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PHTY3140 > L24: Central vertigo assessment > Flashcards

L24: Central vertigo assessment Flashcards

1
Q

What is the image for the central vestibular system?

A
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2
Q

What are 3 higher vestibular functions?

A
  1. Internal representation of body schema
  2. Internal model of the surrounding space
  3. Multisensory motion perception, attention, spatial memory and navigation
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3
Q

What are 3 major vestibular functional groups?

A
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4
Q

What are 4 vestibular nuclei?

A
  1. Superior
  2. Inferior (descending)
  3. Medial
  4. Lateral
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5
Q

What are 2 features of vestibular nuclei?

A
  1. Medial & superior vestibular nuclei get input from semicircular canals
    • Pathology with medial & superior nuclei - lose angular acceleration
  2. Inferior & lateral vestibular nuclei get input from otolith organs
    • Pathology with lateral & inferior nuclei - lose linear acceleration
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6
Q

Medial & superior vestibular nuclei get input from ________.

A

semicircular canals

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7
Q

What if there is a pathology of medial and superior vestibular nuclei?

A

Pathology with medial & superior nuclei - lose angular acceleration

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8
Q

Inferior & lateral vestibular nuclei get input from _______.

A

otolith organs

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9
Q

What if there is a pathology of medial and superior vestibular nuclei?

A

Pathology with lateral & inferior nuclei - lose linear acceleration

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10
Q

Vestibular nuclei receive input from multiple brain areas and the 8th cranial nerve to ________.

A

refine movements by inhibitory and excitatory modulation

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11
Q

What are 4 features of “vestibular nuclei receive input from multiple brain areas and the 8th cranial nerve to refine movements by inhibitory and excitatory modulation”?

A
  1. Vestibular nuclei extend from the medulla to the rostral pons
  2. Branch off to the MLF bilaterally off the midline
    • Mediolateral fasciculus: Transmission of info from vestibular nuclei
    • MS destroys MLF - lose descending input control
  3. Process and relay information with neural outputs to control eye movements, postural movements and spatial orientation
  4. Can also influence ANS - control of BP when changing posture
    • Orthostatic hypotension: Because otoliths do not fire > muscles do not contract > do not keep blood flowing > drop BP > faint
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12
Q

What is Integration of SCC & Otolith Organs?

A

During complex and combined movements, SCC and otolith inputs are summed (sub-additive).

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13
Q

What are 3 features of “omplex and combined movements, SCC and otolith inputs are summed (sub-additive)” for Integration of SCC & Otolith Organs?

A
  1. The weighting of SCC and otolith organ input will vary.
  2. At higher frequency, the weighting of rotational sensitivity decreases, but the weighting of translation sensitivity increases.
  3. Central vestibular pathologies over-rely on certain SCC or otolith organs - poor control of dynamic contributions of those organs.
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14
Q

What is translation?

A

Otolith organs

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15
Q

What is tilt?

A

Otolith organs + SCC

  • Utricle + horizontal SCC
  • Saccule + vertical SCC
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16
Q

By integrating otolith and SCC inputs together, you can discriminate between _____ and _____ (also integrated with visual and proprioception).

A

tilt; translation

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17
Q

What is the image summary?

A
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18
Q

What are 2 Vestibular & Extraocular Nuclei Pathways for the pathways of central vestibular systems?

A
  1. Mediate VOR
  2. Ascending pathways
    • Medial longitudinal fasciculus
    • Dieter’s tract from lateral vestibular nuclei (Dieter’s nucleus)
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19
Q

What are 2 vestibulospinal pathways?

A
  1. Medial vestibulospinal tract
  2. Lateral vestibulospinal tract
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20
Q

What are 2 medial vestibulospinal tracts/pathways?

A
  1. Arises from medial vestibular nucleus
  2. Innervates motor neurons for head & neck
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21
Q

What are 3 lateral vestibulospinal tracts/pathways?

A
  1. Direct efferents to vestibular nuclei, reticular formation and oculomotor nuclei
  2. Coordination of head-eye movements
  3. Indirect efferents go to thalamus, then to the motor cortex, red nucleus, reticular formation, vestibular nuclei and back to the cerebellum
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22
Q

What are 2 vestibulo-thalamo-cortical pathway?

A
  1. Visual vertical
    • Lesion lower than decussation causes ipsilesional tilt ○
    • Lesion higher than decussation causes contralesional tilt
  2. Haptic vertical
    • Lesion in MCA area causes tilting sensation due to breakage of link to vestibular input
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23
Q

What are 4 features of thalamus as a pathway of central vestibular system?

A
  1. Thalamus is the gatekeeper to the cortex
  2. >10 regions attributed to vestibular processing within the thalamus
    1. Ventrolateral & posterolateral thalamus
    2. Thalamus encode vestibular input
  3. Thalamic lesions can present with tilts of subjective visual verticality (SVV) ipsi- or contralesionally
  4. Lesions do not produce OTR
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24
Q

What are 2 features of multi-sensory intergrations in thalamus as a pathway of central vestibular system?

A
  1. Integration of vestibular and somatosensory inputs depends on the posterolateral thalamus.
    • MCA strokes cannot integrate them well
  2. PD demonstrated changes in the SVV after deep brain stimulation of the subthalamic nucleus.
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25
Q

What are 3 features of vestibular-basal ganglia pathways as a pathway of central vestibular system?

A
  1. Vestibular nucleus connects to striatum via thalamus.
  2. The striatum is likely the main input center for vestibular signals in the basal ganglia.
  3. This pathway contributes to motor control.
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26
Q

What are 3 features of cerebral cortex?

A
  1. Several distinct and separate areas of the temporoparietal cortex that receive vestibular and somatosensory afferents •
  2. Multiple network of cortical areas
  3. All vestibular cortex neurons respond to motion stimulation from other senses
    • Treatment - need movements to change coding of somatosensory inputs
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27
Q

What are 2 major areas of cerebral cortex?

A
  1. Parietoinsular vestibular cortex (PIVC)
  2. Medial superior temporal area (MST)
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28
Q

What are 3 features of the vestibular cortex?

A
  1. Areas represented in both hemispheres
  2. Ipsilateral input from the stimulated end organ is the stronger input
  3. Both hemispheres but only one “global” vestibular perspective
    1. e.g. Right handed - right hemisphere is dominant to vestibular input
    2. One cannot perceive 2 different body positions/motions at the same time
    3. Callosal communication very important
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29
Q

What is the bilateral pathways of the vestibular system?

A

Right vestibular nuclei activated > right vestibular cortex activated, but also talk with left cortex.

  • Yaw plane = blue
  • Roll plane = pink
  • Pitch plane = green
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30
Q

What are 3 lesions of the vestibular cortex?

A
  1. Altered perceptions of SVV
  2. Body lateropulsion (pushers)
  3. Rotational vertigo (rare)

Cortical infarcts damage critical areas in voluntary eye control

  • Treatment: Translate motor control to ocular systems to improve balance
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31
Q

What are 2 features of parietal lesions?

A
  1. Latency on visually guided saccades in both hemifields
  2. Impaired smooth pursuit with textured background
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32
Q

What are 3 features of frontal lesions?

A
  1. Inaccuracy of saccades (hypometric)
  2. Latency of saccades
  3. Impaired smooth pursuit
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33
Q

What are 4 symptoms of yaw plane?

A
  1. Horizontal nystagmus
  2. Past pointing
  3. Rotational and lateral body falls
  4. Horizontal deviation of perceived straight ahead
34
Q

What is a lesion of yaw plane?

A

Unilateral lesions of vestibular nuclei

35
Q

What are 4 symptoms of roll plane?

A
  1. Torsional nystagmus
  2. Skew deviation - one eye drops
  3. Ocular torsion
  4. Tilts of head, body and perceived vertical
36
Q

What is a lesion of roll plane?

A

Lesions along the crossed pathways from vestibular nuclei in the medulla to the interstitial nucleus of Cajal (INC) in the midbrain

37
Q

What are 4 symptoms of pitch plane?

38
Q

What is a lesion of pitch plane?

A

Bilateral lesions of vestibular structures

  • Dark green = downbeat
  • Light green = upbeat
39
Q

What are 3 features of Sensory Integration for Balance?

A
  1. Proprioception encodes body motion with respect to surface orientation
  2. Vision encodes body motion with respect to the visual scene
  3. Vestibular encodes body motion in space
40
Q

What are 3 features of variability (across sensory systems in quiet stance) for Sensory Integration for Balance?

A
  1. Vestibular system (SCC & otoliths) are inactive during quiet stance because 5°/sec of sways is too little to be detected.
  2. Proprioceptors are active during quiet stance because they work at a narrower range and they can sense small sways.
  3. So, we need to incorporate movements to help reweigh sensory input.
41
Q

What are 2 features of weighted summation (combined signal is achieved) for Sensory Integration for Balance?

A
  1. The sensory system with the lowest variance has the largest weight, because it is the most reliable.
  2. Although vestibular input has larger variance, we still use it because visual environment and contact surfaces (proprioception) can move in space. Only vestibular provides input about motion in space
42
Q

What are 2 features of reciprocal inhibition (between the systems at the cortical level) for Sensory Integration for Balance?

A
  1. Activation of 1 sensory system = inhibition of the other 2 sensory systems
    • We can manipulate this in treatment
  2. Shift the weight to the more reliable sensory system in order to resolve perceptual conflicts and optimize movement
43
Q

What are 4 situations of shift the weight towards vestibular system Sensory Integration for Balance?

A
  1. Larger perturbations
  2. Higher frequency movements
  3. No visual input, or if the visual environment is moving
  4. When proprioception is more variant
    • Narrow BOS
    • Compliant surfaces
    • Moving surface
44
Q

What are 7 causes of central vestibular pathology?

A
  1. Strokes
  2. Tumors
  3. Neurodegenerative pathologies - widespread diseases
    • Multiple Sclerosis
    • Parkinson’s Disease
    • Cerebellar Disease
  4. Immunological
  5. Toxicity: e.g. Alcohol
  6. Inflammatory
  7. Age
45
Q

What are 6 physiological movements of eyes of the ocular examination for central vestibular pathology?

EXAM QUESTION

A
  1. Ocular alignment
  2. Skew deviation (cover test)
  3. Spontaneous nystagmus
  4. Gaze-evoked nystagmus
  5. Eye ROM
  6. Smooth pursuit
  7. Saccades
  8. Convergence
    1. Common in cerebellar & brainstem pathologies
    2. Uncommon in cerebral pathologies
  9. VOR (HIT)
  10. VOR cancellation
  11. Subjective visual vertical
  12. Head-shaking nystagmus
  13. Positional nystagmus
  14. Optokinetic nystagmus
  15. Pressure-induced nystagmus
46
Q

What are 5 features of ocular alignment of the ocular examination for central vestibular pathology?

A

Prefix + tropia/phoria

  1. Hyper = eye up
  2. Hypo = eye down
  3. Eso = eye in
  4. Exo = eye out

The abnormal eye movements occur when eye is covered.

47
Q

What are 4 features of tropia?

A
  1. Position of eye to maintain binocular focus
  2. Deviation stays when both eyes are viewing
  3. Due to strabismus, skews, squints
  4. If brain cannot correct it, then you get double vision, headaches, giddiness - need prism glasses.
48
Q

What are 4 features of phoria?

A
  1. Position of eye when binocular vision disrupted
  2. Deviation when covering one eye
  3. Due to squint.
49
Q

What are 4 features of skew deviation?

A
  1. Misalignment of the vertical visual axes
    1. Part of ocular tilt reaction - skew eye
    2. Brainstem infarct
  2. Occurs due to loss of tonic input from one side, which holds the eye
  3. Level in the orbit
  4. Vertical diplopia
50
Q

Hypotropic eye is ipsilesional if the injury occurs ______ (lower/higher) than the decussation of the utricle‐ocular motor pathway (medulla)

51
Q

Hypertropic eye is ipsilesional if the injury occurs _____ (lower/higher) than the decussation of the utricle‐ocular motor pathway (MLF, pons, midbrain)

52
Q

What are 6 features of Ocular Tilt Reaction?

A
  1. Skew deviation, head tilt & ocular torsion
  2. Damage to 8th cranial nerve
  3. Vestibular nucleus damage (ipsilesional) - disinhibition
  4. Vestibular pathways damage (MLF, riMLF, INC) - contraversive roll‐tilt
  5. Pons damage - ipsilesional
  6. Midbrain damage - contralesional
53
Q

What are 2 Ipsiversive VOR Ocular Tilt Reaction?

A
  1. Induced by unilateral lesions of vestibular nuclei
  2. Pontomedullary lesions
54
Q

What are 5 disturbance of eye fixation?

A
  1. Stable fixation is maintained by pause cell neurons in the pons
  2. Prevent occurrence of unwanted saccadic pulses
  3. Dysfunction leads to extraneous saccades interrupting fixation
  4. Saccadic intrusions and oscillations
  5. May be normal but usually smaller than in patients
55
Q

What are 6 Saccadic Intrusions & Oscillations with intersaccadic intervals (constant speed)?

A
  1. Square-wave jerks
  2. Macro square-wave jerks
  3. Square-wave oscillations
  4. Saccadic pulses
  5. Double saccadic pulses
  6. Macro saccadic oscillations
56
Q

What are 6 Saccadic Intrusions & Oscillations without intersaccadic intervals (irregular speed, slow & fast phase)?

A
  1. Microsaccadic oscillations
  2. Opsoclunus
  3. Microsaccadic opsoclonus
  4. Ocular flutter
  5. Microsaccadic flutter
  6. Voluntary nystagmus
57
Q

What are 4 features of spontaneous nystagmus?

A
  1. Observed without eye or head movements
  2. May be present in acute peripheral lesions (UVL) or central abnormality (brainstem/cerebellar)
  3. Note direction of nystagmus
    • Peripheral nystagmus has fast phase to unaffected side
    • Central nystagmus - direction unsure Perverted nystagmus - fast phase to lesion side
  4. Note effect of:
    • Gaze including convergence ○ Head shaking
    • Position change: Make nystagmus go into all 9 phase positions - central, R, L, up, down, all quadrants
      • Supine & sitting may change direction of nystagmus - central issue.
58
Q

What are 5 features of peripheral nystagmus?

A
  1. Binocular and conjugate
  2. Beats in a single plane and direction regardless of gaze position
  3. Obeys Alexander’s law
  4. Suppressed by visual fixation (enhanced by removing fixation)
  5. Constant-velocity slow phases.
59
Q

What are 7 features of central nystagmus?

A
  1. Imbalance in central oculomotor tone
  2. Central nystagmus is more obvious with fixation
    • Peripheral nystagmus is less obvious with fixation
  3. Often pure vertical, horizontal or torsional
  4. Can be combination
  5. Nystagmus can be ipsilesional or contralesional
  6. Gaze towards the direction of the fast phase increases frequency and amplitude (like peripheral)
  7. Gaze away from the direction of the fast phase causes it to change direction (unlike peripheral)
60
Q

What are 6 features of downbeating nystagmus?

A
  1. Downbeating nystagmus is more common than upbeating nystagmus
  2. Present with and without fixation
  3. Best evoked on downward gaze or lateral gaze
  4. Vertical amplitude increases with horizontal gaze deviation - often associated with horizontal gaze-evoked nystagmus so may appear oblique on lateral gaze
  5. May be precipitated or exacerbated or changed in direction, by altering head position, vigorous head shaking or hyperventilation
  6. Downbeating - brainstem & cerebellar issues
61
Q

What are 8 etiology of downbeating nystagmus?

A
  1. Mostly due to bilateral deficit of the cerebellar floculus
  2. idiopathic = 38%
  3. Degeneration of cerebellum = 20%
  4. Vascular lesions = 9%
  5. Malformations = 7% Toxic drug damage, multiple sclerosis, paraneoplastic syndromes, tumours of the posterior fosse, vestibular migraine, vitaminB12 & thiamine deficiency, TBI, hypoxic brain injury
  6. Permanent if caused by structural lesions
  7. Reversible if from deficiencies or intoxication
62
Q

What are 7 upbeating nystagmus?

A
  1. Uncommon
  2. Present in center position
  3. Increases on looking up
  4. Lesions of medulla or midbrain
  5. Convergence may increase, suppress or convert to down-beat nystagmus
  6. Associated with abnormal vertical vestibular and smooth pursuit responses and saccadic intrusions
  7. Can present with migraine
    • Frequent migraines cause brain damage - scar tissues
63
Q

What are 7 torsional nystagmus?

A
  1. Usually difficult to see
  2. Present with eyes close to central position
  3. Poorly suppressed by fixation
  4. Exacerbated by changes in head position or head shaking
  5. May be suppressed with convergence
  6. Often occurs in association with OTR or unilateral INO
  7. Internuclear ophthalmoplegia blocks MLF - ipsilesional eye loses adduction - torsional nystagmus
64
Q

What are 5 features of vergence?

A
  1. Tested by moving a target from 50cm towards the patient’s eyes
    1. Paddle pop stick + “I” in 14 font on top
  2. Normal range before the target doubles, one eye abducts 6-10cm
  3. Convergence/accommodation reaction
    • Vergence (conjugate movement inward)
    • Change in lens shape
    • Change in pupil size
  4. Often impaired in midbrain lesions and certain neurodegenerative disorders (PSP)
  5. Pre-existing strabismus predisposes to poor convergence reaction
65
Q

What are 2 Gaze-Evoked Nystagmus?

A
  1. Unable to maintain stable conjugate eye deviation away from the primary position
  2. Central gaze-evoked nystagmus is usually in the direction of the gaze
66
Q

What are the 4 types of Gaze-Evoked Nystagmus?

A
  1. Symmetric gaze-evoked nystagmus
  2. Asymmetric gaze-evoked nystagmus
  3. Rebound nystagmus
  4. Internuclear opthalmoplegia
67
Q

What are 3 features of symmetric gaze-evoked nystagmus?

A
  1. Equal amplitude to right and left
  2. Most commonly caused by drugs
  3. Also found in
    1. Multiple sclerosis
    2. Myasthenia gravis
    3. Cerebellar atrophy
68
Q

What are 3 features of asymmetric gaze-evoked nystagmus?

A
  1. Indicates a structural brain lesion
  2. The larger amplitude nystagmus usually directed toward the side of the lesion (brainstem & cerebellum)
  3. Can be caused by large acoustic neuromas
69
Q

What are 3 features of rebound nystagmus?

A
  1. Gaze held in eccentric position for 10-60sec Upon return to primary position, a burst of nystagmus occurs in the direction of the return saccade
  2. Usually have gaze evoked nystagmus then rebounds in the opposite direction
  3. Look to right - get right nystagmus. Look to left - get left nystagmus.
  4. Due to cerebellar pathology (flocculus/paraflocculus)
70
Q

What are 3 features of internuclear opthalmoplegia?

A
  1. Due to MLF lesions between the oculomotor & abducens nuclei
  2. Disorder of conjugate gaze
  3. Inhibition of adduction of the contralesional eye
  4. Convergence is intact Abducting eye contralesionally gets a nystagmus in the direction of the gaze (dissociated nystagmus)
  5. Bilateral - usually MS
  6. Unilateral - usually vascular
71
Q

What are 7 features of smooth pursuit?

A
  1. Requires a visual target to initiate the eye movement
  2. Maintains an object on the fovea +/- head movements
  3. Trajectory of object must be predictable
  4. Smooth pursuit is not sustainable with velocities >70°/s, frequencies >1 Hz, accelerations >240°/sec
  5. Used instead of the VOR to maintain clear visual viewing from no movement to head movements ≤5 Hz
  6. Different pathologies show abnormality in different speed smooth pursuit
    • ACA, MCA strokes, PD, midbrain lesions, cerebellar lesions interfere with smooth pursuit
    • PD shows abnormality in high speed smooth pursuit
  7. Supranuclear control centre: Ipsilateral parieto-occipito-temporal region
72
Q

What are 6 features of saccades?

A
  1. Fast conjugate eye movements that shift the eyes from one target to another
  2. Mechanism to replace a target onto the fovea if has moved off
  3. Very fast ≤500°/sec
  4. Brief in duration <100 msec
  5. Use saccade if:
    • Smooth pursuit cannot be used secondary to pathology
    • Movement is outside the normal velocity for pursuit
    • The trajectory is unpredictable
  6. Abnormal saccades
  7. Dysmetric (cerebellar pathology)
    • Slow saccade - looks like smooth pursuit
    • PD has issues with saccades
73
Q

Saccade is generated by _____ , mediated by _______

A

cortex; brainstem

74
Q

______ saccade is controlled by mesencephalic reticular formation

75
Q

______ saccade is controlled by pontine reticular formation

A

Horizontal

76
Q

What are 5 VOR tests?

A
  1. Visually enhanced VOR
  2. Head impulse test
  3. Head shaking nystagmus
  4. Dynamic visual acuity
  5. Central vestibular pathology makes slow VOR overactive and fast VOR underactive.
77
Q

What are 4 features Velocity Storage Mechanism: “Leaky” Integrator Model?

A
  1. A bucket with a hole that can be opened to let water leak out. When no more water is poured into the bucket, the water will drain completely.
  2. The velocity storage mechanism is like a “leaky bucket”.
  3. Cupula deflection > excitation signal (input) > velocity storage integrator charges up
  4. Spin a person, and stop suddenly. Measure nystagmus decline, >15-20s decline means central vestibular pathology
78
Q

What are 3 results of VVOR?

A
  1. VOR
  2. Optokinetic reflex
  3. Smooth pursuit
79
Q

What are VVOR tests?

A

Turn the patients head slowly (~0.5 Hz) while the patient visually fixates upon a target. The compensatory eye movements should be smooth.

  • Saccadic VVOR - impairment
80
Q

What are 5 Subjective Visual Vertical (SVV)?

A
  1. SVV is the ability to perceive verticality
  2. Depend on visual, vestibular and somatosensory inputs
  3. It is the most sensitive sign of vestibular tone imbalance in the roll plane
  4. Tilt of SVV is observed in 94% of patients with acute unilateral brainstem lesions that affect central graviceptive pathways (from vestibular nuclei to midbrain)
    • Pontomedullary brainstem lesions = ipsilateral tilts
    • Pontomesencephalic lesions = contraversive tilts
    • Unilateral lesions of posterolateral thalamus or PIVC also cause ipsiversive or contraversive tilts
  5. Not exclusively a central sign - acutely seen in vestibular neuritis, Meniere’s, BPPV (usually resolves within a month)
81
Q

What are 6 features bucket method?

A
  1. Visual field covered completely by bucket
  2. Bucket with midline = vertical
  3. If examiner turns it, then it eliminates haptic cues
  4. Measure degrees of vertical deviation using protractor or iPhone app
  5. Repeat 6‐7x for accuracy
  6. Patients should be within 1‐2°

PHTY3140 (28 decks)

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