The vestibular system Flashcards
Where is the vestibular labyrinth located. What does it consist of? Where and what are the sensory structures?
- The labyrinth is buried deep in the temporal bone.
- The vestibular labyrinth consists of two otolith organs (utricle and saccule), and three semicircular ducts (within bony semicircular canal) that are approximately mutually orthogonal.
- Both ends of each semicircular canal insert into the utricle
- The sensory structure of the otolith organs is called the macula
- At one end of each duct is a dilation, the ampulla; in which sits the ampullary crest which is the sensory structure.
What do the macula of each otolith organ respond to/ detect?
The macula detects linear acceleration;
- For a person standing upright, the macula is horizontal in the utricle and vertical in the saccule
- The utricle is sensitive to tilting of the head whilst the saccule is sensitive to vertically acting forces such as gravity.
The (ampullary crest of the) semicircular ducts respond to/ detect what?
The ampullary crest detects angular acceleration in the plane in which the duct lies;
- Using the signals coming from all six semicircular ducts (both ears) the brain computes the magnitude and direction of the angular acceleration of the head.
Describe the location, production and drainage of endolymph in the vestibular labyrinth
- The membranous sacs within the bone are filled with fluid (endolymph) and are collectively called the membranous labyrinth.
- It is secreted by the stria vascularis epithelium lining the outer wall of the cochlear duct
- It drains into a venous sinus of the dura via the endolymphatic sac.
Describe the location, production and drainage of perilymph in the vestibular labyrinth
- The space between the bony and membranous labyrinths is filled with a CSF-like fluid, called perilymph.
- It is secreted by arterioles of the periosteum (connective tissue layer covering the bone).
- It drains into the subarachnoid space via the perilymphatic duct.
List the 6 main functions of the vestibular system?
- Subserve perception of motion in space and tilt (with respect to gravity)
- Provide reflex balance reactions to sudden instability of gait/posture (vestibulo-spinal reflexes)
- Stabilise the eyes on fixed targets during head movement, preserving acuity (vestibulo-ocular reflexes)
- Assist in control of heart rate and blood pressure during rapid up-down tilts
- Assist synchronisation of respiration with body reorientations
- Provokes motion sickness
Describe the appearance of the macula
The macula is an epithelial sheet of supporting cells, and sensory hair cells.
Describe the innervation of a hair cell
Innervated at its base by two nerve fibres, a vestibular afferent and an efferent.
Describe the appearance of the apical border of the hair cell
- Has a single motile kinocilium, and modified microvilli (stereocilia) which are progressively shorter the further they are from the kinocilium.
- This defines an axis of polarity for a hair cell, with a direction going from the smallest stereocilium to the kinocilium.
- Stereocilia lying along this axis are connected at their tips by tip links.
- The tips contain stretch-activated potassium channels that are regulated by the tip links.
The kinocilium and stereocilia are embedded in what?
Embedded in a gelatinous matrix containing tiny crystals of calcium carbonate, called the otolith membrane
Explain the baseline firing of the primary afferent (at rest)
The hair cell is at rest if no force acts on the otolith membrane to cause the stereocilia to pivot. In this state the tension in the tip links is slight so only about 10% of the potassium channels gated by them are open => small depolarisation.
- This is sufficient to sustain tonic release of glutamate, which maintains baseline firing of the primary afferent.
State the series of consequences that result from a head tilt in the direction of the axis of polarity
- Causes the otolith membrane to pull on the stereocilia, making them pivot
- Tension in the tip links increases
- This opens stereocilia K+ channels, allowing potassium influx to depolarise the hair cell
- Increasing glutamate release (due to calcium influx) proportional to tilt angle and raising the afferent firing rate
State the series of consequences that result from a head tilt in the opposite direction of the axis of polarity
Reduces tip link tension so K+ channels close, the hair cells hyperpolarize and primary afferent firing drops.
Why would a tilt which is perpendicular to the axis of polarity of a hair cell have no effect?
Because stereocilia are not linked in this direction
Tilts in intermediate directions cause what?
graded receptor potentials
How are the axes of hair cells oriented?
The axes of hair cells are orientated in an orderly pattern so a given stimulus will depolarize some hair cells and hyperpolarize others.
The stereocilia of the vestibular hair cells of crest are embedded into what?
embedded in a gelatinous sheet, called the cupula, that bridges the width of the ampulla
Describe how head rotation leads to ME transduction
- Rotation of the head maximally stimulates hair cells in the canals lying in the same plane as the rotation.
- Rotation of the endolymph lags behind head rotation because of its inertia, so the endolymph exerts a pressure distorting the cupula, bending the stereocilia.
- The transduction mechanism is identical to that of hair cells in otolith organs.
For what head rotation speeds are the duct afferents able to transmit signals?
The signals transmitted by the duct afferents measure angular acceleration for slow and fast rotations, but encode velocity for mid-range rotation speeds
How do the semicircular ducts on each side lying in the same plane operate in pairs?
Head rotation that causes depolarisation of hair cells in the horizontal duct of the left ear will hyperpolarise hair cells in the horizontal duct of the right ear.
Other semicircular canal partners (which alternately depolarise and hyper polarise):
- Left Anterior + Right Posterior (LARP)
- Right Anterior + Left Posterior (RALP)
What type of neuronal cell are the primary vestibular afferents, and what nerve do they run in?
The vestibular primary afferents are pseudobipolar cells with their cell bodies in the vestibular ganglion. Their axons run in the vestibulocochlear nerve to enter the vestibular nuclei
How many vestibulocochlear nuclei are there, and where are they located?
There are 4 vestibular nuclei that lie laterally in the medulla and pons - superior, lateral, medial and inferior.
Describe the neural circuitry mediating the vestibule-ocular reflex
- Vestibular nerve fibres originating in the left horizontal semicircular canal project to the medial and superior vestibular nuclei
- Excitatory fibres from the medial vestibular nucleus cross to the contralateral abducens nucleus, which has two outputs.
- One of these is a motor pathway that causes the lateral rectus of the right eye to contract; the other crosses the midline and ascends via the medial longitudinal fasciculus to the left oculomotor nucleus, where it activates neurons that cause the medial rectus of the left eye to contract.
- Finally, inhibitory neurons project from the medial vestibular nucleus to the left abducens nucleus, directly causing the motor drive on the lateral rectus of the left eye to decrease and also indirectly causing the right medial rectus to relax.
The consequence is that turning the head to the left causes eye movements to the right.
Describe the path of superior vestibular neurones in the VOR
Project ipsilaterally to the oculomotor and trochlear nuclei to generate vestibulo-occular reflexes allowing for vertical gaze stabilisation
Describe the neural circuitry mediating the vestibulo-cervical reflex, and for what?
Axons form the medial vestibular nucleus descend in the medial longitudinal fasciculus to reach the upper cervical level of the spinal cord.
This pathway regulates head position by reflex activity of neck activity in response to stimulation of the semicircular canals caused by head rotations.
Describe the neural circuitry mediating the vestibulo-spinal reflex, and for what?
- The inputs from the otolith organs project mainly to the lateral vestibular nucleus, which in turn sends axons in the lateral vestibulospinal tract to the spinal cord.
- These axons terminate monosynaptically on extensor motor neurons, and they disynaptically inhibit flexor motor neurons; the net result is a powerful excitatory influence on the extensor (antigravity) muscles
=> mediates balance and the maintenance of upright posture
Describe the importance vestibulocerebellar circuits
- Integrating and modulating vestibular signals to enable adaptive changes to the VOR
- Distinguish head tilts from translational movements
- Distinguish passive movements of the head and body from those that are self-generated
Major target = flocculonodular lobe
Describe the vestibular pathways to the thalamus and cortex which are especially important to our sense of self-motion and orientation in space
The superior and lateral vestibular nuclei send axons (in the medial lemniscus) to the ventral posterior nuclear complex of the thalamus. From here neurons project (via the internal capsule) to the parietoinsular vestibular cortex which lies at the temporo-parietal boundary
Why is central vestibular processing described as inherently multi sensory?
The vestibular nuclei are important centers of integra- tion, receiving input from the vestibular nuclei of the opposite side, as well as from the cerebellum and the visual and somatosensory systems.
Define vertigo.
False perception of movement in space
Define vestibular ataxia
Instability of gait or posture
What happens to the ability of the brain to stabilise the eyes in unilateral vestibular lesions?
Vestibular nystagmus
The eyes start moving in the direction of the lesion
State a consequence of a bilateral loss of vestibular functions, in terms of a loss of the VOR and VCR/VSR
Loss of VOR:
Oscillopsia = Everything appears to be shaking – the eyes aren/t able to fixate on visual targets while the head is moving
Loss of VCR/VSR:
Diminished head and postural stability => gait deviations + difficulty balancing
What are some other consequences of vestibular loss?
- Slight impairment of orthostatic control
- Severe nausea and vomiting
- Loss of coordination on directional reorientation, motion intolerance,
- Oversensitivity to visual motion in the environment
What are the effects of loss of canal function on one side?
There is unopposed signal coming from the intact side meaning that there is partial impairment of sensitivity to rotation in the ‘on’ direction of the defunct canal
Why would a unilateral canal lesion cause vertigo?
The unopposed tonus of the intact canal gives a signal as if the head is rotating to the intact side.
Patient may feel like they’re spinning even though they’re not.
Why would acute unilateral vestibular disorder cause vestibular nystagmus?
Unopposed tonus of the intact canal causes the eyes to be driven to the lesioned side – this is a vestibulo-ocular reflex (because it thinks that your head is rotating towards the intact side)
State a common cause of vestibular vertigo that lasts:
a. Seconds
b. Minutes
c. Hours
d. Days
e. Fluctuating/continuous
f. Silent
a. Seconds Benign Paroxysmal Positional Vertigo (BPPV) b. Minutes Vertebrobasilar insufficiency c. Hours Meniere’s Syndrome d. Days Vestibular neuritis e. Fluctuating/continuous Uncompensated vestibular lesion f. Silent Acoustic neuroma
What is BPPV and how is it treated?
Benign paroxysmal positional vertigo:
- It is caused by otoconial debris (small crystals of calcium carbonate/ ‘ear rocks’) in the canals and is provoked by head movement
- Debris floating in the canal stimulates the ampulla and generates false signals of head rotation
Treatment:
Particle repositioning manoeuvre = turning the head vigorously in the opposite direction to that which provokes the vertigo, through 360 degrees, flushing out the debris
