each (except C1) innervates a single dermatome; 8 cervical, 12 throacic, 5 lumbar, 5 sacral, 1 coccygeal
Spinal cord internal structure
white matter (axons and glia) surround H-gray matter (neuronal cell bodies and glia) with central canal (CSF) in middle
White matter subdivisions
posterior funiculus, lateral funiculus, anterior funiculus
Posterior Funiculus
ascending somatosensory fibers ( fasiculus gracilis: sacral and lumbar info/medial; fasiculus cuneatus: thoracic and cervical info/lateral)
Lateral funiculus
descending tracts to the spinal cord (lateral coritcospinal tract, rubrospinal tract, etc) and ascending tracts from cord (lateral spinothalamic, post spinocerebellar, etc)
Anterior funiculus
smaller ascending and descending tracts; crossing of spinothalamic tract
Gray matter subdivisions
dorsal, ventral and lateral horns
Dorsal horn
sensory (receives sensory input; mediates synapses; neurons give rise to ascending efferent pathways)
Ventral horn
motor (houses alpha and gamma motoneurons and interneurons; neurons innervate extrafusal and intrafusal muscle fibers)
Lateral horn
intermediolateral cell column from T1-L2/3 only; thoracolumbar sympathetic outflow
Rexed lamination
subdivides gray matter into 9 cellular laminae plus an area X surrounding central gray
Primary sensory afferent inputs and spinal cord
Receives them from dorsal root ganglia at each segmental level and relays them to the brain stem, cerebellum, or thalamus (may or may not synapse in cord first)
Alpha and gamma motoneurons
housed in spinal cord; innervate extrafusal and intrasfusal muscles respectively of body and extremities
Intermediolateral cell column
from T1-L2/3; gives rise to pregang sympathetic fibers which synapse in the paravertebral and prevertebral ganglia
Preganglionic parasymp neurons in S2-4
housed in spinal cord; fibers synapse in terminal ganglia within walls of pelvic viscera
dorsal root lesion (dorsal rhizotomy)
hypesthesia or anesthesia
ventral root lesions
may lead to complete flaccid paralysis and atrophy of muscles; involvement of autonomic pregang fibers may result in autonomic dysfunction
spinal cord transection
destruction of ascending and/or descending tracts produces sensory motor or mixed deficits
spinal cord hemisection
Brown-Sequard syndrome: loss of fine touch/vibration/proprioception ipsilaterla and below lesion; loss of pain/temp contralateral to and below lesion; spastic paralysis ipsilateral to and below lesion
brainstem from rostral to caudal
midbrain-pons-medulla
Integrative functions of the brainstem
nuclei regulate consciousness, motor, respiratory, and cardiovascular activity via reticular formation in core
conduit functions of brainstem
ascending sensory tracts and descending motor tracts pass through brainstem
cranial nerve functions of brainstem
cell bodies of cranial nerves are located in brainstem; CN nuclei arranged in funcitonal columns
CN functional columns from medial to lateral
somatic motor, brachial motor, visceral motor, visceral sensory, somatic senosry, special sensory
Somatic motor CNs
innervate skel muscles in head and neck that are derived from myotomes (CN III, IV, VI, XII)
BRachial motor CNs
innervate skel muscles derived from brachial arches: mm of mastication, facial expression, pharynx, larynx, middle ear, trapezius (CN V, VII, IX and X, XI)
Visceral motor CNs
pregang parasymp innervation to cardiac m, smooth m, glands (CN III, VII, IX, X)
Visceral sensory- special CNs
taste (CN VII, IX, X)
Visceral sensory- general CNs
control of cardiorespiratory and digestive fucntions (CN IX and X)
Somatic sensory CNs
convey touch, pain, temp, position and vibration from skin/muscles/joints of head (CN V, VII, IX, X)
Special sensory
hearing and balance (CN VIII)
Midbrain topography
Tectum= colliculi and CN IV; cerebral aqueduct; anterior= cerebral peduncles, CN III
Rostral midbrain
cerebral aqueduct, periaqueductal gray, sup colliculi, oculomotor nucleus, Edinger-Westphal nucleus, red nucleus , corticospinal tract (middle of crus cerebri), medial lemniscus, spinothalamic tract
caudal midbrain
cerebral aqueduct, peraqueductal gray, inf colliculi, trochlear nucleus, mesencephalic nucleus of CN V, corticospinal tract, medial lemniscus, spinothalamic tract
Pons topography
Cerebllar peduncles on posterior surface; basilar sulcus for basilar a, CN V in middle, CN VI, VII, VIII at bottom
Medulla topography
gracile and cuneate tubercles, corticospinal tract (pyramids), CN IX, X and XII emerge from ant sulci
Posterior Cerebral A and superior cerebellar a
supply lateral aspects of midbrain including corticospinal tract (middle of crus cerebri)
occlusion of PCA
Weber's syndrome
Basilar and posterior communication aa
supply medial aspect of midbrain
Lateral aspect of rostral pons
superior cerebellar a; basilar a--> short circumferential branches
occlusion of superior cerebellar a
lateral pontine syndrome
Penetrating branches of basilar (paramedian arteries)
supply medial pons inc pontine nuclei, medial lemniscus, and corticospinal tract
occlusion of basilar a
medial pontine syndromes
Pontine tegmentum and dorsolateral quadrant of pons blood supply
AICA, long circumferential branches of the basilar, and superior cerebellar a
occlusion of AICA
lateral pontine syndrome
lateral aspects of rostral medulla blood supply
vertebral a and PICA
occlusion of vertebral a/ PICA
lateral medullary syndrome (of Wallenberg)
medial aspects of rostral medulla blood supply
(inc corticospinal tract) anterior spinal a and penetrating branches of the vertebral a
occlusion of ant spinal a and penetrating branches of vertebral a
medial medullary syndrome
posterior spinal artery
supplies lateral aspect of caudal medulla
medial aspects of caudal medulla blood supply
(inc coritcospinal tract) ant spinal a and penetration branches of vertebral a
role of somatosensory system
allows us to sense touch, temp, proprioception, and pain
Basic pathway for sensory stimula to be perceived
stimulus> sensory receptors>spinal cord>medulla/brainstem>thalamus>cortex
dorsal root ganglion
cell bodies of sensory neurons; innervating neck on down; pseudounipolar cell bodies with peripheral and central processes
Exteroreceptive sensory receptors
code info from external world mainly via skin; inc mechanoreceptors (touch), thermoreceptors, nociceptors (sharp and burning pain)
Proprioceptive sensory receptors
code info about muscle length/tension and joint angles via muscle afferent receptors (golgi tendon organs and muscle spindles) and joint and tendon afferents
Interoceptive sensory receptors
code info about changes insid eht body; visceral afferent receptors; localize sensation and pain very poorly
sensory neuron stimulus transduction
stimulus activates receptors and ion channels> generates receptor potenital> if strong enough, generates APs> APs conveyed to spinal cord
Intensity of stimulus is encoded by:
each neuron: freq of AP firing (rate code) and many neurons: number of neurons fighting (spatial summation code)
A-alpha fibers
large, myelinated, conduct APs fast; muscle spindles
A-beta fibers
large, myelinated, conduct APs fast; light touch, vibration, pain
A-delta fibers
thin, myelinated, conduct APs moderately fast; nociceptors (fast pain) and cooling receptors
C fibers
unmyelinated, conduct APs slowly; nociceptors (slow pain) and warm receptors
Compound action potential (whole peripheral nerve)
clinical diagnostic to determine whether axons are missing, damages or demyelinated; used to diagnose peripheral neuropathies
Slowly adapting receptors
respond best to sustained, unchaning stimulus; sense pressure and shape of objects
Rapidly adapting receptors
respond only when stimulus changes (on/off); sense impact and motion of objects on skin
Superficial receptors receptive field size
small receptive field size
Deep receptors receptive field size
large receptive field size
Innervation density
high in very sensitive areas (fingers, face) low in insensitive areas (back, calves) using 2 point discrimination
mechanoreceptors
mediate tactile/touch; very senstive to force (low threshold); silent without stimulation' myelinated axons, fast conduction
Merkel disks
fine touch- sharpest resolution of surface texture; @ epidermal/dermal junction; multiple small spots for receptive field; several innervated by single myelinated axon; slowly adapting, encodes amount of force
Meissner's corpuscles
fine touch; epiderm-dermal junction; single spot receptive field; corpuscle closes stack of flattened epith cells; myelinated axons; rapidly adapting response encodes on/offset of skin indentation
Ruffini Endings
in dermis; sense stretch to determine shape; large and diffus receptive field; encapsulated ending; myelinated axons surrounds collagen fibrils; slowly adapting
Pacinian corpuscles
in dermis; high freq vibration; most sensitive mechanoreceptor, even distribution; large and diffuse receptive field; fluid filled capsule; myelinated axon; rapidly adapting
Meissner's vs Pacinian
Meissners: low freq vibration and lots of indentation to be activated
Pacinian: high freq vibration and only require tiny amounts of skin indentation
Hair follicle receptors
respond to movement of hairs; receptive field around base of hair follicle; bare axon wraps base of follicle, axon is myelinated; rapidly adapting response to encode velocity of hair movement
best at 2 point discrimination
Merkel (Meissner's is ok)
Thermoreceptors
encode skin temp; discharge continuously at normal skin temp
cooling receptors
increase firing rate when skin is cooled; stop firing when warm; free nerve endings with myelinated axons; small receptive fields, infreq distribution
warming receptors
increase firing when skin is above 32; stop when cool; free nerve endings with unmyelinated axons (c fiber); very small receptive fields
Nociceptors
respond to stimuli that damage or threaten skin; ~70% of all sensory neurons in DRG; provide almost all innervation to tooth pulp and cornea
A-mechanonociceptors
axon myelinated (a-delta); respond to intense mech force/extreme heat; free nerve endings; small receptive fields; slowly adapting to detect entire time
polymodal nociceptors
unmyelinated axon (c fibers); intense mech force, high heat, noxious chemicals; free nerve endings; small receptive fields; slowly adapting; mediate slow, aching, burning quality of pain; difficult to localize
dorsal column system
sensory pathway for light touch, 2 pt discrimination, vibration, joint position
basic pathway for dorsal column system:
stimulus-> sensory receptors-> spinal cord-> medulla/brainstem-> thalamus-> cortex
spinal cord and dorsal column system
-first place in CNS that sensory info goes
-ea level gives rise to 1 spinal n. and 1 DRG on each side
-ea innervates 1 dermatome
spinal neurons
gray matter on inside of spinal cord containing cell bodies of neurons
nucleus/ nuclei
clusters of neuronal cell bodies that connect functional systems
tracts
bundles of projecting axons (fibers) with similar connections/ functions--> course through white matter on outside of spinal cord
Major sensory tracts in dorsal columns
-fasciculus gracilis
-fasciculus cuneatus

convey tactile, vibration, joint position info to brain
major sensory tracts: anterolateral
(anterior funiculus)
convey pain, temp info to brain and some crude touch
anatomy of spinal cord (horns)
dorsal horn: sensory input

ventral horn: contains motor neurons that send efferent info to muscles
general regions of spinal cord gray matter are divided into...
rexed laminae
Laminae I/II
gray matter most lateral
receive nociceptive primary afferent input from dorsal roots
(marginal zone and substantia gelatinosa)
Laminae III/IV
gray matter
receive tactile/vibration afferent input form dorsal roots
damage to dorsal column system
causes loss in fine touch and vibration sensation below the spinal level of the lesion
primary afferent input for dorsal column system
all mechanoreceptors afferents that mediate fine touch
(Merkel, Meissner, Pacinian, Ruffini, hair follicle afferents)
dorsal column system and spinal cord entry
central process of afferents enter medial spinal cord through medial part of dorsal root
dorsal column system spinal cord ascent
-mostly ipsilateral
-a few local branches synapse in dorsal horn onto spinal nn that send axons across and to anterolateral tract (crude touch)
fasciculus gracilis
-medial dorsal column
-carries info from T7 and below
fasciculus cuneatus
-lateral dorsal column
-carries info from T6 and above
lumbar region and dorsal columns
fasciculus gracilis only
thoracic region and dorsal columns
segment T7 and below have f. gracilis only
T6 and above have both
cervical region and dorsal columns
both f. gracilis and cuneatus
somatotopy of axons in dorsal columns
(med) leg->trunk->arm->neck (lat)
cervical and lumbar cord differences in matter
cervical: lots of white matter, many axons, distinct dorsal columns

lumbar: lots of gray matter, big ventral horns
termination of axons in dorsal column nuclei
mechanoreceptor axons ascend and terminate onto 2nd order neurons in Dorsal Column nuclei: nucleus gracilis and nucleus cuneatus
dorsal column 2nd order neurons
send projections across sensory decussation in caudal medulla, turn and ascend in medial lemniscus
dorsal column nuclei
-N. Gracilis (medial, leg and trunk), cuneatus (lat, arm and neck)
-(med) leg-->trunk-->arm->neck(lat)
-as column ascends, sensory fibers are added laterally
medial lemniscus
-bundle of fibers originating in medulla
-made of axons of 2nd order neurons with cell bodies in dorsal column nuclei
medial lemniscus ascent
caudal medulla --> pons --> midbrain --> thalamus
receptor type info still segregated (merkel with merkel)
lesions of medial lemniscus
-contralateral deficits in fine touch, 2 pt discrimination, vibration, joint position
termination of medial lemniscus
2nd order axons asecnding in medial lemniscus terminate in the ventral posterior lateral (VPL) nucleus of the thalamus onto 3rd order thalamic neurons
VPL
and somatotopy
-receives info about neck and body
-neck is medial, feet are lateral
lesions of VPL nucleus in thalamus
contralateral deficits in fine discrimination, vibration, joint position
3rd order thalamic neurons from dorsal column system
from VPL pass laterally through posterior limb of the internal capsule--> fans out as corona radiata rostrally
3rd order thalamic neurons form dorsal column system termination
terminate in somatosensory cortex (S1) in postcentral gyrus
somatorsensory cortex somatotopy
medial=legs, lateral=face
lesions of S1 cortex
contralateral deficits in fine discrimination, vibration, joint position
convergence of thalamic neurons
receptirve field of one cortical neuron in S1 ma ultimately receive input from 300-400 mechanoreceptors in skin
Primary somatosensory cortex (S1)
-all sensory info from thalamus goes to S1 cortex first (contains 4 Brodmann's areas 3a, 3b, 1, 2)
Brodmann's area 3b
-receives input from cutaneous slowly and rapidly adapting receptors
-derives info about details of edges of objects and texture
Brodmann's area 1
-input from cutaneous rapidly adapting receptors
-dervies info about kinesthesis (limb movement)
Brodmann's area 2
-input from deep tissue and complex touch from skin
-combines info about finger & limb position with edge info to determine 3D shape
Secondary somatosensory cortex (SII)
-receives neurons form all 4 SI areas
-project to insular cortex which projects to temporal lobe (imp for tactile memory and recognition)
Posterior parietal cortex
-where some SI neurons project
-Brodmann's 5&7: integrate tactile info with visual info-->project to motor areas of frontal cortex
-where body is, where stimulus is
pain
a complex, cognitive perception of sensory stimulus in the context of the environment, previous experiences and emotherions--> product of brain's abstract interpretation of sensory experience
analgesia
lack of pain
anesthesia
lack of sensation
allodynia
pain from a normally non-painful stimulus like light touch
paresthesia
unpleasant, abnormal sensation; tingling, pricking, tickling
acute vs chronic pain
acute: critical protective function

chronic: continues after healing or in absence of injury serving no useful purpose
nociceptive pain
-pain from tissue damage
-activation of nociceptors in skin, inflamm chemicals, nerve receptors
-NSAIDs responsive typically
neuropathic pain
-direct damage to nerves in the peripheral or central NS
-often burning, lancinating, electrical quality, allodynia common
anterolateral system
-info about pain and body temp
-made of several pathways of neurons terminating at diff brain levels
anterolateral system input
-noxious mechanical, thermal or chemical stim
-to free nerve endings of A-delta or C-fiber nociceptors
A-delta fibers in anterolateral system
-myelinated
-mediate pain first
-immediate, short-lasting, pricking quality
C fibers in anterolateral system
-unmyelinated
-mediate second pain
- delayed, long lasting, burning quality
anterolateral system and spinal cord
central processes of nociceptors enter spinal cord dorsal horns (lateral party)--> synapse right away onto 2nd order neurons in Lamina I/II
anterorlateral 2nd order neurons
-cross to contralateral side within 2-3 segments and ascend in anterolateral quadrant tracts (ventral lateral funiculus)
lesion of anterolateral tract
contralateral loss of pain and temp complete by 2-3 segments below the lesion
anterolateral termination in higher brain centers
-3 paths all start in spinal cord but terminate in diff places
-spinothalamic tract, spinoreticular tract, spinomesencephalic trat
Spinothalamic tract
-majority of 2nd order ascending fibers terminate onto 3rd in thalamus
-mediates discriminative aspects of pain and temp (location and intensity)
in thalamus, axons from body terminate in 2 nuclei:
VPL and Central lateral nucleus
VPL
-3rd order axons project to ipsilateral SI cortex
-relay for discriminative somatosensory info from body
-recognizes both dorsal column medial lemniscus and spinothalamic inputs (but segregation of neurons occurs)
Central Lateral Nucleus
-3rd order neurons project to many areas of cortex, partic limbic cortex (affect, emotion)
-involved in emotional suffering
-CL nucleus is not somatotopically organized
thalamus and nociceptive info
Processes info--> crude pain and temp sensation is beginning to be appreciated and emotional rxns to pain are initiated
thalamus and relaying info
relays info to cerebral cortex (SI) by 3rd order neurons that pass through posterior limb of internal capsule and corona radiata to SI cortex
similarities of spinothalamic tract and dorsal column system
-project to VPL of thalamus
-somatottopically organized
-discriminates and localizes stimuli
Spinoreticular tract
-2nd order neurons ascend and terminate in medulla and pons--> reticular formation
-mediates changes in level of attention to painful stimuli
spinomesencephalic tract
-2nd order neurons terminate in midbrain in superior colliculus and in a region of gray matter surrounding cerebral aqueduct called periaqueductal gray (PAG)
-stimulates central modulation of pain
-sends neurons back down to stim. endogenous pain inhibition
thalamic neurons of anterolateral tract project to cortex areas:
-somatosensory cortex
-cingulate gyrus
-insular cortex
thalamic neurons of anterolateral tract to somatosensory cortex
SI areas 3b, 2, 1 and SII

localizes stimulus on body
thalamic neurons from anterolateral tract in cingulate gyrus
-part of limbic system
-processing of emotional component of pain, fear, anxiety, etc
thalamic neurons form anterolateral tract in insular cortex
processes info on the internal, autonomic state of body (heart races, breathing rapid, etc)
integrates sensory, affective, and cognitive components of pain
lesions of insular cortex
-asymbolia for pain
-pts can perceive noxious stimuli as painful and localize the pain to body part, but don't display appropriate emotional responses
descending pathways that inhibit pain
-painful stimuli can be suppressed by endogenous pain control systems
-reticular formation has prominent role
descending pathways inhibiting pain neurons
-cell bodies in PAG in midbrain--> send axons down to the Raphe nucleus in medulla and to Locus Ceruleus of pons--> send axons down spinal cord where they synapse on inhibitory interneurons or directly on to spinothalamic tract projections to suppress noxious transmission
referred pain
-area to which the pain is referred corresponds to the dermatome innervated by the spinal segment to which the visceral afferents project
(MI= left chest and arm, T1-T4)
Trigeminal nerve
-opthalmic (V1), maxillary (V2), mandibular (V3)
-peripheral afferent neurons
-fine touch afferents, nociceptive afferents, thermoreceptors
trigeminal ganglion
-on each side of head
-cell bodies of sensory neurons innervating head/face
-homologous to DRG for body
trigeminal nuclei for fine touch
-fibers synapse first in main sensory nucleus in pons
trigeminal nuclei for pain and temp
-fibers synpase first in spinal trigeminal nucleus (from pons to cervical spinal cord)
-homologous to spinal dorsal horn for body
-caudal nucleus: extends from obex to spinal cord
thalamic nuclei for trigeminal system
Ventral posterior medial (VPM) nucleus for both fine touch and pain/temp (but they stay segregated)
somatotopy of VPM
(medial) tongue--> intra-oral cavity--> face (lateral)
primary afferent input for trigeminal system
mechanoreceptor fibers enter from 3 branches of CN V
major primary pathway for trigeminal system
fine touch mechanoreceptors synapse in chief sensory nucleus of V in pons on ipsilateral side
2nd order neurons for trigeminal system
send fibers that cross to other side of the pons and form the trigeminal lemniscus (which joins medial lemniscus)--> ascends to VPM of thalamus--> terminates on 3rd order thalamic neurons
minor pathway for crude touch in trigeminal system
a few mechanoreceptors enter pons but descend directly in spinal tract of V to spinal nucleus of V where they synpase--> 2nd order neurons cross midline--> ascend in trigeminothalamic tract to VPM
minor pathway for oral cavity in trigeminal system
-dorsal trigeminal tract
-a few mechanoreceptors enter the pons and synapse in cheif sensory nucleus--> 2nd order neurons don't cross-->ascend on ipsilateral side to VPM
3rd order VPM thalamic neurons in trigeminal system
send projections through posterior limb of the internal capsule and corona radiata and terminate in the lateral aspect of the SI cortex (near lateral fissure)
primary afferent input for trigeminal pain and temp
nociceptors form the face enter CN V at pons, immediately descend in spinal trigeminal tract without synapsing, terminate in spinal trigeminal nucleus of V
2nd order neurons for pain/temp in trigeminal system
send axons that corss to other side of medulla and ascend as the trigeminothalamic tract to VPM of thalamus
3rd order neurons for pain/temp in trigeminal system
neurons in VPM project through the posterior limb of internal capsule and corona radiata up to lateral SI cortex (some others to reticular formation)
trigeminal neuralgia
-lancincating, severe pain that last seconds to minutes
-region of V2/3
-treat with carbamazepine (anticonvulsant works on Na+ channels)
Temperomandiulbar joint disorder
-chronic pain localized at TMJ or in muscles of mastication
-recurrent headaches, toothaches
lesions of thalamus and cortex
contralateral deficits in all sensation
lesion on one entire side of cord
-ipsi loss of fine discrim, joint position, vibration below lesion
-contra loss of pain and temp 2-3 segments below lesion
-some contra loss of crude touch
alternating sensory loss in body (fine discrim on one side, pain and temp on the opposite side)
usually idicates a unilateral lesion in the spinal cord
lesions in brainstem (above caudual medulla) or higher
contra loss of tactile and pain/temp in body
dorsal lesion above caudal medulla
contra loss of tactile and pain/temp
Lesion of VPL or VPM in thalamus
loss is contralateral
lesion at cortex
loss is contralateral
rhizomy (cutting of dorsal roots)
-lose fine discrim, joint position, vibration, pain/temp in dermatome innerv by cut dorsal roots
-surgeons typically cut dorsal roots adjacent to affected dermatomes
cordotomy (surgical cutting of anterolateral fiber tracts in spinal cord)
-cut 2-3 segments rostrally
-one side: lose pain and temp on contra side
-both sides: lose pain/temp both
-only for terminally ill
Peripheral nerve lesion causes
trauma, diabetes, neuropathy
peripheral nerve lesion deficit
lack of fine discrimination, pain/temp in skin, only in parts of limbs (glove and stocking)

affects multiple dermatomes
complete cord transection causes
trauma, fx or dislocated vert causing cord compression, penetrating injuries, tumors, MS
complete cord transection deficit
bilateral loss of all sensation below lesion and loss of motor control
anterior cord syndrome causes
fx vert--> contusion of spinal cord

infarct form anterior spinal artery embolism (blood clot)
anterior cord syndrome deficit
-bilateral loss of pain and temp below lesion
-spares dorsal columns- fine touch OK
-can get weakness from effect on motor neurons
posterior cord syndrome causes
trauma, extrinsic compression from tumors, syphalis (tabes dorsalis)
posterior cord syndrome deficit
loss of fine touch below level of lesion

pain and temp OK
central cord syndrome causes
-syringomyelia (tube-like enlargement of central canal)
-gliosis or cysts in central part of cord
-hyperextension of cervical spine (usually lower cervical or upper thoracic)
central cord syndrome: small lesion deficit
-cuts anterolateral fibers that cross in ant commissure
-bilateral loss of pain and temp in affected dermatomes: cape-like
-dorsal columns usually spared
central cord syndrome: large lesion deficit
-bilateral loss of pain/temp
-bilateral loss of fine touch below lesion
-motor neuron loss
-may spare sacral part of anterolateral tracts
Brown-Sequard syndrome (hemisection of cord) causes
penetrating injuries, tumor compressing ascending pathways, MS, herniated disk
(usually incomplete)
Brown-Sequard deficit
-ipsi loss of fine touch below lesion
-contra loss of pain and temp by 2-3 segments below lesion
unilateral lesion in VPL or VPM or SI cortex causes
stroke, hemorrhage, brain tumor, MS, trauma affecting one side of thalamus
unilateral lesion in VPL deficit
contralateral loss of fine touch and pain/temp in body

sensation in face is intact bc VPM is intact
unilateral lesion in VPM deficit
contralateral loss of fine touch and pain/temp in face and head
unilateral lesion in SI cortex deficit
contra loss of fine touch and pain/temp in body and/or face
(feet fibers most medial, head most lateral)
brain stem lesion in lateral medulla deficit
-contra loss of pain/temp in body
-contra loss of pain/temp in face
-ipsi loss of pain/temp in face

medial lemniscus ok=body fine touch OK
light path
cornea-anterior chamber-lens-vitreous-retina
function of the cornea
-protective function
-eye's outermost lens (65-75% of eyes total focusing power)
nourishment for the cornea
-no blood vessels
-tear and aqueous humor filling chamber behind it
5 tissue layers of the corneum
1. epithelium
2. Bowman's membrane
3. stroma
4. Descemet's membrane
5. endothelium
corneal epithelium
-blocks passage of foreign material
-smooth surface to absorb oxygen and nutrients
-lots of nerve endings=sensitive
-highly regenerative stratified squamous
corneal Bowman's membrane
-collagen
-if injured, can scar
corneal stroma
-90% of cornea's thickness
-water and collagen
-gives strength, elasticity, form
-necessary for light-conducting
corneal Desccemet's membrane
-protective barrier against infection and injury
-collagen and endothelial cells
-regenerated
corneal endothelium
-very thin
-pumps XS fluid out of stroma
Refractive errors
myopia: nearsighted, eye too long
hyperopia: far sighted, eye too short
uvea: 3 parts
-choroid
-ciliary body
-iris
choroid
-vessel layer (a&v, loose CT, melanocytes)
-chorocapillary layer (fenestrated capillaries in one plane)
-Bruch's membrane (amorphous hyaline membrane)
ciliary body
-expansion of stroma of choroid near the lens
-vitreous body, sclera, post. chamber
-ciliary processes project to lens
iris
-covers lens
-regulates amt of light reaching retina
anterior aspect of iris
-vascular, loose CT with interspersed melanocytes
-number and type of melanocytes determines eye color
posterior surface of iris
-double layer of pigmented epith to absorb light
-2 muscle masses rest on it and regulate iris opening (pupil diameter)
dilator pupillae m.
-radially arranged myoepithelial cells
-btw vascular and pigmented layers of iris
-symp innervation
sphincter pupillae muscle
-concentric smooth muscle bundles at pupil margin
-parasymp innerv
Anterior chamber
-contains aqueous humor
-avascular
-maintains intraocular pressure
-btw cornea and iris/lens
aqueous humor circulation
-produced by ciliary processes in post chamber--> anterior chamber--> trabecular meshwork--> canal of Schlemm-->venous system
-no direct cxn btw trebec and canal: humor percolates through tissue into canal
Open angle (chronic) glaucoma
-80-85% cases
-obstruction in drainage of eye
-passes too slowly through meshwork drain
-pressure builds and can damage optic nerve
angle-closure glaucoma
-blindness in 24-48 hours
-angle btw iris and cornea narrows, blocking draining of aq humor
clinical signs of glaucoma
-increased pressure
-increased cupping of optic nerve head (inc cup:disc)
-visual field defect will reveal a selective peripheral loss of sensitivity
lamina cribosa
network of collagen through which fibers of optic nerve exit--> may be altered in glaucoma
lens
-very transparent: avascular, little ECM
-2nd to corneal refractive power
-supported by system of fibers (suspensory ligaments or zonules) attached to ciliary body
Lens structure
-capsule: ECM surrounding lens
-epithelium: ant. surface
-lens fibers: body of lens, no organelles
accommodation
-lens thinner when focused on distant objects, relaxed ciliary muscles
-dynamically changes focus of eye
vitreous body
-nearly acellular
-maj macromolecules: type 2 collagen, hyaluronic acid
-nutritive function
cataracts
-occur as lens ages
-nuclear, cortical or posterior capsular
-replace lens to accommodate again
retina regions
-neural or sensory retina
-retinal pigment epithelium
retinal layers
-Bruch's
-RPE
-outer segments
-inner segments
-outer limiting membrane
-outer nuclear layer
-fiber layer
-inner nuclear layer
-inner synaptic layer
-ganglion cell layer
-optic fiber layer
-inner limiting membrane
fovea
-small pit
-region lateral to optic nerve
-used for high acuity vision
anterior retina
-number of neural elements declines
-becomes a single layer of unpigmented epithelium covering ciliary body
layer of photoreceptor outer and inner segments
-most posterior (last thing for light to reach)
-rods and cones
outer nuclear layer
nuclei of rods and cones
outer plexiform layer
location of synapses of rod and cone axons with next layer of neurons (bipolar)
inner nuclear layer
nuclei of bipolar neurons (also nuclei of horizontal and amacrine neurons and Muller glia)
inner plexiform layer
synapss of bipolar axons with ganglion cells
ganglion cell layer
ganglion cell nuclei
nerve fiber layer
axons of ganglion cells that converge to form optic nerve
inner limiting lamina
basement membrane fo Muller glial cells
Photoreceptor segments
-Inner: organelles for protein synthesis and energy production
-Outer: flattened membrane discs with photosensitive visual pigments (where proteins go via cilum)
rods
-long, slender outer segments
-numerous except at fovea
-very light sensitive
cones
-conical outer segments with membrane discs
-responsible for high acuity and color vision
-only photoreceptor in fovea
foveal development
-multiple anatomical events
-core packing increases postnatally from an initially uniform dist.
-foveal pit develops after a thickening of retina
-site of incipient fovea is avascular all along
RPE
-simple, cuboidal, MELANIN-containing epithelium btw neural retina and Bruch's membrane
-provides outer blood-retinal barrier
RPE functions
-absorbs scattered light
-transports nutrients and ions
-spatial buffering
-re-isomerization of all-trans retinal
-outer segment renewal
-secretes GFs for maintenance
retinal blood supply
-outer: choriocapillaries
-inner: central retinal artery from opthalmic artery
without foveal specialization...
-albinism because normally increased melanin contributes to avascularization (for high acuity vision)
in each eye, you have:
-100 million rods for vision in very low light
-5 million cones for day-time vision
cones and cone system
-photopic
-less sensitive, fast
-don't saturate
-high spatial resolution
-less pigment
rod and rod system
-scotopic
-more sensitive, slow
-saturate
-poor spatial resolution
-more pigment
photoreceptors response to light
hyperpolarization
univariance
-photoreceptors cannot register the wavelenth of photons they catch
-depends on number of photons
Visual pigment g-coupled protein cascade
-light activates photopigments-->stim G-protein (transducin) amplification--> activates cGMP phosphodiesterase--> breakdown of cGMP-->channels close-->decrease Na+-->hyperpolarization
countering effects of light
-decrease in ca2+ depresses PDE activity and enhances guanylate cyclase activity
-increases cGMP in OS
-counters light effects
retinitis pigmentosa
-defect affecting rods
-rhodopsin, PDE, GMP gated ion channels, arrestin
congenital stationary night blindness
-affects rods
-rhodopsin, transducin, PDE, rhodopsin kinase
cone, cone-rod, and macular degeneration
-affects cones
-GCAP1, guanylate cyclase, ABCR
rod monochromacy
-affects cones
-GMP gated ion channel, cone transducin
red/green vision defects and blue-cone monochromacy
-affects cones
-cone-opsin
Receptive field concept
-every neuron (that is higher order than photoreceptors) has a receptive field
-retinal area (of photoreceptors) that when stimulated influences the activity of that neuron
Hyperpolarization=universal response of photoreceptors to light
-as they hyperpol, release less NT
-light turns them OFF--> "off cells"
-hyper and depolarize in a graded fashion, release NT in graded fashion
when a cone is depolarized...
-releases excitatory NT glutamate
-occurs when light is NOT present
parallel pathways
-even though the cones all act in the same way in response to light, activity of a single cone gives rise to two parallel pathways
On center Bipolar cells
-"on center" cells-- light in center turns them on (metabotropic)
-invaginating contacts onto cone
-sign reversing of cone output (which is off-center)
-light depolarizes them (glutamate from photoreceptors would hyperpol-- inhibitory action)
Off center bipolar cells
-ionotropic receptors
-flat contacts on to cones
-classical excitatory synapses (sign CONSERVING)
-light-->hyperpolarizes
why does cone system have 2 parallel channels but rod system only has one?
-organization allows one channel to provide info to the ganglion cell concerning brighter than background stimuli (ON center channel) and the other, darker than background stimuli (the OFF center channel)
bipolar cells talk to:
-amacrine cells (lateral cxns; transient depolarizing responses)
-ganglion cells (produce APs)
physiological types of ganglion cells
-on center or off center
-either can have either sustained or transient responses
-melanopsin ones are photosensitive
parasol ganglion cells
-exhibit M cell behavior
-large cells with large receptive fields --> more transient responses
-project to M (magnocellular layers of LGN)
midget ganglion cells
-exhibit P cell behavior
-smaller cells with small receptive fields have more sustained responses
-project to P (parvocellular layers of LGN)
Horizontal cells
-elaborate system of inhibitory interneurons that synaptically interconnects photoreceptors
-ie every cone has a reciprocal synaptic relationship with all of its neighboring cones
rod monochromacy
-absence of cone-based vision in the eye
-intense glare in bright conditions
-poor acuity, poor fixation, nystagmus, visual field defects, etc
rod monochromacy causes
-mutations in CNG channel subunits or GNAT2 (cone transducin)
-cones are unable to hyperpolarize in response to light
red-green dichromacy
-missing the function of the one of the three cone types
-protanopia and dueteranopia are x-linked
congenital color vision defects
-present at birth
-constant type and severity
-both eyes equally affected
-visual acuity unaffected
acquired color vision defects
-onset after birth
-flucuating type/severity
-monocular differences
-reduced visual acuity
-predom. tritanopia
-equal male/female incidence
Retinitis Pigmentosa
-rhodopsin mutations alter ROD function via disrupting transport to OS
-difficulty seeing in dim light
-gradual loss of peripheral vision
-rods secrete cone-surviving factor so eventually lose cones
-inherited
Usher's syndrome
most common form of deaf-blindness

defect in transport proteins (ciliary defect)
geniculo-striate system
-conscious visual perception
-retina--> LGN-->striate cortex-->extrastriate cortex
retino-tectal system
-directing eye movements and visual attention
-retina --> superior colliculus --> pulvinar --> extrastriate cortex
pupillary constriction
-pregeniculate body--> pretectum-->EW nucleus--> ciliary ganglion-->pupillae constric mm
-consensual light reflex (both eyes) d/t linking via post. commissure
pupillary dilation
-pregenic body--> projection to midbrain retic formation--> descends to thoracic cord--> symp chain--> superior cerv gang--> pupillae dilator mm.
-symp: emotion can cause dilation
accommodation pathway
retina-->LGN-->visual cortex --> pretectum --> crossover --> EW nucleus--> ciliary gang --> contraction to plump up lens to see close objects
contraction of ciliary m
thickening of lens

(flattening of lens is passive)
When attention is directed to nearby objects...
-convergence of the 2 eyes
-contraction of ciliary m to thicken lens
-pupillary constriction to increase depth of field
how accommodation differs form pupillary reflex
-accomm can be voluntarily controlled
-reg by neg feedback mech that automatically adjusts focal power of lens
-pathway includes cerebral cortex
Retinal topography= visual field topography
-cornea and lens of the eye create an image of the visual field on the retina
retinotopy
-fibers in adjacent gang cells in each hemiretina stay together
-fibers from each nasal hemiretina cross
-preserved in LGN
-up is down, L is R
Cortical over-representation of the fovea
-fovea contains more gang cells than periphery--> more fibers and cells--> more cortical area (magnif)
-acuity at center of gaze is much better than periphery
fMRI responses
-used to identify brain sites that respond best to stimulation at different visual field eccentricities
hemianopia and quadrantanopia
-loss of vision in a hemifield or quadrant
homonyous
corresponding loss of vision in each eye
heteronomous
non-corresponding loss in each eye
functional specialization of visual cortex
-many intervening stages--> hierarchy of visual areas
-multiple pathways--> parallel processing
Symptoms of trauma to extrastriate cortex....
-lesions at higher levels will become more functionally specific
-lesions can result in selective loss of function (agnosias) rather than blindness
Extrastriate visual area organization
-what is it--> temporal lobe pathways for recognition of objects
-where is it--> parietal lobe for localization esp directing visual attention to an object of interest
lesions up to and including V1
-produce blindness
-all different functional pathways are cut
lesions of hMT+
-selective loss of motion perception
(sees someone enter room, then they're on the other side and don't know how they got there)
lesion of V4/V8
-cerebral achromatopsia (loss of color vision due to brain injury)
lesion of FFA
-Prosopagnosia = inability to recognize familiar faces
-often accompanies cerebral achromatopsia
lesions of PVA (primarily on right)
-attentional neglect
outer ear
pinna and external auditory meatus (canal)
middle ear
-begins at tympanic membrane
-tympanic cavity, ossicular chain and Eustacian tube
inner ear
-begins at oval window
-includes cochlea and vestibular structures
ear canal (external auditory meatus)
-concha to eardrum
-outer third is cartilaginous
-inner 2/3 is bony
-provide boost in high freq sound intensity
Middle ear bones
tympanic membrane--> handle of malleus--> vibrates --> incus --> stapes -->footplate on oval window
Ossicles of middle ear amplify sound vibration by
-a lever mechanism (2dB of gain)
-the area different between the tympanic membrane and the footplate of the stapes (23 dB)
-buckling of tympanic membrane
protective feedback to dampen vibration of ossicles
-tensor tympani attached to handle of the malleus
-stapedius muscle attached to neck of stapes
Where is inner ear contained
-petrous apex of the temporal bone
-encased in a bony labyrinth
sections of the bony labyrinth
-vestibule, cochlea, semicircual canal
Modiolus
-core of the cochlea
-highly porous bone that allows passage of auditory nerve fibers from internal aud meatus to hair cell synapse
osseous spiral lamina
-coils around center of cochlea
-partial division of upper and lower cochlear chambers into scala vestibuli and tympani
-pt of attach for basilar membrane
cochlear chambers all connect at the
helicotrema
scala media
-membranous labyrinth of the cochlea following the shape of the osseous cochlea
-sup. border: Reissner's membrane
-inf. border: basilar membrane
Sensory organ of hearing in membranous labyrinth
-organ of Corti
Along lateral wall of membranous labyrinth..
-stria vascularis: highly vascular tissue that is responsible for the metabolic environment of the scala media
organ of Corti
-longitudinally along length of basilar membrane
-one row inner hair cells
-3 rows outer hair cells
-cell bodies surrounded by supporting cells
Perilymph
-high Na+, low K+
-in scala vestibule and tympani
Endolymph
-high K+, low Na+
-in scala media
stria vascularis
-maintains ionic concentrations of endolymph
communication between endolymphatic sac and membranous labyrinth
-via endolymphatic duct and vestibular aqueduct
innervation of hair cells
-contacted by dendrites of afferent bipolar neurons whose cell bodies are in the spiral ganglion
-90-95% contact inner hair cells
afferent fibers and hair cells
-many afferent fibers synapse on the same inner hair cell
-single afferent fibers branch to synapse with several outer hair cells
Efferent fibers and hair cells
-cell bodies in the superior olivary complex of brainstem
-synapse directly on outer hair cells and on afferent fibers of inner hair cells
tonotropic organization of cochlea
-high freq stim.= near narrower base (stiff, near stapes)
-low freq stim= near wider apical side of basilar membrane
outer hair cells as amplifiers
-change length to amplify motion of the basilar membrane-->generate vibrations that travel backwards--> vibrate tympanic membrane--> generate otoacoustic emissions
-contain mt's for motile props
-12,000 total (strial side)
inner hair cells as sensory receptors
-main transducer
-20 afferent fibers and 20 independent synapses per
-3500 total (modiolar side)
cuticular plate
-apical portion of all hair cells
-thickened region
-in conjunction with supporting cells forms the reticular lamina
stereocilia
-stiff, hair-like structures that deflect with mech disturbances
-rooed in the cuticular plate of each hair cell
-connected to each other by filamentous cross-links and tip-links
traveling wave
-produced as pressure waves are transmitted from middle ear to the cochlea--> cochlear fluid is displaced--> wave like motion along basilar membrane
hair cell function and synaptic stimulation
-movement of endolymph produces deflection of stereocilia --> opens ion channels of stereocilia --> +ions flow in --> depolar --> NT release stimulation auditory nerve fibers
conductive hearing loss
occlusion or dysfunction of the external and/or middle ear
sensorineural hearing loss
dysfunction of the cochlea and/or auditory nerve
function of vestibular apparatus
-maintain upright posture
-adjust head position in response to changes in posture
-coordinate eye movements with each other and to compensate for head movement
bony labyrinth
-space in temporal bone
-lined with membrane
-gap filled with perilymph
membranous labyrinth
-filled with endolymph
-divided into cochlear and vestibular labyrinths
Maculae
-in utricle and saccule (vestibular)
-detect linear acceleration
otolithic membrane
-cover hair cells in macula epith
-made of Ca2+ carbonate crystals (make it denser than endolymph)
maculae sensory pathway
-movement of membranous lab-->endolymph movement lags in vestibule-->inertia --> stereocilia deflection toward kinocilium leads to hair cell deplarization--> tip links open membrane channels --> depolarization
macula orientation
-utricle: horizontal (forward-backward, side-side)
-saccule: vertible (forward-backward, up-down)
crista ampullaris
-in each semicircular canal
-detects angular movement
-sensory epith covered by gelatinous material = the cupola
crista ampullaris pathway
rotation of head--> rotation of bony lab --> movement of endolymph in membranous lab --> inertia makes endolymph lag and be in opp direction --> deflect cupola --> deflect stereocilia toward kinocilia --> hair cells depolarize and inc NT release --> synpase with aff and eff fibers nasally
functional pairs of semicircular canals
-R horiz/ L horiz
-R sup/ L post
-R post/ L sup
CN VIII (vestibulocochlear)
-bipolar cells
-nuclei in vestibular (scarpa's) gang --> lateral end of internal acoustic meatus
-central processes synapse onto vestibular nuclei --> low pons and medulla
vestibular nuclei
-caudal pons (superior and lateral)
-rostral medulaa (medial and inferior)
lateral vestibulospinal tract function
-maintains balance and posture
-input to vestibular nuclei via CN VIII
LVST route
-descends ipsilaterally from lateral vestibular nucleus to all spinal cord levels
LVST mech
-excites extensor muscles of neck, back and lower limbs (antigravity muscles)
-inhibits flexor muscles
-modified by info from inner ear and cerebellum
MVST function
-adjust head position in response to postureal changes
-coordinates eye movements with ea other
-coordinates eye movements to compensate for head movements
MVST pathway to adjust head position
-descends bilaterally from medial vestibular nucleus to cervical spinal cord levels
MVST pathway to coordinate eye movement with each other
-projects superiorly and bilaterally along medial longitudinal fasciculus (MLF) from vestibular nuclei to paramedian pontine reticular formation (PPRF)--> projects to the ipsilateral abducens nucleus --> contralateral oculomotor nucleus
central pathways for vestibulocular reflex (VOR)
-semicirc canals detect head movement toward L--> send signal to vestibular nuclei--> project to brainstem nuclei controlling extraoc. muscles--> contract--> move eyes to R to maintain foveation
nyastagmus
-rhythmic oscillations of the eyeballs
-from rotation of head, observing a moving object, temp-generated convection currents
train moving from R-->L, experience...
R nyastagmus
movement of warm water in L ear canal...
L-beating nystagmus

(COWS)
movement of cold water in L ear canal...
R-beating nystagmus

(COWS)
where do auditory nerve fibers synapse
in cochlear nucleus
recognition of sound pathway
-dorsal and ventral cochlear nuclei--> contralateral inf colliculus via lateral lemniscus
localization of sound pathway
ventral cochlear nucleus--> superior olivary complex in pons --> binaural convergence --> projects to inf colliculus
Inferior colliculus role is auditory pathways
-relays both recognition and localization pathways
-to medial geniculate nucleus of thalamus
-MGN fibers terminate in 1* aud cortex in superior temporal lobe
Wernicke's area
-speech interpretation
-cuases expansion of L cortex
topography in auditory system
-limited use
-multiple decussations and commissures so info from each ear ascends on both sides of brain
topography of auditory receptor array
-thin end of basilar membrane (basal) = high freq
-thick end (apical) = low freq
-thus, tono-topic
receptive field of an auditory nerve
-region os basilar membrane to which it is responsive
-best freq= characteristic freq
freq tuning curve
-describes how well a cell responds to higher and lower freq's
-increasing sound intensity makes tuning curve broaden
preservation of freq sensitivity
-preserved in relative positions of fibers and cells within each pathway
-maps are found in most maj auditory nuclei (ie inf colliculus, 1* and 2* auditory cortex)
Cortex around A1
-responsible for higher order processing of sound
-Wernicke's for speech analysis
-Broca's for speech production
lesions of auditory cortex
-affect perception of complex sounds like speech
-ie wernicke's aphasia (doesn't produce speech bc doesn't understand)
unique quality of cells in auditory cortex
-can be selectively responsive to complex features of sounds
-ie audiogram showing speech sounds are composed of an initial formant that changes over time, followed by a sustained tone
higher order cortical areas for auditory
-can contain cells that are selectively responsive to combos of tones
how do ears locate a sound
-use binaural time and intensity differences in the two ears
Superior olivary complex and auditory system
-contains cellular structures uniquely designed to detect auditory time and intensity differences
temporal coincidence
-circuitry in superior olivary complex that can create a neural code for location in space
-neurons need simultaneous input from each ear to fire
vertigo
illusory sense of environmental or personal rotation
(vestibular)
dysequilibrium
inability to maintain a normal gait and upright posture
(cerebellum, proprioception, vestibulospinal, motor)
diplopia
-usually binocular, can be mono
(CN disorders, retinal detachment)
syncope
loss of consciousness with loss of postural tone
(CV, pulmonary, hematologic, neurologic)
vestibular system
-semicircular canals, utricle, saccule
-endolymph is circulated by inertia to maintain equil during head motion
cochlear system
-sound is converted to vibration and transmitted through cochlear duct
activation of the unilateral horizontal canal
eyes deviate contralaterally
activation of the anterior canals
eyes deviate up
activation of the posterior canals
eyes deviate down
Deviation of eyes to L...
R system activates and L system deactivates to push you out of equil.

applies only during VOR
Head turn to the left:
-activates L vestibular system
-inhibits R vestib system
-allows eye deviation to R
nystagmus in vestibular disorders
-slow phase beats towards hypoactive vestibular system
-fast pahse towards hyperactive side
fast phase of nystagmus
-mediated by the cortex
-rapidly corrects slow deviation and tries to maintain straightforward gaze
-5 brief episodes of dizziness, no hearing loss
-once acute hearing loss, vertigo, imbalance
-slow phase nystagmus to R
-ischemic stroke in R vesitbular system
-in labyrinthine artery (accompanies CN VII, VIII into internal acoustic meatus)
-acute vertigo when getting out of bed for 15-30s
-episodes triggered by turning over on R side in bed
-slow phase to L
-recently had dental work-- head tilted way back
-BPPV on R side
benign paroxysmal positional vertigo (BPPV)
-otoconia detach from wall of utricle and fall into a SCC
-activate the system on that side by creating currents in the endolymph
Dix-Hallpike maneuver
-for diagnosing BPPV
-turn head toward side you think is affected--> push person down as fast as you can--> fast phase toward ground, slow phase away from ground
Epley maneuver
-treating BPPV
-pt's head slowly rotated through sequential positions, flushing ocotonia thorugh SCC, stay upright after for 24-48 hrs
-get otoonia into utricle where they can reanneal
sound vibrations and window flexing
-round window flexes outward at scala tympani, thereby allowing oval window to flex inward into scala vestibule and vice versa
-nystagmus with fast to R
-recurrent vertigo when straining, loud music, pushing R ear
-R peri-lymphatic fistula (activating)
perilymphatic fistula
-activating
-allows leakage of endolymph --> current activates vesitbular system
-abrupt episodes of vertigo, nausea, vomiting
-slow phase to L
-also thrown to floor
-now has diminished hearing on R
-R Meniere's disease (activating)
Meniere's Disease
-abnormal accumulation of endolymph
-mixes with perilymph from cochlear system, activates vestib system
-triggered by barometric pressure and high salt intake
Tumarkin's otolithic crisis
-sudden falls, being thrown to the floor
-d/t interruption of vestibulospinal tract activity --> lose equilibrium
Pike's peak audiogram
-lose low freq hearing, then high freq hearing, middle freq intact
-seen in Meniere's over time
-persistent severe vertigo
-cough, rhinorrhea, fever
-slow phase to L
-generalized imbalance
-L vestibular neuritis (inhibiting)
vestibular neuritis
-2nd most common cause of vertigo
-inflamm of vestib. nerve (not gang)
-slow phase towards abnormal side
-hearing preserved
-symptoms for 48 hrs to 6 weeks
-2 mo in hospital for periotonitis
-severe balance problem
-no vertigo or hearing loss
-can't read signs while driving
-no nystagmus
-Aminoglycoside induced ototoxicity
-treatment for peritonitis killed hair cells so fluid moves but nothing is activated
-severe vertigo and spatial disorientation
- decreased hearing on R
-hyperventilation --> fast phase to L with severe vertigo, nausea, vomiting
-cerebello-pontine angle tumor on R (inhibiting)
Cerebello-pontine angle tumor
-vestibular schwannoma
-meningioma
Cerebello-pontine angle tumor and hyperventilation
-reduces CO2, altering endolymph production
-compromised vestibular system cannot fully compensate for because of tumor
-car sickness as child
-vertigo often followed by unilateral pulsatile headache
-more freq around menses
-dix-hallpike: severe downbeat nystagmus
-migraine manifesting as dizziness
-paroxysmal episodes of severe vertigo
-confusion
-vertigo assoc with perception of environmental tilt
-seizure
-"tornade epilepsy"
-abnormal cortex firing gives perception of vertigo