Week 6 - The Vestibular Sense Flashcards

1
Q

What is the vestibular sense?

A

= The ‘balance sense’

In reality, it’s a modality that mixes info on balance, posture and gravity to give us spatial orientation/awareness. To do this (and get information on acceleration and movement) the brain must combine proprioception and equilibrioception (and to get equilibrioception we use the vestibular sense)

Is essential for coordinated movement

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2
Q

Equilibrioception

A

Equilibrioception is the sense of balance. It is a physiological sense in humans and animals to prevent them from falling over as they move or stand.

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3
Q

The vestibular sense (in an example)

A

The vestibular sense gives us information on acceleration and movement through space and works by assessing our position in relation to gravity.

eg. if you get in an elevator, the visual, olfactory, somatosensory and auditory information is all constant however, we know we are moving

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4
Q

The vestibular labyrinth definition/function

A

= a set of connected, fluid-filled tubes in the inner ear, extending from the cochlea

Provides information on body position, relative to gravity and is critical for balance aka equilibration

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5
Q

Structure of the Vestibular System

A

There are 5 regions of interest:

  • 2 otolith organs consisting of the utricle and sacculus which are used to detect linear acceleration and static position
  • 3 semicircular canals which detect rotational acceraltions of the head
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6
Q

What are the rotational accelerations of the head detected by the semicircular canals?

A

Pitch = nodding up and down
- aka rotation around the y axis or rotation around the coronal plane/movement along the sagittal plane

Yaw = shaking of the head
- aka rotation around the z axis or rotation around the sagittal plane/movement along the transverse plane

Roll = an ear to the shoulder type movement
- aka rotation around the x axis movement along the coronal axis

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7
Q

x,z and y orientations

A

Z = vertical axis. Movement of the head up and down (pitch) is movement along this axis whilst yaw (head shaking) is movement around this axis

y = transverse/horizontal from ear to ear axis. Movement of the head side to side (yaw) is movement along this axis whilst pitch (nodding) is rotation around this axis

X = front to back axis. Movement of the head up and down (pitch) is movement along this axis whilst roll is rotation around this axis

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8
Q

Otolith Organs

A

The utricle and saccule form the otolith organs which are used to detect linear acceleration
- the vestibular hair cells sit in the otolith organs and semicircular canals
- They extend hairs (stereocilia) into a gelatinous layer
- on top of the jelly layer are the otolith stone (caCo3) or the otoconia. These stones exert weight onto the gelatinous layer and therefore onto the stereocilia of hair cells

During linear acceleration, gravity will move the otoconia causing a displacement of pressure being exerted down on the gelatinous layer and therefore hair cells. This change in downward pressure causes hair cells to deflect and mechanoreception occurs to drive signal transduction

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9
Q

Semicircular Canals

A
  • Semicircular canals are filled with endolymph fluid
  • at the base of each canal aka the ampulla is a dome like shape (cupula).
  • there is one dope per canal, so signal transduction occurs when the head moves through any of the three planes, as the endolymph moves and deflects the cupula and hair cells to trigger signal transduction through mechanorecpetion
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10
Q

Hair cells in the Semicircular Canals

A

Hair cells are the receptor and is a sensory neuron, as the whole cell is sensing movement
- when the hair cells be they fire action potential which activate aferents of the vestibular nerve

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11
Q

If the hair cell is the receptor what is the stimulus for detection in the semicircular canals?

A

Acceleration aka a change in velocity

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12
Q

The vestibular nerve

A

Vestibular information is carried along the vestibular branch of CN8 (vestibulocochlear nerve)

  • it projects to multiple vestibular nuclei in the medulla and pons of the brainstem and there to the cerebellum

However, some vestibular nerve fibres bypass the brainstem and ascend straight to the cerebellum. These are the only sensory nerve fibres that directly innervate the cerebellum

Additionally, some fibres descend to the spinal cord (specifically portions of CN8. innervated by hair cells of otolith organs)
Fibres also descend from the cerebellum to the spinal cord

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13
Q

Importance/Function of the Vestibular System

A
  • informs if we are horizontal, moving forward/backward, up/down, rotating etc
  • enables planned postural corrections (conscious-requires actions arising from the MI motor cortex activity)
  • enables coordinated reflexes (often subconscious/automatic, but can override)
  • eg. postural reflexes such as the labyrinthine righting reflex- brings the head back to normal position relative to centre of gravity when displaced
    eg. not falling on your face. Whe we strip a strong signal from the vestibular labyrinth arrives at multiple vestibular nuclei in the brainstem sending bilateral messages aka reflex motor messages to the psinal cord and cerebellum to trigger us to lift our head or extend the arm etc
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14
Q

What is the minimal detectable rotational accelleration?

A

is roughly 2degrees/second (detection threshold of the semicircular canal)
and after about 20 seconds fluid in the canal catches up and stops moving so there’s no perceived acceleration after this time.

So, there’s two ways to feel we are not moving when we are;
1. when rotational acceleration is less than 2 degrees a second
2. when we’ve been acellerating at a constant speed for more than 20 seconds

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15
Q

The leans as a vestibular illusion (chat gpt)

A

The Leans is a vestibular illusion that can occur in individuals who have experienced prolonged exposure to a roll motion, such as pilots, astronauts, or people on boats.

The vestibular system is responsible for detecting changes in head position and movement, and is located in the inner ear. During prolonged exposure to a roll motion, the vestibular system can adapt to the motion and begin to perceive it as normal. When the motion stops, however, the vestibular system may continue to signal that the body is rolling, even though it is not.

This can create the sensation of leaning to one side or the other, even when the body is upright. The individual may also experience a sense of disorientation or instability. The Leans is a type of vestibular illusion because it is a misperception of body position and motion that is created by the vestibular system.

To counteract the Leans, individuals can try to reset their vestibular system by looking at a fixed point in the distance or by performing specific exercises designed to stimulate the vestibular system.

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16
Q

Recap; The vestibular system allows us to detect…..

A

acceleration in rotational planes (z,y,x)

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17
Q

Vestibulo-ocular link

A

Describes the inter-relation of visual and vestibular information and is the structures behind the vestibulo-ocular reflex (VOR) which uses information from the vestibular labyrinth of the inner ear to generate eye movements that stabilize gaze during head movements.

These ‘bridges’ are in the brainstem and is important for visual stability

18
Q

Examples of the Vestibulo-ocular reflex (VOR)

A

1) Rotate the head left and keep your gaze straight
2) Rotate your head right and keep your gaze straight

19
Q

How does the Vestibulo-ocular reflex work?

A

Within the brainstem, projections from the vestibular branch of CN8 ascends to vestibular nuclei in the brainstem, then ascend and integrates with cranial nerves in the midbrain that control eye movement, including CN6 (the abducens) and CN3 (oculomotor).

The VOR requires coordinated activity of all three.

eg. If you turn your head left the following occurs;
1. Excitatory impulses are sent from the left semicircular canals (inner ear) to the vestibular nuclei of the brainstem by the vestibular branch of CN*

  1. From the medulla, axons of the vestibular nuclei ascend to the pons where a synapse occurs with the abducens and oculomotor cranial nerves. Importantly, the axons of vestibular nuclei can ascend ipsilaterally or contralaterally
  2. fibres that ascend contralaterally, excite the abducens nerve whilst ipsilateral fibres of the vestibular nuclei inhibit the ipsilateral nucleus abducens nerve
  3. The excited regions of the abducens nerve triggers activation of the lateral rectus muscle in the right eye and has projections to the midbrain that activate the oculomotor nerve to contract muscles medial to the left eye (medial rectus).
    The inhibition of the ipsilateral abducens nerve triggers inhibition of the lateral rectus in the left eye and through projections via the midbrain inhibits the right oculomotor nerve and therefore inhibits the right medial rectus
  4. The eyes therefore look right
20
Q

What occurs when there is damage or impairment in the VOR?

A

Loss of VOR is problematic as it means gaze cannot be maintained

  • Nystagmus (dancing eyes) = loss of control of the eye muscles, meaning they move rapidly and cannot be stabilised
  • this affects vision, depth perception, coordination and balance
  • eg. oscillopsia (jumping vision) – where words and objects don’t appear stable as they jump and shake

-eg. vertigo and balance issues if the nystagmus is due to vestibular dysfunction

21
Q

What are the two ways to test the VOR?

A
  1. Head tilt test
  2. Caloric Reflex Test
22
Q

Head Tilt Test

A

Is a way to test the VOR in individuals with dizziness

It involves quickly tilting the head left and right and checking for constant line of sight, or if line of sight moves with head movement

23
Q

Caloric Reflex Test

A

Is a way to test the VOR in individuals with dizziness

in this ice water or warm water (or ait) is irrigated into the external auditory canal via a syringe. This causes a convection current that causes endolymph to flow

Warm water >44 degrees causes endolymph to flow into the ipsilateral horizontal canal resulting in an increase in firing in the vestibular afferent nerve. So both eyes will turn to the contralateral ear

Cold water <30 decrees causes endolymph to flow our of the horizontal canal leading to decreased firing in the vestibular afferent nerve. Both eyes will therefore turn to the ipsilateral ear

Absent reactive eye movement would suggest an issue with horizontal semicircular canals in the side being tested

24
Q

Vestibular Dysfunction

A

Issues in any part of the path eg. with CN8, the vestibular nuclei of the brainstem, the cerebellum or inflammation of the semicircular canals or otoconia can cause vestibular dysfunction

In the vestibular labyrinth, there are the following potential issues;
1. Labyrinthitis = infection leading to inflammation of the inner ear. This increases the pressure exerted on fluid in the inner ear and increases the sensitivity of hair cells
2. Benign Paroxysmal Positional Vertigo (BPPV) = pieces of loose otolith become displaced from the utricle and sit at the base of the cupula. As a result less gravitational force is exerted on fluid in the cupula so there is less deflection of hair cells.
- treatment for this is physio as rotating the head can get the otoconia to sit on the fluid again

  1. Vestibular Neuritis = inflammation of the nerve. This is the second most common cause of vertigo often seen together with labyrinthitis. in this condition, impulses can fire to tell us we’re moving when we are in fact stationary
  2. Vestibular Nuclei or Cerebellar issues (eg. Brain damage by a stroke or traumatic brain injury)
    - 10% of cerebellar infarcts leads to vertigo
25
Q
  1. Labyrinthitis
A

= infection leading to inflammation of the inner ear. This increases the pressure exerted on fluid in the inner ear and increases the sensitivity of hair cells

26
Q
  1. Benign Paroxysmal Positional Vertigo (BPPV)
A

= pieces of loose otolith become displaced from the utricle and sit at the base of the cupula. As a result less gravitational force is exerted on fluid in the cupula so there is less deflection of hair cells.
- treatment for this is physio as rotating the head can get the otoconia to sit on the fluid again

27
Q
  1. Vestibular Neuritis
A

= inflammation of the nerve. This is the second most common cause of vertigo often seen together with labyrinthitis. in this condition, impulses can fire to tell us we’re moving when we are in fact stationary

28
Q
  1. Vestibular Nuclei or Cerebellar issues
A

(eg. Brain damage by a stroke or traumatic brain injury)
- 10% of cerebellar infarcts leads to vertigo

29
Q

Symptoms of Vestibular Dysfunction

A
  • Dizziness
  • Poor balance
  • Disorientation
  • Stumbling/Falling
  • Blurred vision
30
Q

EtOH (ethanol) and vestibular dysfunction

A
  • Affects the cerebellum resulting in impaired gait and balance
  • Affects VOR causing nystagmus and oscillopsia
  • Affects Cupula/endolymph homeostasis causing vertigo
31
Q

Position Alcoholic Nystagmus and Vertigo (aka the spins)

A
  • Under normal conditions, there is an equilibrium between the specific gravity in the gel of the cupula and the pressure of the endolymph fluid
  • When we drink alcohol two things of importance occurs;
    1. ethanol flows into the cupula
    2. ethanol flows into the endolymph
    and these two events occur at different rates

Phase 1 PAN:
- in phase one ethanol enters the cupula at a faster rate than the endolymph, causing the cupula to become lighter making the endolymph relatively heavier in comparison
- The light cupula and heavy endolymph ratio is associated with more hair cell firing

Over time ethanol diffuses also into the endolymph and the endolymph and cupula regain equilibrium (associated with a silent or intermediate period 3 - 5 hours post alcohol intake has stopped)

Phase 2 pan
- as ethanol is metabolised, the cupula returns to its normal specific gravity first. This means it is heavier and less likely to move with the endolymph - therefore exhibiting reduced firing. Phase 2 pan occurs 5 - 10 hours post alcohol cessation

Positional vertigo can persist for many hours after BAC = 0 (blood alcohol content)

32
Q

Positional Vertigo (chat gpt)

A

Positional vertigo, also known as benign paroxysmal positional vertigo (BPPV), is a common condition of the inner ear that causes dizziness and a spinning sensation. It occurs when small calcium crystals called otoliths become dislodged from their normal position in the inner ear and enter the semicircular canals, which are responsible for sensing rotational movements of the head.

When the head is moved in certain positions, such as rolling over in bed or looking up, the dislodged otoliths can move within the semicircular canals, sending confusing signals to the brain about the head’s position and causing vertigo. BPPV is typically a short-lived condition that can be effectively treated with specific head and body movements known as canalith repositioning maneuvers. In some cases, medication may also be prescribed to manage symptoms

33
Q

Confusion Motion Sickness (chat gpt)

A

Confusion motion sickness is a type of motion sickness that occurs when the body experiences conflicting sensory signals about movement and orientation. This can happen, for example, when a person is in a moving vehicle and the visual cues from the outside environment indicate movement in one direction, while the sensory signals from the inner ear indicate a different movement or orientation.

34
Q

Motion Sickness in the Vestibular System

A

Motion sickness has several causes based on confusion motion sickness in which there is a vestibular and visual mismatch.

  • if demanding/high-speed integration is needed (ie a rollercoaster) = overload motion sickness
  • if one system (vestibular or visual) says ‘still’ and the other says ‘moving = confusion motion sickness (eg. back of car on long trip)
  • if the brain has adopted new synchrony -> Mal de debarquement syndrome (ie getting off of a boat)
35
Q

What causes motion sickness

A

Motion sickness doesn’t occur in those congenitally born without a vestibular system - so we know the vestibular system is involved in this

Visual input is also important, as not having a view of the road ahead makes you 3x more likely to get motion sickness

Ancestry also plays a role - as North East Asians are more susceptible to getting road sickness

Biological sex; females (XX) are more susceptible than males (XY)
- and even more so during different points of the menstrual cycle

36
Q

Genetics and motion sickness (Hromatka et al 2015)

A
  • asked what mediates genetic determinants of motion sickness (including sex)
  • Used Genome Wise Association Studies point to 3 things; genes related to ;
    1) glucose homeostasis (link to cupula gel/endolymph homeostasis - as this influences density
    2) Inner ear development (thinner/wider canals can change pressure)
    3) nervous system development (including synapse development in vestibular inputs to brainstem)

In all cases the vestibule system was heavily implicated

37
Q

Describe the details of the case study discussed by Miyahara et al., 2009

A

5yo female admitted to the ED vomitting, with abdominal pain and a headache.
Vomiting persisted for 8 hours, but she was afebrile (no temperature), consisted of no blood/bile, heart rate and BP was normal

Was initially diagnosed gastroenteritis and prescribed IV fluids. Then was diagnosed with cyclic vomitting

She however, continued to have episodes of this until after 13 months the girls mum advised that before the events began her head would sway

At this point, additional testing was performed, she was normal in an otoscopic exam (so no blockage in the outer ear), she had no vertigo or nystagmus (so no vestibular deficits). She did however, have a VOR deficit in the right ear (suggesting a deficit in the inner ear) and a hearing deficit (so likely had a deficit with the cochlea and vestibular labrynth)

Was given a differential diagnosis ; Meniere’s disease

38
Q

Meniere’s Disease

A

First described in 1861, idiopathic endolymphatic hydrops (excess fluid in the inner ear)

-presents as recurrent spontaneous episodic vertigo, fluctuating hearing loss, aural fullness or pressure and tinnitus

Doctors at the time said it’s like being completely drunk but sober

The cause of fluid build-up is unknown but could involved;
- improper fluid drainage due to blockage or anatomic abnormality
- abnormal immune response to viral infection
- unknown genetic factor

Has no cure but treatments include;
- antiemetics to stop nausea/vomiting
- antihistamines to stop vertigo

In the case of Miyahara et al., the patient was given isosorbide a diuretic to stop the endolymphatic fluid buildup in the semicircular canals

39
Q

Vestibular Hypofunction

A

Approx 1.8 mill people have bilateral vestibular hypofunction (caused by traumas, toxins, infection, autoimmune conditions, vascular insult or bilateral Meniere’s)
- or sometimes defects in canals or the vestibular nerve

Any head movement makes vision jump and blur, simple tasks like walking take considerable effort and there’s more than thirtyfold increase fall risk

There is no treatment - just vestibular rehab
However, there is emerging evidence that cochlear implants could be adjusted to innervate the vestibular system to correct this

40
Q

Vestibular Implants

A

There’s already ~740,000 people with cochlear implants in the world. The same technology could be used for the vestibular nerve to correct vestibular hypofunction or deficits

41
Q

Vestibular issues in children

A

sensory processing issues in kids are becoming more common including vestibular and p/k processing issues

Common symptoms;
- slouching or leaning on desks or tables
- difficulty maintaining balance in activities
- fearful of movement activities
- constant moving or fidgeting

and adults are getting worse too