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Neuroscience > Test 5 > Flashcards

Test 5 Flashcards

1
Q

CN I

A

olfactory nerve

olfaction

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2
Q

CN II

A

Optic nerve

vision

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3
Q

CN III

A

Oculomotor nerve

levator palpebrae superior and all extra ocular muscles, except for superior oblique and lateral rectus

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4
Q

CN IV

A

Trochlear nerve

superior oblique muscle; causes depression and intorsion of the eye

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5
Q

CN V

A

Trigeminal nerve

sensations of touch, pain, temp, jt position, and vibration for the face, mouth , anterior 2/3 of tongue, nasal sinuses, and meninges

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6
Q

CN VI

A

Abducens nerve

Lateral rectus muscle; causes abduction of the eye

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7
Q

CN VII

A

facial nerve

  • Muscles of facial expression, stapedius muscles, and part of digastric muscle
  • parasympathetics to lacrimal glands, and to sublingual, submandibular, and all other salivary glands except parotid
  • taste from anterior 2/3 of tongue
  • Sensation fro a small region near the external auditory meatus
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8
Q

CN VIII

A

vestibulocochlear nerve

  • hearing and vestibular sensation
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9
Q

CN IX

A

Glossopharyngeal

  • stylopharyngeus muscle
  • parasympathetics to parotid gland
  • sensation from middle ear, region near the external auditory meatus, pharynx, and posterior 1/3 of tongue
  • taste from posterior 1/3 of tongue
  • chemo- and baroreceptors of carotid body
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10
Q

CN X

A

Vagus nerve

  • Pharyngeal muscles (swallowing) and laryngeal muscles (voice box)
  • parasympathetics to heart, lungs, and digestive tract down to the splenic flexure
  • sensation from pharynx, meninges and a small region near the external auditory meatus
  • taste from epiglottis and pharynx
  • chemo and baroreceptors of the aortic arch
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11
Q

CN XI

A

spinal accessory nerve

  • sternomastoid and upper part of trapezius muscle
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12
Q

CN XII

A

hypoglossal nerve

  • intrinsic muscle of the tongue
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13
Q

cerebellopontine angle

A

region where CN 7-9 exit brainstem

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14
Q

where does olfactory nerve exit

A

Cribriform plate

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15
Q

where does optic nerve exit

A

optic canal

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16
Q

where does oculomotor nerve exit

A

superior orbital fissure

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17
Q

where does trochlear nerve exit

A

superior orbital fissure

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18
Q

where does trigeminal nerve exit

A

V1: superior orbital fissure
V2: foramen rotundum
V3: foramen ovale

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19
Q

where does abducens nerve exit

A

superior orbital fissure

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20
Q

where does facial nerve exit

A

auditory canal (stylomastoid foramen)

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21
Q

where does vestibulocochlear nerve exit

A

auditory canal

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22
Q

where does glossopharyngeal nerve exit

A

jugular foramen

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23
Q

where does vagus nerve exit

A

jugular foramen

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24
Q

where does spinal accessory nerve exit

A

jugular formanen

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25
Q

where does hypoglossal nerve exit

A

hypoglossal formen

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26
Q

how does smell get to temporal lobe?

A

Special chemoreceptors in the nasal mucosa of the upper nasal cavities detect odor.

Axons of these neurons travel via short olfactory nerves through the cribriform plate to synapse on the olfactory bulbs

sensory information is relayed via olfactory tracts to the primary olfactory cortex in the temporal lobe

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27
Q

Anosmia

A

Unilateral deficits: usually not noticeable because the contra nostril can compensate

bilateral deficit: anosmia, and patients will often c/o decreased taste due to the important contribution of olfaction to perception of flavor

-caused by head trauma, viral infections, nasal obstruction, neurogenerative diseases, intracranial lesion at base of frontal lobes

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28
Q

Parasympathetic fibers of CN III

A

pupillary constrictor muscles

ciliary muscles of lens (for near vision)

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29
Q

Course of CN III

A

exist ventrally at the interpeduncular fossa
-preganglionic parasympathetics - synapse in ciliary ganglion in orbit

  • postganglionic parasympathetics - continue to pupillary constrictor muscles and ciliary muscles in orbit

travel through cavernous sinus and exit skull at the superior orbital fissure

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30
Q

course of CN IV

A

exits dorsally at the inferior tectum

travel through cavernous sinus and exit skull at the superior orbital fissure

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31
Q

course of CN VI

A

exits ventrally at the pontomedullary junction

travel through cavernous sinus and exit skull at the superior orbital fissure

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32
Q

Course of CN V

A

exists ventrolateral pons and then enters a small fossa (Meckel’s cave)

ophthalmic division- enters cavernous sinus to exit at the superior orbital fissure

maxillary division- exits via foramen rotundum

mandibular division - exist via foramen ovale

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33
Q

Mesencephalic trigeminal nucleus (midbrain)

A
  • Proprioception
  • includes jaw jerk reflex
  • cross and ascend via mesencephalic trigeminal tract -> central pathways are still being investigated
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34
Q

chief trigeminal sensory nucleus (pons)

A
  • fine/discriminative touch and dental pressure

- cross and ascend via trigeminal lemniscus -> VPM -> PSC

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35
Q

Spinal trigeminal nucleus (Pons and medulla)

A
  • Pain temp and crude touch

cross and ascend via trigeminothalamic tract -> VPM -> PSC

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36
Q

What happens the jaw with unilateral lesions to cortex or corticobulbar?
in UMN vs LMN

A

UMN: causes no deficit in jaw movement
UMN control to CN V motor nucleus is bilateral

LMN: lesions to the nerve LMN causes ipsilateral jaw weakness. jaw will deviate towards side of lesion (weak side)

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37
Q

trigeminal neuralgia

A

Most common CN V disorder

  • brief severe pain lasting from seconds to a few minutes
  • cause is unkown
  • most often in V2 or V3 sensory distribution
  • painful episodes triggered by chewing, shaving, etc
  • facial sensation is normal on exam
  • initial treatment is with medications
  • –> if medications are unsuccessful, more aggressive treatment can be useful
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38
Q

lesions to the nerve or the CN V sensory nucleus

A

ipsilateral loss of facial sensations (primary fibers donot cross before entering the nucleus)

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39
Q

lesions to ascending tracts or face area of PSC

A

contralateral loss of facial sensations (fibers cross after exiting the nucleus)

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40
Q

jaw jerk reflex

A
  • Tap on the chin with the mouth slightly open
  • the reflex is minimal or absent in normal individuals
    • the response is the jaw jerking slightly forward or absence of movement
    • bilateral UMN lesions could cause hyperactive (brisk)) jaw jerk reflex
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41
Q

monosynaptic pathway

A
  • sensory axons heading to the mesencephalic trigeminal nucleus also send axons to synapse on the trigeminal motor nucleus
  • motor axons from trigeminal motor nucleus travel via V3 to the muscles of mastication
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42
Q

Parasympathetic fibers of facial nerve

A

Lacrimal glands (tears) and salivary gland (saliva)

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43
Q

sensation of the facial nerve

A

small area near external auditory meatus

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44
Q

CN VII nucleus

A
  • nucleus is in the lower Pons

- fibers loop dorsally around the CN VI nucleus at the floor of the 4th ventricle to form the facial colliculus

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45
Q

Course of CN VII

A

nerve exits brainstem ventrolaterally at the pontomedullary junction in a region called the cerebellopontine angle

enters internal auditory meatus to travel in auditory canal along with CN VIII. then enters the facial canal and travels to the stylomastoid foramen to exit skull

-divides intofive major branches to controlmuscles of facial expression

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46
Q

Parasympathetics of CN VII preganglions

A
  • Preganglionic orginate in superior salivatory nucleus

- two branches greater petrosal nerve (lacrimation) and chorda tympani (salivation)

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47
Q

Taste from CN VII

A

taste to anterior 2/3 of tongue
Primary sensory neurons synapse in nucleus solitaries
-ascend via Central tegmental tract -> VPM -> Cortical taste area
—-taste projects to bilateral cortical taste areas

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48
Q

sensation of facial nerve

A

small area of skin near external auditory meatus

sensory fibers synapse in CN v sensory nuclei

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49
Q

CN VII: LMN facial weakness

A

ipsilateral CN VII consists of LMN that innervate the ipsilateral muslces of facial expression

Lesions to ipsilateral CN VII cause weakness of the ipsilateral half of the face

LMN to forehead and eye muscles get bilateral innervation from cortex
LMN to below eye get contralateral innervation only from cortex

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50
Q

CN VII: UMN facial weakness

A

Lesions to contralateral PMC cause weakness of contra facial muscles below the eye

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51
Q

Bell’s Palsy

A

Most common CN VII disorder

  • unilateral facial weakness of the LMN type
  • –> sever cases eye willnnot close, loss of salivation, lacrimation, and taste from ipsilateral anterior 2/3 of the tongue

cause unknown, can be from viral, inflammatory or immune disorder

recommended treatment is 10 days of oral steroids after onset

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52
Q

corneal reflex

A

afferent- sensation to the cornea of the eye is from CN V
Efferent- innervation to facial muscles is from CN VII

Eye closure in response to lightly touching the cornea

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53
Q

What make sup te outer ear , middle ear and inner ear?

A

Outer -external acoustic meatus

Middle ear- tympanis membrane, ossicles and e7stachian tube

Inner- semicircular canals, vestibule ,cochlea, cn VIII

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54
Q

What are the two branches of the vestibulocochlear nerve

A

Cochlear branch and the vestibular branch

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55
Q

Cochlear branch of vestibulocochlear nerve

A

Hearng and detection of sound waves

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56
Q

Vestibular branch of vestibulocochlear nerve

A

Vestibular sensation and head position (relative to space/gravity) and head movement (relative to body)

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57
Q

How does CNVIII travel

A

Exits the brainstem at te oontomedullary junction.
Enters subarachnoid space to enter internal auditory meatus

Travels with CN VII in auditory canal through temporal bone to enter the cochlear and vestibular organs

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58
Q

Bony and membranous labyrinth

A

Bony labyrinth is filled with fluid called perilymph.
The structures of the membranous labyrinth are suspended in the perilymph

Membranous labyrinth is filled with fluid called endolymph. Contains semicircular canals, utricle and saccule and cochlear duct

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59
Q

What is cochlea?

A

Snail shaped organ formed by spiraling, fluid-filled tube

-contians the scala vestibuli and scala typani with the cochlear duct in between them

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60
Q

What is basilar membrane

A

Is between the cochlear duct and scala tympani and it extends the entire width of the cochlea

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61
Q

Organ of corti

A

Is in the cochlear duct, residing on the basilar membrane

— consists of hair cells, techtorial membrane and terminals of cochlear nerve

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62
Q

How do we convert sound to neural signals?

A

Sound waves hit tympanic membrane causing vibration of ossicles. This causes vibration of the oval window causing movement of the perilymph.

Movement of the perilymph causes te adjacent basilar membrane and attached hair cells to move and thus bend.

Bending of hair cells bend results in excitation, stimulating the cochlear nerve.

High freq sounds activate hair cells closer to tenoval window and lower freq sounds activate hair cells closer to the apex of teh cochlea

63
Q

Auditory pathways travel where

A

Axons of the CN VIII travel to the dorsal and ventral cochlear nuclei

  • fibers from both nuclei cross over via the trapezoid body. Ventral cochlear fibers synapse bilaterally in the superior olivary nuclei
  • fibers ascend in the lateral lemniscus to the inferior colliculus
  • fibers cross and ascend in brachium of inferior colliculus to the MGN
64
Q

Small CNS lesions and hearing?

A

Rarely cause unilateral loss of hearing because auditory information projects bilaterally in brainstem and cerebrum

65
Q

Areas of the primary auditory cortex?

A

Heschel’s gyri area 41

Conscious awareness of teh intensity of sounds auditory association cortex (sup temporal gyrus)

Compares sounds with memories of other sounds and classifies sounds (area42) (as language , music, noise, etc)

Wernicke’s area 22- language comprehension

66
Q

Unilateral hearing loss

A

Damage to external auditory canal, middle ear,cochlea, organ of corti, cochlear nerve, or cochlear nuclei

Loss of hearing in one ear interferes with the ability to locate sounds because the timing of auditory information from each ear is compared to locate sounds

67
Q

Hearing loss is categorized as…

A

Conductive and sensorineural

68
Q

Conductive hearing loss

A

Caused by abnormalities in outer or middle ear

Wax build up, otitis media, tympanic membrane tear

69
Q

Sensorineural hearing loss

A

Caused by disorders of cochlea or CN VIII

Prolonged exposure to loud noise, ototoxic drugs, meniere’s disease, acoustic neuroma

70
Q

Basic hearing can be tested with….

A

Different frequencies

Finger rubbing, ticking watch, tuning fork

71
Q

Acoustic neuroma

A

Compresses CNVIII where it enters internal auditory meatus

Most common tumor at teh cerebellopontine angle

Almost always unilateral
Causes slow,progressive unilateral hearing loss

Patients also c/o tinnitus (ringing in ears) and balance problems

Mean age of onset is 50 yo

As tumor grows, can then include CN VII and CN V

Removed surgically

72
Q

Vestibular apparatus

A

For ed by the semicircular canals and vestibule (contains utricle and saccule)

Also has a bony labyrinth with perilymph.
Structures of the membranous labyrinth are suspended in the perilymph. Membranous labyrinth is filled with fluid called endolymph. Contains utricle and saccule (otolith organs), semicircular canals, and cochlear duct

Semicircuar canals have small opening at each end into the utricle

73
Q

What do Semicircular canals detect?

A

Detect angular rotation of teh head (speed up or slow down the rotation of teh head)

The canals are perpendicular to each other

74
Q

What are teh tree pairs of canals?

A

-right and left anterior
—45 deg anterior tonfrontal plane

Right and left posterior
—45 deg posterior to frontal plane

Right and left Horizontal
—30 deg above horizontal plane

75
Q

Semicircular canals working as coplanar pairs

A
  • right posterior and left anterior canals
  • right anterior and left posterior canals
  • right and left horizontal canals
76
Q

Ampulla

A

Bulge located at one end of each semicircular canal

  • hair cells are located on crista ampullaris and have cilia connected to them
  • teh cilia of teh hair cells project up into the cupula
  • movement of endolymph causes cupula tonbend
  • this results in deflection of the cilia causing excitation or inhibition of hair cells
77
Q

What do hair cells lead to neural firing?

A

Hair cells convert displacement due to angular head rotaton into neural firing and send axons into the vestibular nerve

78
Q

How does each SCC move in its own plane during angular motion

A

Each SCC respond best to motion in its onw plane.

When angular motion occurs within their shared plane, each SCC of tge pair reproduces reciprocal signals

Excitatory signals from one canal occur simultaneously with inhibitory signals from te other canal

During ipsi head rotations , ipsi afferents are excitated

Brian detect direction of head movement by compairing input from coplanar planes

79
Q

Otolith organs

A

Respond to linear motion and static head tilt with respect to the gravitational axis

Otoliths are calcium carbonate crystals are embedded in te top of the gelatinous layer to give it mass

80
Q

Utricle

A

Excitation occurs during horizontal linear motion and head tilt

81
Q

Saccule

A

Excitation occurs during vertical Linear motion

82
Q

Maccula

A

Are contained inside the utricle and saccule

Contain short HC projecting up into a gelatinous layer

Otoliths are embedded in the top of the gelatinous layer to give it mass

Linear motion and head tilt causes otoconia to move and hence gelatinous layer and HC to move

HC convert displacement into neural firing and send axons into the vestibular nerve

83
Q

Vestibular nuclei

A

They lye on the lateral floor of the 4th ventricle in pons and rostral medulla

Adjust posture, muscle tone, and eye position inresponse to movements of teh head in space

Have many connections with cerebellum, brainstem motor systems, and extraocular systems

Sends awareness of head position to parietal association cortex that is integrated with visual and tactile information to contribute tonspatial awareness

84
Q

Lateral vestibular nucleus

A

Gives rise tonlateral vestibbulospinal tract

Extends entire length of cord

Important role in maintaining balance and extensor tone

85
Q

Medial vestibular nucleus

A

Largest of teh vestibbular nuclei

Gives rise to medial vestibbulospinal tract

Extends to cervical spine

Important role in controlling head and neck position

86
Q

Medial longitudinal fasciculus MLF

A

Pathways connecting vestibbular nuclei to oculomotor, trochlear, and abducens nuclei

Fibers from mainly superior vestibular nucleus and also inferior vestibular nucleus ascend in MLF to CN III,IV and VI nuclei

Function to match eye movements resulting in conjugate gaze in all direction

Mediates the vestibulo-ocular reflex in which eye movements are adjusted for changes in head position

87
Q

Vestibular nuclei send information toooo….

A

Send to mainly the flocculonodular lobes and the vermis of cerebellum. Regions called vestibulocerebellum

  • lateral temporoparietal junction and posterior insula. Head position and movement
  • CN XI nucleus to influence head position
  • reticular formation. To influence reticulospinal tracts (posture and gait) and autonomic centers for nausea and vomiting
88
Q

True vertigo

A

Spinning sensation of movement. Themselves or room spinning

Can be caused by lesions anywjhere along the vestibular pathways from the labyrinth,CnVIII, vestibular nuclei, cerebellum , to the cortex.

Most often is from peripheral vestibular disorders (affect structures of the inner ear)

89
Q

Eye movement disorders and pathways are divided into two levels:

A

Nuclear and infranuclear pathways

Supranuclear pathways

90
Q

Nuclear and infranuclear pathways

A

CN II, IV, an dVI their peripheral nerves and teh extraocular muscles

91
Q

Supranuclear pathways

A

Brainstem and forebrain circuits that control eye movements

—connect with CN III,IV, and VI nuclei

92
Q

Extra ocular muscles muslces origination

A

Common tendinous ring at apex of orbit

Muslces insert into the sclera

93
Q

Oblique eye muscles

A

Torsional movements

- eye is slightly rotated about its axis

94
Q

Superior oblique

A

Inserts n superior surface
-Produces primarily intorsion
—

95
Q

Inferior oblique

A

Inserts on inferior surface
—produces primarily extorsion
—movement of teh upper pole of teh eye outward

96
Q

With teh eye adducted the sperior oblique causes

A

Depression

97
Q

With teh eye abducted the inferior obllique causes

A

Elevation

98
Q

Innervation to extraocular muscles

A

LR by CN VI
SO by CN IV

And teh rest supplied by CN III

(LR6 SO4)3

99
Q

CN III has two major branches

A

Superior division

Inferior division

100
Q

Superior division of CN III

A

Innervate levator palppebrae superior (elevates eyelid)

Innervates superior rectus

101
Q

Inferior division of CN III

A

Contains parasympathetic fiber to pupillary constrictor muscles and ciliary muscles of teh lens

Innervates teh other extraocular muscles (except LR and SO)

102
Q

Oculomotor nuclei

A

In the upper midbrain (level of superior colliculi and anterior to PAG)

CN III exits anteriorly between posterior cerebral artery and superior cerebellar artery

-Parasympathetic fibers run in teh superficial an dmedial portion of CN III
—

103
Q

Trochlear nuclei

A

-In the lower midbrain (level of teh inferior colliculi and anterior to PAG)

-CN IV
—

104
Q

Abducens nuclei

A

In the mid/lower , posterior pons (floor of 4th ventricle)

CN VI exits at the pontomedullary junction

-Ascends and exits teh dura to enter Dorello’s canal

  • has long,ascending, vertical course to reach teh orbit
  • highly susceptible to downward traction injury produced by elevated ICP
105
Q

Diplopia

A

-Can be caused by abnormalities in several locations
—mechanical problems: orbital fx with muscle entrapment

—the extraocular muscles: orbital myositis

  • the neuromuscular junction: myasthenia gravis
  • CN III,IV, VI and their central pathways

-the supraanuclear ocular pathways
—ingestion of toxins
—anticoagulant medications

106
Q

Dysconjugate gace

A

Occurs when an extraocular muscle iis not working properly and teh result is diplopia

Over time will cause suppression ofone of the images, which will resultt in amblyopis (decreased vision in one eye)

-early intervention is extremely important

107
Q

PComm aneurysm

A

Highly suspected in pts with a painful CN III palsy involving the pupil

  • CN III palsy may be subtle or complete
  • a Pcomm aneurysm is considered teh diagnosis until proven otehrwise
  • emergency CT angiogram needed immediately
108
Q

Trochlear palsy

A

CN IV causes depression and intorsion, so with these movements unopposed the eye will rest in hypertropia and extorsion

  • causes vertical diplopia
  • diplopia can be improved by tucking chin and by tilting head away from the affected eye (these head movements produce the movements that the eye muscles would normally do)
109
Q

Relationship between compensatory head position and eye movement abnormalities

A

Head movement is always in teh direction of teh action normally produced by the affected muscle

110
Q

Right CN IV palsy how would the head move?

A

The head down/chin tucked, and head tilted to the left (CN IV acions are normally depression and intorsion)

111
Q

Abducens palsy

A

CN VI causes eye abduction

Lesion to teh CN VI will result in horizontal diplopia

Diplopia worse when objects are far and better when looking at objects that are near

112
Q

Which way will your patient turn his/her head in attempt to compensate for horizontal diplopia?

A

Towards the affected eye (lateral rotation of the head)

113
Q

Common cause of abducen palsy

A

Downward traction from elevated ICP

Infection
Neoplasm
Aneurysms
Microvascular damage
Etc
114
Q

Pupillary light reflex

A

Light entering one eye activates CN II which projects to the optic tracts

Extrageniculate fibers project to the pretectal area of the midbrain

Synapse occurs at the pretectal nuclei

Fibers then project bilaterally to synapse at the Edinger-westphal nuclei
- cross at teh posterior commissure

Then fibers travel with CN III. Synapse occurs at teh ciliary ganglia on the orbit

Post ganglionic prasympathetic fibers then target pupillary constrictor muscles

115
Q

Light shown in one eye causes

A
  1. Pupillary constriction (diract response in that eye

2. Pupillary constriction (consensual response) in the other eye

116
Q

Ciliary muscles

A

Adjusts thickness of the lens in response to changing viewing distances

The lens focuses the image on the retina

Visual cortex signals pretectal nuclei that image is out of focus. Parasympathetics to teh ciliary muscle are activated to adjust the shape of the lens

117
Q

Sympathetic Pathway: Pupillary dilation

A

Visual cortex sends signal to autonomic nuclei in the hypothalamus

Dscending neurons travel in lateral brainstem and cervical cord to the T1-T2 level

Synapse occurs on preganglionic sympathetic neurons in teh intermediolateral cell column

Preganglionic sympathetic neurons enter the sympathetic trunk

Ascend to synapse on superior cervical ganglion

Postganglionic sympathetic neurons ascend beside the ICA to the orbit to the synapse on pupillary dilator muscle

118
Q

Superior tarsal muscle

A

Elevates upper eyelid during increased sympathetic outflow

119
Q

Orbitalis muscle

A

Prevents eye from sinking back in the orbit

120
Q

Pupillary abnormalities

A

Can have many causes:
- Peripheral or central lesions, sympathetic or parasympathetic lesions, or disorders of the iris muscle or visual pathways

Can be bilateral or unilateral

121
Q

Anisocoria

Why is it more obvious in a lit room than a dark room? Why?

A

Pupillary asymmetry

In a room with light, it should be constricting, but will stay a “blown pupil” due to loss of teh pasasympathetic for pupillary constriction

122
Q

CNIII lesion

A

With a complete lesion, the pupil is very large “blownn pupil”

Will also likely see ptosis (drooping of upper eyelid) and eye movement abnormalities associated with CN III function

123
Q

Horner’s syndrome

A

Lesion affecting teh sympathetic pathway to face and eye

TRIAD
Consists of ipsi: Ptosis, miosis (decr pupillary size), anhidrosis (decr sweating of face and neck)

Can be caused by a lesion anywhere that affects the sympathetic pathway to face and eye.

124
Q

17 yo male present sto teh ER with a GSW to L side of neck just above the clavicle with a L lung collapse

The pt exhibits…?

A

L ptosis
L miosis: L2mm R 4mm
L forehead smooth to touch compared to R: Hit his parasympathetic pathways

125
Q

Ptosis

A

Drooping of upper eyelid

-upper lid comes down further over the iris in the affected eye

126
Q

Common causes of Ptosis

A

horners syndrome
CN III palsy
Myasthenia gravis, orbital mass , excess skin folds

127
Q

Widended palpebral fissure

A

Sagging of lower face due to UMN lesion can slightly widen the palpebral fissure and pull the eyelid down slightly as well

Examine entire eyelid using iris as a reference point

Examine the facial muscles below the eye

128
Q

Supranuclear control of eye movement

A

Pathways in teh CNS for eye movement control via activation of CN III, IV, VI nuclei: horizontal, vertical, vergence

Also generate eye moment for other purposes: saccades, smooth pursuit, vergence, reflex eye movements

129
Q

HOrizontal eye movement circuit

A

Actions of CN III, IV, VI nuclei coordinated through the medial longitudinal fasciculus.

Cn VI nucleus acts as horizontal gaze center.

130
Q

To move eyes to the left… what does the CN VI do

A

Neurons from teh L CN VI nucleus project to L lateral rectus

Other neurons from L CN VI nucleus project to R CN III nucleus to R medial rectus

131
Q

Paramedian pontine reticular formation

A

Serves as ahorizontal gaze center via input to CN VI nuclei

132
Q

Vertical eye movement circuit

A

Brainstem centers for controlling vertical movement are in teh upper midbrain reticular formation and pretectal area

133
Q

Cortical control of eye movements

A

-input to teh PVC and visual association cortex

Multiple pathways descend from teh cortex to control eye movement circuits.

Frontal eye fields- best-known cortical area that controls eye movement

134
Q

Saccades

A

Rapid eye movement to switch gaze from one object to another

-velocities of 700/sec

135
Q

Smooth pursuit

A

Allows for the stable viewing of moving objects

-100/sec

136
Q

Vergence

A

Movement of eyes toward or away from midline as targets move towards or away from the viewer

137
Q

Reflex eye movement

-Nystagmus

A

Composed of slow eye movementt in one direction interrupted repeatedly by fast movement in teh opposite direction. Ex falling asleep in class

Normal nystagmus occurs during attempts to view a visual scene moving in front of the eyes

Nystagmus abnormal when it occurs at rest

138
Q

Reflex eye movements

-Vestibul-ocular refelx VOR

A

Stabilizes teh eyes on a visual image during head movements

  • Inputs from vestibular nuclei travel in the MLF to control the extraocular eye muscle nuclei
  • cerebellum and proprioceptors of cervical SC also influence VOR
139
Q

VOR demonstration

A

Focus on your finger in front of your and turn your head side to side, noting the stable image of your finger

140
Q

What do we mean by dizziness?

A

Vague term

lightheadedness, faintness, nausea, unsteadiness

141
Q

Benign paroxysmal positional vertigo

A

Sudden change in head position resulting in vertigo and nystagmus.

Otoconia from nearby macula dislodge and float into a SCC. usually caused by trauma or virus. the new position of otoconia causes abnormal movement of the endolymph and bending of cupula causing abnormal signals in CN VIII

142
Q

vestibular neuritis

A
  • inflammation of vestibular nerve
  • caused by virus
  • causes several day of intense vertigo, disequilibrium, nystagmus, and nausea with symptoms subsiding over a few weeks ago,
  • medications during acute phase may suppress vertigo and N/V
143
Q

Meniere’s disease

A
  • excess fluid and pressure in endolymph system
  • causes recurrent episodes of intense vertigo, fullness in ear, fluctuating hearing koss and N/V
  • medications during acute phase may suppress vertigo and N/V and with extreme cases vestibular nerve may be severed to relief symptoms
144
Q

motor function of the Glossopharyngeal muscle

A
  • movement of stylopharangeaus muscle: elevates the pharynx during swallowing and speech.
  • motor fibers arise from nucleus ambiguous in medulla
145
Q

CN X lesion will cause..

A

asymmetric elevation

  • soft palate will be lower on the side of the lesion
  • uvula will deviate towards the normal side
146
Q

CN XI LMN lesion will cause…

A

SCM: weakness of turning head towards opposite the lesion
UT: ipsilateral weakness of L shoulder shrug

147
Q

CN XI UMN lesion will cause…

A

SCM: UMN descend to the ipsilateral CN XI nucleus. wekness of turning head toward opp side

UT: UMN descend to the CONTRA CN XI nucleus. weakness on contra shoulder shrug

148
Q

CN XII UMN lesion will cause…

A

UMN from tongue area o fPMC travel with corticobulbar tract to synapse on contralateral CN XII nuclei

Ipsilateral lesion of PMC or UMN will cause contralateral tongue weakness

149
Q

CN XII LMN lesion will cause…

A

Ipsilateral lesion to CN XII nucleus or nerve fibers will cause ipsi tongue weakness
-tongue will deviate toward weak side

150
Q

Dysarthria

A

abnormal articulation of speech

  • motor articulary disorder
  • range from mild to unintelligible speech
  • occur with dysfunction of muscle of articulation
  • common causes: CVA,MS,ALS or anyotehr muscular disorder
151
Q

dysphagia

A

Impaired swallowing

  • can lead to aspiration of food, choking
  • caused by esophageal strictures, neoplasms,local lesions
  • can occur withdysfunction CN V, VII, IX, X, XII
  • aspiration pneumonia
152
Q

gag reflex

A

Protective reflex preventing entry of foreign objects into alimentary and respiratory passageways.
-CN IX and CN X

153
Q

Pseudobulbar affect PBA

A
  • uncontrollable bouts of laughter or crying w/o any appropriate emotional reasons
  • CN VII,IX,X, and XII
  • lesions of the corticobulbar pathways or brainstem can also produce this very unsual syndrome
  • common causes: CVA,MS,ALS, TBI, tumors, etc

Neuroscience (6 decks)

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