Cerebellum and Cranial Nerves Flashcards

1
Q

What is the Cerebellum used for?

What do lesions to the cerebellum lead to?

UMN syndrome or LMN syndrome?

A

motor output

lesions lead to deficits in motor output and mobility

lesions to cerebellum do not result in UMN syndrome (does not cause spasticity, hyper, pathological reflexes)

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2
Q

Does lesion to cerebellum cause UMN syndrome?

A

NO

lesions to cerebellum do not result in UMN syndrome (does not cause spasticity, hyper, pathological reflexes)

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3
Q

Cerebellum: motor or sensory?

A

not only a motor effector but takes sensory input

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4
Q

Cerebellum Function (5)

A
  1. coordinates activity, fluid movement and postures
  2. comparison of motor activities to intend plan and modify it if not achieved (continual loop)
  3. modification of motor output based on sensory input and motor output: continuous loop
  4. compensation for motor tasks: predictive / anticipatory
    big role in predictive movement: feed forward, anticipatory *if cerebellar lesion hard time with anticipatory balance but less impaired with reactive balance
  5. major role in learning new motor programs because of its modifying function
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5
Q

If Cerebellum Damaged

A

learning new motor programs is limited: challenge in PT because we depend on motor learning – here plasticity cannot occur

*if cerebellar lesion hard time with anticipatory balance but less impaired with reactive balance

depending on where lesion is in the cerebellum can change deficits

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6
Q

Vestibulocerebellum

another name

receives input from _____ and outflow to ________

lesions result in _________

what happens in lesion?

A

archicerebellum

receives input from and outflow to the vestibular nuclei

lesions result in inability to use vestibular inputs (even though vestibular input comes in)

luckily the pons can help to some extent

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7
Q

if lesion to vestibulocerebellum can vestibular input still come in?

A

YES

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8
Q

Spinocerebelleum

another name

role

receives input from _____ and outflow to ________

lesions result in _________

what happens in lesion?

A

paleocerebellum

input: from spinocerebellar tracts (alot from spinal cord)
outflow to:

movement completion: termination of movement
muscle tone: initiate–>accelerete –>peak –>deccelerate –>terminate

lesion of the spinocerebellum results in overshooting when reaching for something reach past object: abnormality in maintaining the muscle tone (ie in a rebound test)

big effect on muscle tone–spasticity is excessive tone
if i hold my arm out, agonists and antagonsits are being used to keep my arm in this position

(regulating muscle tone and in adapting the body to changing circumstances. )

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9
Q

Rebound Test

A

hold arm straight, ability to maintain tone because firing of muscles is equal and opposite on all sides maintaining muscle tone

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10
Q

What does lesion to spinocerebellum cause?

A

abnormality in maintaining the muscle tone (ie in a rebound test)

NOT IN FLACCIDITY
NOT IN RIGIDITY
but ability to maintain an EVEN tone

ie doorbell: lesion to spinocerebellum- amount of pressure put onto the doorbell did not stay the same because could not maintain an even pressure/tone

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11
Q

Cerebrocerebellum

  1. another name
  2. role
  3. receives input from _____ and outflow to ________
  4. lesions result in _________

what happens in lesion?

A
  1. neocerebellum
  2. control of rapid movements, sudden movements (throw a ball and he quickly reacts to catch it)
    precise movement control
    motor planning
  3. lateral cerebral hemispheres recieve input from pontine nuclei and has output to the thalamus, motor cortex, and premotor cortex
  4. dysmetria
    disdiadokinesia
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12
Q

Vestibulocerebellum (online)

input/output

function

damage

A

The vestibulocerebellum,receives a substantial amount of its input from the vestibular nerve. This is unique since no other portion of the cerebellum receives direct input from a sensory nerve.

Additionally, there are connections from the vestibular nuclei to the vestibulocerebellum.

The vestibulocerebellum is an important regulator of the vestibular system.
Most important function of this is to allow adaptation to vestibular damage.

Damage to this region will result in vertigo and nystagmus.

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13
Q

Spinocerebellum (online)

input/output

function

damage

A

important in regulating muscle tone and in adapting the body to changing circumstances.

receives extensive input from the spinal cord. several direct and indirect spinocerebellar pathways terminate in the spinocerebellum

The input from muscles and the spinal cord reflex pathways are necessary for proper regulation of muscle tone and movement.

Since the spinocerebellum includes both vermal and paravermal zones of the cerebellum, there are connections with both the fastigeal nuclei and the interposed nuclei.

The fastigeal nuclei, in turn, connect to the reticular formation can affect muscle tone and crude movements via the reticulospinal tracts.

The interposed nuclei connect predominantly to the contralateral red nucleus through the superior cerebellar peduncle, origin for the rubrospinal tract that mainly influences limb flexor muscles.

-Therefore, the spinocerebellum can influence both muscle tone and coordination of the extremities.

-cerebellum is important in determining the appropriate response to changing situations.
For example, when attempting to resist a force on the extremities, a sudden release of force would result in a rebound of the the limb. The ability to rapidly check this motion requires feedback from muscle stretch and tension receptors.

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14
Q

Neocerebellum (online)

input/output

function

damage

A

The neocerebellum receives the vast majority of its input from the pontine nuclei. The pontine nuclei receive input from the majority of the cerebral cortex via corticopontine fibers. The pontine nuclei project exclusively through the middle cerebellar peduncles to the cerebellum, where these axons terminate as mossy fibers. It is the largest input to the cerebellum and almost exclusive input to the neocerebellum (which comprises most of the lateral hemispheres of the cerebellum).

involved in regulating the cerebral cortical motor output. The best-known effect of this is in procedural learning. —Activities such as riding a bike or learning to ski involve activity of the cerebellar hemispheres.

Damage to the lateral hemispheres results in lack of coordination of limb movement, with overshoot and undershoot (intention tremor).

The discussion to this point has largely focused on control of balance and of skilled voluntary movements. In addition to these functions. the cerebellar vermis receives visual input from the superior colliculus and is involved in coordinating eye movements. It also coordinates speech. Drunken speech, for example, derives from the effect of alcohol on the vermal portions of the cerebellum.

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15
Q

Signs of Cerebellar Dysfunction

5 traits

A
  1. Dysmetria
  2. Asynergia/dysnergia
  3. Rebound phenomena
  4. Tremor
  5. Hypotonia
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16
Q

Dysmetria

what is it

word root

what happens as a result

A

inability to accurately judge speed (of movement), force (of movement), or distance needed for task

“difficulty” + “measurement”

miss the target, too much force, too little force, cannot grade the amount of force needed for the task

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17
Q

Asynergia/Dysnergia

what is it

A

movement decomposition
lack movement fluidity

parts of the body working together in a particular/effective way to accomplish a task in synergy

motor planning that needs cerebellum to function normally is not occurring

movement is fractionated

decomposition: movement is less fluid, more robotic, less smooth movement. broken into short static components, because amount of control to make it fluid is gone and the nervous system reconstructs the movement to accomplish the task

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18
Q

Rebound Phenomena

  • instructions
  • normal result
  • abnormal result
A

hold arm out in front of you
do not let me push you down
when PT removes hand, pt should have only one upswing–but in a cerebellar issue it swings around

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19
Q

Tremor

what is cerebellar tremor due to?

why is cerebellar tremor different than PD tremor?

A

cerebellar tremor is due to not maintaining stable tone
-need equal and opposite tone of flexors and extensors, adductors and abductors, agonists and antagonists

different from tremor seen in PD that is due to almost the opposite

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20
Q

Hypotonia

A

amount of tone that normally goes through the arm is lower rather than higher

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21
Q

Signs of Cerebellar Dysfunction (6)

findings

A
  1. findings usually ipsi-lateral (different than the contra-lateral in stroke or spinal cord lesion)
  2. ataxic gait: wide BOS, tremor and shaking
  3. dysarthria: cerebellar speech
    —-need motor control of mouth/lips/tongue/ lower jaw/ and soft palate
    —-sounds myffy
    if diaphragm involved, not able to control pitch and volume
  4. Nystagmus: rapid involuntary beating of eye in specific direction (direction indicates location of lesion) and impaired extra-occular movements
  5. loss of motor learning: feet forward loss, makes therapy difficult
  6. inability to learn from movement errors-may be aware made error but cannot correct it
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22
Q

are cerebellar dysfunctions contralateral or ipsilateral?

A

ipsilateral

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23
Q

What type of gait from cerebellar dysfunction?

A
  1. ataxic gait: wide BOS, tremor and shaking
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24
Q

dysarthria

what is it

A

cerebellar speech
—-need motor control of mouth/lips/tongue/ lower jaw/ and soft palate
—-sounds myffy
if diaphragm involved, not able to control pitch and volume

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25
Q

Nystagmus

A

apid involuntary beating of eye in specific direction (direction indicates location of lesion) and impaired extra-occular movements

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26
Q

What aspect of cerebellar dysfunciton makes PT difficult?

A

loss of motor learning: feet forward loss, makes therapy difficult

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27
Q

ataxia

A

lack of order (in their movements), better to say nystagmus, rebound, tremor, dysmetria etc because ataxia can be about a lot of things

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28
Q

coordination assessment

A

Dysmetria: Finger Nose Finger

Disdiachokinesia: difficulty in moving in two opposite directions

eye movements

part of vestibular exam

VOR1, VOR2

Tracking, sacaads

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29
Q

Dysmetria Assessment

A

Finger nose Finger

patient touches your finger and then your nose
different ranges, speeds, locations: i move my finger side to side/across midline/ speeds range/ location

note accuracy under different conditions (more than speed)

heel to shin test: slide heel of one foot across the shin of the other leg (may be too weak to do that, and get a false positive)

do not mistake weakness, spasticity, sensory loss for dysmetria!

Not Cerebellar findings, do not make this mistake!

  • -LMN lesion in arm is a weakness
  • -spasticity: cannot do the full movements
  • -visual loss
  • -sensory loss
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30
Q

what may be mistaken for dysmetria?

A

do not mistake weakness, spasticity, sensory loss for dysmetria!

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31
Q

Which are cerebellar findings?

  • -LMN lesion in arm is a weakness
  • -spasticity: cannot do the full movements
  • -visual loss
  • -sensory loss
A

Not Cerebellar findings, do not make this mistake!

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32
Q

Disdiadochokinesia

  1. what is it
  2. how is it tested
  3. what mistakes made
  4. what needs this
  5. False positive
A

1) “difficulty” “two”

difficulty moving in two opposite directions

two opposite movements, rapid and alternating movements

tested at different speeds

rapid and alternating movements
hands or feet

2) sit with hands on knees with palms up switch to palms down now as fast as you can–provocative, fast

can also do heel-toe: alternate heel/toe touching the ground

3) do not mistake weakness, spasticity, contracture, or sensation for a positive test result

4) what needs it:
1. all functional movements require combinations: flexors/extensors, IR/ER, AD/ABductors

  1. lengthening, shortening, correct force, correct timing, correct speed (accelerate, deccelerate), correct “choice”
  2. speaking requires rapid alternating movements: tongue and lips in rapid speech and therapists test for this
    5) false positive: spasticity, contracture, sensory loss, visually dominant (cannot do it with eyes closed)
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33
Q

Mistaken test result for disdiadochokinesia

A

do not mistake weakness, spasticity, contracture, or sensation for a positive test result

alse positive: spasticity, contracture, sensory loss, visually dominant (cannot do it with eyes closed)

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34
Q

when is disdiadochokinesia relevant that we need it fore

A
  1. all functional movements require combinations: flexors/extensors, IR/ER, AD/ABductors
  2. lengthening, shortening, correct force, correct timing, correct speed (accelerate, deccelerate), correct “choice”
  3. speaking requires rapid alternating movements: tongue and lips in rapid speech and therapists test for this
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35
Q

Testing on practical (4)

A

Dysmetria: Finger Nose Finger or
heel to shin test: slide heel of one foot across the shin of the other leg (may be too weak to do that, and get a false positive)

Disdiachokinesia: difficulty in moving in two opposite directions

finger-nose-finger:
patient touches your finger and then your nose
different ranges, speeds, locations: i move my finger side to side/across midline/ speeds range/ location. note accuracy under different conditions (more than speed)
do not mistake weakness, spasticity, sensory loss for dysmetria!

rebounding: hold arm straight, ability to maintain tone because firing of muscles is equal and opposite on all sides maintaining muscle tone

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36
Q

Cranial Nerves

Motor or Sensory?
Peripheral or Central?

A

peripheral nerves mediate motor and sensory function

transmit impulses to the CNS–not purely peripheral structures because have central component

Sensory Motor and reflex functions

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37
Q

Cranial Nerve lesion abnormalities:

where can they be (4)

A

lesion at any of these areas can qualify as cranial nerve abnormality

  1. Nerves
  2. Nucleus
  3. Pathways to/from cortex, diencephalon, cerebellum,
  4. brainstem
  5. receptor (muscle, reflex, etc)
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38
Q

Effects of Cranial Nerve Lesion

Nagi model application

A

examine the impairment, functional limitation, and disability level

ie vestibulochochlear nerve lesion

  • impair: nystagmus and vertigo
  • functional limitation: disequilibrium
  • disability: cannot work
39
Q

Olfactory Nerve

  • seonsory or motor
  • why is it unique
  • where do olfactory tracts project to location and lobe
A

only sensory afferent impulses of sense of smell

only sensory modality with direct access to cerebral cortex without going through the thalamus (relay station for senses)

the olfactory tracts project mainly to the UNCUS of the TEMPORAL LOBE (near hippocampus)

–projections to hippocampus suggests role in memory

40
Q

CN1 Lesion

name 2 pathologies
disable?

A

classical pathology: olfactory groove meningioma

basal skull fractures another potential cause (unilateral or bilateral)

can be part of a larger pathology

not disabling but can affect QOL

41
Q

CN1 Testing

what is more important in smell?

what is used in testing?

how is it done?

A

detection of the smell is more important than the actual identification

the non-noxious odors are used in tests

noxious odors may be used in sensory stimulation

test unilaterally and bilaterally

42
Q

CN1 Pathology

loss of ____

A

Anosmia: loss of smell (unilateral vs bilateral)

  • sudden loss: infarct, trauma
  • gradual loss: tumor

olfactory hallucinations: associated with seizure disorders (auro smell often before seeizure comes) or limbic system lesion

43
Q

CN2

  • sensory or motor
  • pathway
A

Optic Nerve

arise from RETINA of the eye

optic nerves pass through the optic CANALS and converge at the optic CHIASM

they continue to the THALAMUS where they synapse

from there optic RADIATION FIBERS run to the visual cortex in the occipital lobe

functions solely by carrying SENSORY afferent impulses for vision to the occipital lobe

44
Q

Function of CN2 (4)

A

acuity: central vision (focus on something directly)
fields: peripheral vision

pupillary dilation and contraction (light reflex)

accommodation reflex [eyes converge together to focus on moving subject nearer or farther]

45
Q

CN2 Lesion

A

monocular blindness: associated with optic neuritis of Multiple Sclerosis

Bitemporal hemionopsia: loss of vision in temporal fields, associated with pituitary tumors

Homonymous Hemianopsia: loss of vision in temporal fields of one eye and nasal fields of the other. Associated with optic tract lesions-CVA

Homonymous Quadrantanopsia: defect in SAME quadrant of each eye (such as left and right superior temporal)

46
Q

Bitemporal hemionopsia:

casue

A

loss of vision in temporal fields

associated with pituitary tumors

47
Q

Homonymous Hemianopsia:

cause

A

loss of vision in temporal fields of one eye and nasal fields of the other.

Associated with optic tract lesions-CVA

48
Q

Homonymous Quadrantanopsia:

case

A

defect in SAME quadrant of each eye (such as left and right superior temporal)

upper: temporal lobe lesion
lower: parietal lobe lesion

49
Q

visual confronting testing

A

patient covers one eye, looks at examiners nose

examiner brings fingers from behind patients eyes in all four quadrants

patient should signal awareness of object a few cm past the plane of their eyes
(ie R eye: right side move finger, left side move finger covering left eye)

record normal vs restricted in each quadrant for each eye

50
Q

CNII and CNIII Pupillary Light Reflex

stimulus
direct reflex
consensual reflex
document as

A

stimulus: penlight into eye

Direct Reflex: constriction in primary eye (shining light into)

Consensual reflex: constriction in opposite eye

Document as present, absent, diminished

51
Q

Pupillary light reflex interpretation

A

Sensory input: CNII afferent impulses from retina

Motor output: CNIII oculomotor nerve

52
Q

stimulate R eye and neither pupil constricts

stimulate L eye and both pupils constrict

A

problem:

Sensory input: CNII afferent impulses from retina
or
RIGHT retina

53
Q

stimulate R eye and right pupil does not constrict but left does

stimulate L eye and right pupil does not constrict left pupil does

A

Right occulomotor nerve
Motor output: CNIII oculomotor nerve

sensory paths in are intact but motor response impaired

54
Q

stimulate R eye and right pupil constricts but left does not

stimulate L eye and right pupil constricts but left does not

A

problem with occulomotor nerve
or
left retina

55
Q

CNII Accommodation

A

bring object 1-2 feet away from patients face towards nose as patient stares at object

NORMAL: constriction and convergence of both eyes

ABNORMAL: lack of constriction and/or convergence of both eyes

56
Q

Pupillary light reflex documentation

A

PERLA: pupils equal, round, light reactive, accommodating

Anisocoria : unequal pupil diameter

Argyll Robertson Pupil: pupil small and doesnt react to light but accommodates

Fixed pupil: non reactive to light, or accommodating

57
Q

Anisocoria

A

unequal pupil diameter (on pupil wider)

58
Q

Argyll Robertson Pupil:

A

pupil small and doesnt react to light but accomodates

59
Q

Fixed pupil:

A

non reactive to light, or accommodating (brainstem damage or damage to CN 2 or 3)

60
Q

CN 3, 4, 6

A

occulomotor
trochlear
abducens

pursuit: slow eye movements used to maintain vision on moving target

H test

61
Q

H TEST

A

inferior oblique(3) _________________superior rectus(3)

medial rectus(3) _____________________lateral rectus (5)

superior oblique(4)_________________inferior rectus (3)

62
Q

Testing Pursuit

A

test unilaterally and bilaterally

follow my finger

common complaints: diplopia, blurred vision, unequal tracking
document areas of mac and minimal diplopia

EOMI-extra ocular muscles intact

63
Q

Saccades

A

rapid movement of the eye from one point of fixation to another

ie looking up from a page to someone walking accros the room with or without moving your head

64
Q

Testing Saccades

instructions

what we look for (9)

A

patient seated
have patient look from one finger to another without moving head
test in all 4 planes to assess extraocular ms

note deviations in for each eye, each movement, smoothness, speed, do both eyes move at similar speeds, nystagmus, vertigo, diplopia, blurring

65
Q

CN3

role
what innervates
role

A

Oculomotor nerve

responsible for 73% of eye movements

tested along with CN4 and CN6

TEst all movements in order:

SR: superior movement
IR: inferior movement
Medial Rectus: nasal movement
Inferior oblique: superior nasal
Levator palperbrae-open eyes wide (if not, ptosis)
66
Q

Trochlear Nerve

A

superior oblique–inferior nasal motion
with lesion, eye cannot track past midline
consistent with midbrain lesion

67
Q

CN 6

A

Abducens:
single function

lateral rectus: abduct they eye past midline

with lesion unable to move eye laterally past midline

common injury due to length of nerve and increased susceptibility to ICP

(teach to move head and body to see)

68
Q

EOM

A

extra ocular movement intact

69
Q

strabismus

A

weakness/paralysis of the EOM (extra ocular movement)

70
Q

Lateral Strabismus

A

wall eyed. loss of medial rectus

71
Q

Medial Strabismus

A

cross eyed, loss of lateral rectus

72
Q

Hypertropia

A

eyes turned upward, loss of downward gaze

73
Q

Hypotropia

A

eyes turned downwards, loss of upward gaze

74
Q

CN5

A

trigeminal nerve

primary sensory, some motor

3 sensory to face from pons

  1. optic (sensory)
  2. maxillary (sensory)
  3. mandibular (sensory and motor)-muscles of mastication

Trigeminal Neuralgia

75
Q

Trigeminal Neuralgia

A

also called tic douloureux, the trigeminal nerve’s function is disrupted.

dental, MS, brainstem nucleus of trigeminal nerve, or ideopathic

pain

76
Q

Testing CN7

A

squeeze eyes shut-obicularis oris

zygomaticus: smile wide
frontalis: wrinkle forehead

frown

purse lips

Grimace: tighten neck

77
Q

Facial Nerve Lesions

A

CN7
central corticobulbar droop of lower contralateral face

peripheral droop of entire ipsilateral face

78
Q

CN7

role

A

motor: muscles of facial expression
sensory-to stapes, hyperaccusis
taste: anterior 2/3 of tongue
tearing, unilateral

79
Q

2 types of bells pasley

A

PNS lesion: ipsilateral droop of full side of face

CNS facial droop: lower contralateral face

80
Q

CN 8

A

vestibulocochlear nerve
vestibular component-balance, stable eye and head poisiton

cochlear component: hearing

81
Q

Vestibular Ocular Reflex

A

VOR
primary output of vestibular nerve

allows eyes to track a moving object regardless of head position or movement

deficits can be peripheral or central

82
Q

Testing VOR

A
  • patient sitting
  • examiner places finger arms length from patients eyes
  • patient moves head from side to side keeping eyes focused on a finger
  • test vertically and horizontally, diagonally, in different positions

VOR1: person moves head, object stable

VOR2 testing: finger moves in opposite directions to head movement

83
Q

Abnormal VOR findings

A
  • loss of focus
  • nystagmus
  • vertigo
  • imbalance
  • disequilibrium
  • nausea
84
Q

Nystagmus

A

oscillating eye movement
slow phase and fast phase, named for FAST phase
Torsional and linear components
Type of nystagmus can be diagnostic

85
Q

Hallpike Dix +

A

To complete the test, the patient is brought back to the seated position, and the eyes are examined again to see if reversal occurs

86
Q

Vertigo

A

Hallucination of movement
usually spinning, can be jumping, telescoping, pulsing
vertigo is NOT dizziness
differentiate from lightheadedness (hypotension)

87
Q

Central vs Peripheral Vestibular Findings

A

Central Lesion in pons, cerebellum, parietal cortex
-MS parietal, cerebellum, or brainstem strokes, TBI, tumor

Peripheral Lesion of the nerve itself or supporting structures
-BPPV, vestibular neuritis, labyrinthis, meniers, otoxicity, accoustic neuroma

88
Q

Central vs Peripheral Vestibular Nystagmus

A
Central: 
Nystagmus Direction changes
Rotary or linear nystagmus and not both
nystagmus can be seperate from vertigo
unable to suppress with fixation
Peripheral
unidirectional nystagmus
rotary AND linear components nystagmus
nystagmus matches with vertigo
suppresses with fixation
89
Q

BPPV: Benign Paroxysmal Positional Vertigo

A

calcium carbonate crystals (autoconia) in SEMICIRCULAR CANALS

most common vestibular complaint

tx relatively simple

dx with hallpike dix test

90
Q

Hallpike Dix Manouver

A
  1. pt in long sitting
  2. look up and over LEFT shoulder
  3. brought rapidly into head hanging position, neck extended about 20 degrees
  4. wait 20-60 seconds for nystagmus (torsional/horizontal)
  5. nystagmus clears
  6. return to sitting position
  7. reversal of nystagmus
91
Q

CNIX, CNX

A

glossopharyngeal (9) and vagus (10)

posterior 1/3 of tongue
gag reflex
all parasympathetic
recurrent laryngeal nerve to vocal cords

92
Q

Test CN9 and 10

A

Dysphagia: difficulty swallowing
Dysphonia: hoarseness or quietness of voice
Absent gag reflex
deviation of soft palate to normal side (CN IX and X are damaged on one side (not uncommon), stimulation of the normal side elicits only a unilateral response, with deviation of the soft palate to that side; no consensual response is seen. Touching the damaged side produces no response at all.)

93
Q

CN11

A

Spinal Accessory

trapezius: shrug shoulders
SCM: rotate head to left and right

94
Q

CN 12

A

hypoglossal

motor to tongue

CENTRAL lesion-tongue deviation away from side of lesion without atrophy of fibrillations

PERIPHERAL Lesions: tongue deviate toward side of lesion with atrophy and fibrillations

component of dysphagia (difficulty with swallowing. )and dysarthria (inability to speak clearly due to problems with control of the motor apparatus of speech)