Case 4 Flashcards
what is the frequency range that humans can detect sound? what is the upper limit in the average adult closer to?
from about 20 Hz to 20 kHz
15-17 kHz
which frequencies is the ear most sensitive to? what does this correspond to?
The ear is most sensitive between 500 and 4000 Hz, which roughly corresponds to the frequency range most important for understanding speech.
external ear
- what does it consist of
- what do these structures do
- what does the configuration of the external auditory meatus do?
- The external ear consists of the pinna (auricle), concha, and external auditory meatus.
- These structures collect sound waves and focus them on the tympanic membrane.
- The configuration of the external auditory meatus selectively boosts the sound pressure (around 30-100 times) for frequencies around 3 kHz via passive resonance effects. This amplification makes humans especially sensitive to frequencies in the range of 2–5 kHz.
how does the ear recognise the elevation of a sound source?
The ear recognises the elevation of a sound source because the vertically asymmetrical convolutions of the pinna are shaped so that the external ear transmits more high-frequency components from an elevated source than from the same source at ear level.
middle ear
- what does it do
- how is it done
• The middle ear converts vibrations in air pressure into movements of the ossicles.
• The middle ear ensures transmission of the sound energy across the air–fluid boundary by boosting the pressure measured at the tympanic membrane greatly by the time it reaches the inner ear.
• Two mechanical processes occur within the middle ear to achieve this large pressure gain:
1. Focusing the force impinging on the relatively large-diameter tympanic membrane on to the much smaller-diameter oval window.
2. A second and related process relies on the mechanical advantage gained by the lever action of the three ossicles (malleus, incus and stapes) which connect the tympanic membrane to the oval window. Sound causes large movements of the tympanic membrane, which are transformed into smaller but stronger vibrations of the oval window.
what is the pressure at the oval window like? why? what does this allow?
• The pressure at the oval window is great because it has a smaller surface area to the tympanic membrane AND because the force on the oval window membrane is greater than that on the tympanic membrane.
The force applied on the oval window is greater than that on the tympanic membrane because behind the tympanic membrane is air, whereas behind the oval window is fluid. Therefore, more force needs to be applied at the oval window.
• The pressure exerted on the oval window is about 20 times greater than at the tympanic membrane, and this increase is sufficient to move the fluid in the inner ear.
what are the two muscles in the middle ear? what are they innervated by?
- The tensor tympani – innervated by mandibular nerve (V3)
2. Stapedius - innervated by facial nerve (CN VII).
what does contraction of the muscles in the middle ear cause? what is it important for? what frequencies is it greater for? when doesn’t it work?
- Contraction of these muscles causes the chain of ossicles to become more rigid, and sound conduction to the inner is greatly diminished.
- The onset of a loud sound triggers a neural response called the attenuation reflex.
- Sound attenuation is much greater at lower frequencies than at high frequencies.
- The automatic contraction of these muscles occurs a few microseconds after a loud noise, and so doesn’t provide protection against sudden loud noises.
describe the anatomy of the cochlea
• At the base of the cochlea are two membrane-covered holes:
1. The oval window – this is below the footplate of the stapes
2. The round window
• In the cross-section of the cochlea, we can see that it is divided into three fluid-filled chambers: the Scala vestibuli, the Scala media and the Scala tympani.
• Reissner’s membrane separates the scala vestibuli and the scala media.
• Basilar membrane separates the scala tympani and the scala media.
• Sitting on the basilar membrane is the organ of Corti, which contains auditory receptor neurons; hanging over this organ is the tectorial membrane.
• At the apex of the cochlea, the scala media is closed off, and the scala tympani becomes continuous with the scala vestibule at a hole in the membranes called the helicotrema. This allows the perilymph in these two scale to mix.
• At the base of the cochlea, the scala vestibuli meets the oval window and the scala tympani meets the round window.
what happens when there is inward movement of the oval window (due to force applied by the ossicles)?
the fluid of the inner ear is displaced, causing the round window to bulge slightly and deforming the cochlear partition
what is the role of the basilar membrane?
The basilar membrane has two structural properties that determine the way it responds to sound:
1. The membrane is wider at the apex than at the base by a factor of about 5.
2. The stiffness of the membrane decreases from the base to apex, the base being about 100 times stiffer.
When sound pushes the footplate of the stapes at the oval window, perilymph is displaced within the scala vestibuli, and endolymph is displaced within the scala media because Reissner’s membrane is very flexible.
Sound can also pull the footplate, reversing the pressure gradient.
Sound causes a continual push-pull motion of the footplate.
The displacement of the endolymph in the scala media makes the basilar membrane bend near its base, starting a wave that propagates toward the apex.
The wave travels up the basilar membrane. The distance this wave travels up the basilar membrane is dependent on the frequency of the sound. The higher the frequency, the shorter the distance it will travel up the basilar membrane. This is because if the frequency is high, the stiffer base of the membrane will vibrate a good deal, dissipating most of the energy, and the wave will not propagate very far.
what is the role of the organ of Corti?
- The auditory receptor cells, which convert mechanical energy into a change in membrane polarisation, are located in the organ of Corti.
- The organ of Corti consists of hair cells (auditory receptors), the rods of Corti, and various supporting cells.
- The auditory receptors are called ‘hair cells’ because each one has about 100 hairy-looking stereocilia extending from its top.
- The critical event in the transduction of sound into a neuronal signal is the bending of these stereocilia.
what is the role of auditory receptors/hair cells?
- These are involved in the mechano-electrical transduction of sound waves.
- The hair cells are sandwiched between the basilar membrane and the reticular lamina.
- The rods of Corti span these two membranes and provide structural support.
- The stereocilia at the tips of the hair cells extend above the reticular lamina into the endolymph, and their tips end either in the tectorial membrane (outer hair cells) or just below the tectorial membrane (inner hair cells).
- Hair cells form synapses (neurotransmitter is glutamate) on neurons whose cell bodies are located in the spiral ganglion.
- Axons from the spiral ganglion enter the auditory nerve, a branch of the auditory-vestibular nerve, which projects to the cochlear nuclei in the medulla.
describe & explain transduction by hair cells
• When the basilar membrane moves in response to the a motion at the stapes, the entire foundation supporting the hair cells moves because the basilar membrane, rods of Corti, reticular lamina, and hair cells are connected.
• Because the tectorial membrane holds the tips of the outer hair cell stereocilia, the lateral motion of the reticular lamina relative to the tectorial membrane bends the stereocilia on the outer hair cells one way or the other.
• The stereocilia are graded in height and are arranged in a bilaterally symmetric fashion:
Displacement of the hair bundle parallel to this plane toward the tallest stereocilia depolarises the hair cell.
While movements parallel to this plane toward the shortest stereocilia cause hyperpolarisation.
Displacements perpendicular to the plane of symmetry do not alter the hair cell’s membrane potential.
- There is a special type of cation channel on the tips of the stereocilia, called the TRPA1 channel.
- When the hair cells bend, the TRPA1 channels open, causing an influx of Na+ and K+ ions. This generates changes in the hair cell receptor potential.
- Each channel is linked with an elastic filament called tip link, to the wall of the adjacent cilium.
- When the cilia are straight, the tension on the tip link holds the channel in a partially opened state, allowing a small leak of K+ from the endolymph into the hair cell.
- Displacement of the cilia in one direction increases tension on the tip link, increasing the inward K+ current.
- Displacement in the opposite direction relieves tension on the tip link, thereby allowing the channel to close completely, preventing inward K+ movement.
- The entry of K+ into the hair cell causes a depolarization, which in turn activates voltage-gated calcium channels.
- The entry of Ca2+ triggers the release of neurotransmitter, probably glutamate, which activates the spiral ganglion fibers lying postsynaptic to the hair cell.
- The hair cell has a resting potential between –45 and –60 mV.
• K+ serves both to depolarise and repolarise the cell, enabling the hair cell’s K+ gradient to be largely maintained by passive ion movement alone.
The apical end (including the stereocilia) protrudes into the scala media and is exposed to the K+ rich, Na+ poor endolymph, which is produced by dedicated ion pumping cells in the stria vascularis (stria vascularis resorbs Na+ and secretes K+).
The basal end of the hair cell body is bathed in perilymph which is K+ poor and Na+ rich.
The compartment containing endolymph is about 80 mV more positive than the perilymph compartment (this difference is known as the endocochlear potential), while the inside of the hair cell is about 45 mV more negative than the perilymph (and 125 mV more negative than the endolymph).
• The resulting electrical gradient across the membrane of the stereocilia (about 125 mV; the difference between the hair cell resting potential and the endocochlear potential) drives K+ through open transduction channels into the hair cell, even though these cells already have a high internal K+ concentration.
K+ entry via the transduction channels depolarizes the hair cell, opening voltage-gated Ca2+ and K+ channels located in the membrane of the hair cell soma.
The opening of somatic K+ channels favours K+ efflux, and thus repolarization. The efflux occurs because the perilymph surrounding the basal end is low in K+ relative to the cytosol.
• In addition to modulating the release of neurotransmitter, Ca2+ entry opens Ca2+-dependent K+ channels, which provide another avenue for K+ to enter the perilymph.
what are the different types of hair cells? how are they arranged? what does each do?
• There are two types of hair cells: Inner hair cells and Outer hair cells.
• There is one row of inner hair cells and three rows of outer hair cells (five at the apex).
• The inner hair cells are the actual sensory receptors. About 95% of the fibres of the auditory nerve that project to the brain arise from the inner hair cells.
One spiral ganglion fibre receives input from only one inner cell.
Each inner cell feeds about 10 spiral ganglion neurites.
• The terminations on the outer hair cells are almost all from efferent axons that arise from cells in the superior olivary complex (this is the first site of convergence of sound from the right and left ears).
- Outer hair cells act like tiny motors that amplify the movement of the basilar membrane during low-intensity sound stimuli.
- Because of this action, the outer hair cells in the basilar membrane are referred to as the cochlear amplifier.
- Cochlear amplification occurs as a result of motor proteins present in the membranes of the outer cells.
- Motor proteins can change the length of outer hair cells.
- Outer hair cells respond to sound with both a receptor potential and a change in length.
- The hair cells’ motor is driven by the receptor potential, and it does not use ATP as an energy source.
- The hair cells’ motor system is extremely fast, as it must be able to keep up with movements induced by high frequency sounds.
- The hair cells’ motor is a protein called prestin. This is tightly packed into the membranes of the outer hair cells, and it is required for outer hair cells to move in response to sound.
- When the outer hair cells amplify the response of the basilar membranes, the stereocilia on the inner hair cells will bend more, and the increased transduction process in the inner hair cells will produce a greater response in the auditory nerve.
describe the auditory pathway
• Afferents from the spiral ganglion enter the brain stem in the vestibulocochlear nerve.
• At the level of the medulla, the axons innervate the dorsal cochlear nucleus and ventral cochlear nucleus ipsilateral to the cochlea where the axons originated.
Each axon branches so that it synapses on neurons in both cochlear nuclei.
• Cells in the ventral cochlear nucleus send out axons that project to the superior olive (superior olivary nucleus) on both sides of the brain stem.
• Axons of the olivary neurons ascend in the lateral lemniscus (a lemniscus is a collection of axons) and innervate the inferior colliculus of the midbrain.
Many efferents of the dorsal cochlear nucleus follow a route similar to the pathway from the ventral cochlear nucleus, but the dorsal path bypasses the superior olive.
• Although there are other routes from the cochlear nuclei to the inferior colliculus, with additional intermediate relays, all ascending auditory pathways converge onto the inferior colliculus.
• The neurons in the inferior colliculus send out axons to the medial geniculate nucleus (MGN) of the thalamus, which in turn projects to auditory cortex.
what are important points to remember with the auditory pathway?
- other pathways
- feedback
- deafness in one ear
• It is important to note that there are many parallel auditory pathways from the cochlear nuclei to the auditory cortex of the brain.
• Projections and brain stem nuclei other than the one described above contribute to the auditory pathways:
For example – the inferior colliculus sends axons not only to the MGN but also to the superior colliculus (where the integration of auditory and visual information occurs) and to the cerebellum.
• There is extensive feedback in the auditory pathways:
For example – brain stem neurons send axons that contact outer hair cells, and auditory cortex send axons to the MGN and inferior colliculus.
• Each cochlear nucleus receives input from just the one ear on the ipsilateral side; all other auditory nuclei in the brain stem receive input from both ears.
This explains the clinically important fact that the only way by which brain stem damage can produce deafness in one ear is if a cochlear nucleus (or auditory nerve) on one side is destroyed.
The anterior inferior cerebellar artery supplies the cochlear nuclei, and unilateral occlusion can produce deafness in one ear.
what are the monaural pathways? what are they for?
- A second major set of pathways from the cochlear nucleus bypasses the superior olive and terminates in the nuclei of the lateral lemniscus on the contralateral side of the brainstem.
- These particular pathways respond to sound arriving at one ear only and are thus referred to as monaural.
where is the middle geniculate nucleus found? what is it made up of?
in the thalamus
• The MGN has several divisions, including;
The ventral division, which functions as the major thalamocortical relay.
The dorsal and medial divisions, which are organized like a belt around the ventral division.
why is the auditory thalamus/middle geniculate nucleus important? where does input arise from? what happens in the MGN?
- It is an obligatory relay for all ascending auditory information destined for the auditory cortex.
- Most input to the MGC arises from the inferior colliculus, although a few auditory axons from the lower brainstem bypass the inferior colliculus to reach the auditory thalamus directly.
• The MGN is the first station in the auditory pathway where selectivity for combinations of frequencies is found. There is also selectivity for specific time intervals between the two frequencies.
via what do axons leaving the MGN project to the auditory cortex?
via the internal capsule in an array called the acoustic radiation
what does the auditory cortex consist of?
6 layers: Layer I contains few cell bodies, and layers II and III contain mostly small pyramidal cells. Layer IV, where the medial geniculate axons terminate, is composed of densely packed granule cells. Layers V and VI contain mostly pyramidal cells that tend to be larger than those in the superficial layers.
where is the primary auditory cortex (A1) located? in what form does it receive input?
on the superior temporal gyrus in the temporal lobe
- it receives point-to-point input from the ventral division of the MGN; thus, it contains a precise tonotopic map - these are known as isofrequency bands
- the belt areas of the auditory cortex receive more diffuse input from the belt areas of the MGC and therefore are less precise in their tonotopic organization.
what are the ways that information about sound intensity are coded?
• Information about sound intensity is coded in two interrelated ways:
1. The firing rates of neurons in auditory nerve.
2. The number of active neurons in auditory nerve.
• The loudness we perceive is thought to be correlated with the number of active neurons in the auditory nerve (and throughout the auditory pathway) and their firing rates.
• Firing rates of neurons:
As a stimulus gets more intense, the basilar membrane vibrates with greater amplitude, causing the membrane potential of the activated hair cells to be more depolarised or hyperpolarised.
As a result, the nerve fibres with which the hair cells synapse fire action potentials at greater rates.
• Number of activated neurons:
More intense stimuli produce movements of the basilar membrane over a greater distance, which leads to the activation of more hair cells.
In a single auditory nerve fibre, this increase in the number of activated hair cells causes a broadening of the frequency range to which the fibre responds.
what is tonotopy? where do tonotopic maps exist?
- When auditory axons in the auditory-vestibular nerve synapse in the cochlear nuclei, they do so in an organized pattern based on characteristic frequency.
- Nearby neurons have similar characteristic frequencies, and a systematic relationship exists between position in the cochlear nucleus and characteristic frequency.
- In other words, there is a map of the basilar membrane within the cochlear nuclei.
- Systematic organization of characteristic frequency within an auditory structure is called tonotopy.
- Tonotopic maps exist on the basilar membrane within each of the auditory relay nuclei, the MGN, and auditory cortex.
because of the tonotopy present throughout the auditory system, the location of active neurons in auditory nuclei is one indication of what?
the frequency of the sound
what is phase locking? why is it important?
- When auditory nerve neurons fire action potentials, they tend to respond at times corresponding to a peak in the sound pressure waveform, i.e., when the basilar membrane moves up.
- The result of this is that there are a bunch of neurons firing near the peak of each and every cycle of sound pressure waveform.
- No individual neuron can respond to every cycle of a sound signal, so different neurons fire on successive cycles.
- Nonetheless, when they do respond they tend to fire together.
- The resultant “phase locking” that results provides temporal information from the two ears to neural centres that compare interaural time differences.
- The evaluation of interaural time differences provides a critical cue for sound localization and the perception of auditory “space.”
summarise how different frequencies are represented
At very low frequencies, phase locking is used.
At intermediate frequencies, both phase locking and tonotopy are useful.
At high frequencies, tonotopy must be relied on to indicate sound frequency.
what is the ‘volley principal’ of auditory information transfer?
- When a bunch of neurons fire at a peak of the sound wave, they need time to recover.
- This means that a second bunch of neurons fire action potentials at the second peak; a third bunch at the third peak; until eventually the first bunch of neurons has recovered.
- This cycle is repeated so that all the ‘peaks’ of a low-frequency sound wave (up to about 3-4kHz) are covered.
- This is the “volley principal” of auditory information transfer.
how does sound need to be localised?
in two planes: the horizontal plane and the vertical plane
describe the localisation of sound in the horizontal plane
• Humans use two different strategies to localize the horizontal position of sound sources, depending on the frequencies in the stimulus:
For frequencies below 3 kHz, interaural time differences are used to localize the source.
For frequencies above 3 kHz, interaural intensity differences are used instead.
• Parallel auditory pathways originating from the cochlear nucleus serve each of these strategies for sound localization.
what does the neural circuitry that modulates interaural time differences consist of? how are the ITD compensated for?
Interaural Time Differences (<3kHz):
• The neural circuitry that modulates interaural time differences consists of binaural inputs to the medial superior olive (MSO) that arise from the right and left anteroventral cochlear nuclei.
• The MSO contains cells with bipolar dendrites that extend both medially and laterally.
The lateral dendrites receive input from the ipsilateral anteroventral cochlear nucleus.
The medial dendrites receive input from the contralateral anteroventral cochlear nucleus.
• The MSO cells work as coincidence detectors, responding when both excitatory signals arrive at the same time.
• The axons that project from the anteroventral cochlear nucleus evidently vary systematically in length to create delay lines.
• These anatomical differences compensate for sounds arriving at slightly different times at the two ears, so that the resultant neural impulses arrive at a particular MSO neuron simultaneously, making each cell especially sensitive to sound sources in a particular place.
interaural intensity differences
- why do we have them
- where are the circuits that modulate the position of a sound source by IID found?
- describe what happens
- When high-frequency (> 3kHz) sounds are directed toward one side of the head, an acoustical “shadow” of lower intensity is created at the far ear.
- The circuits that modulate the position of a sound source on this basis are found in the lateral superior olive (LSO) and the medial nucleus of the trapezoid body (MNTB).
- Excitatory axons project directly from the ipsilateral anteroventral cochlear nucleus to the LSO.
- The LSO also receives inhibitory input from the contralateral ear, via an inhibitory neuron in the MNTB.
- This excitatory/inhibitory interaction results in a net excitation of the LSO on the same side of the body as the sound source.
- For sounds arising directly lateral to the listener, firing rates will be highest in the LSO on that side; in this circumstance, the excitation via the ipsilateral anteroventral cochlear nucleus will be maximal, and inhibition from the contralateral MNTB minimal.
- In contrast, sounds arising closer to the listener’s midline will elicit lower firing rates in the ipsilateral LSO because of increased inhibition arising from the MNTB.
- For sounds arising at the midline, or from the other side, the increased inhibition arising from the MNTB is powerful enough to completely silence LSO activity.
- Note that each LSO only encodes sounds arising in the ipsilateral hemifield; it therefore takes both LSOs to represent the full range of horizontal positions.
where are ITD and IID processed?
where are the two pathways eventually merged?
• In summary, there are two separate pathways—and two separate mechanisms— for localizing sound in the horizontal pane:
Interaural time differences are processed in the medial superior olive.
Interaural intensity differences are processed in the lateral superior olive.
• These two pathways are eventually merged in the midbrain auditory centers.
describe localisation of sound in the vertical plane
- This is dependent on the curvature and shape of the pinna.
- Specialized neurons within the dorsal cochlear nucleus appear to use this information to determine the elevation of the sound source.
- The ascending projection of the dorsal cochlear nuclei bypasses the superior olivary complex to reach the inferior colliculus directly.
what does the vestibular system use to transduce movements?
hair cells
where are the hair cells (for auditory system) contained?
within sets of interconnected chambers called the vestibular labyrinth
what does the vestibular labyrinth consist of? what is function of each part? why are the functions different?
- otolith organs (saccule & utricle) - detect the force of gravity and tilts of the head
- semicircular canals - sensitive to head rotation
• These structures are sensitive to different kinds of movement not because their hair cells differ, but because of the specialised structures within which the hair cells reside.
to what and how does each hair cell of the vestibular organs transmit impulses?
Each hair cell of the vestibular organs makes an excitatory synapse with the end of a sensatory axon from the vestibular nerve, branch of the vestibulocochlear nerve (CN VIII).
where are the cell bodies of the vestibular nerve axons found?
in Scarpa’s ganglion
what are the membranous sacs within the bone (vestibular system) filled with? what is it collectively called?
endolymph - they are collectively called the membranous labyrinth
what is endolymph high and low in?
high in K+ and low in Na+
where is perilymph found? what’s it high and low in?
between the bony walls (the osseous labyrinth) and the membrnaous labyrinth
low in K+ and high in Na+
where are the vestibular hair cells located? how are they situated?
in the otolith organs and in ampullae, located at the base of the semicircular canals next to the utricle
Within each ampulla, the vestibular hair cells extend their hair bundles into the endolymph of the membranous labyrinth.
what causes neurotransmitter to be released onto the vestibular nerve fibres?
- Movements of the stereocilia toward the kinocilium (this is the largest single cilium in the hair bundle – similar to the auditory system) in the vestibular organs opens mechanically gated transduction channels located at the tips of the stereocilia.
- This causes depolarisation of the hair cell, causing neurotransmitter release onto (and excitation of) the vestibular nerve fibres.
what does the biphasic nature of the receptor potential mean?
The biphasic nature of the receptor potential means that some transduction channels are open in the absence of stimulation, with the result that hair cells tonically release neurotransmitter, thereby generating considerable spontaneous activity in vestibular nerve fibres.
what’s important about the orientations of hair cell bundles? how are they polarised?
• The hair cell bundles in each vestibular organ have specific orientations.
• As a result, the organ as a whole is responsive to displacements in all directions.
In a given semicircular canal, the hair cells in the ampulla are all polarized in the same direction.
In the utricle and saccule, a specialized area called the striola divides the hair cells into two populations with opposing polarities. (otoconia are calcium carbonate crystals that form the striola which in turn rests on the otolithic membrane)
what do the otolith organs detect?
• These detect changes of head angle, as well as linear acceleration of the head, such as tilting the head.
otolith organs form the static system and detect linear acceleration
what do both the otolith organs contain?
sensory epithelium, the macula, which consists of hair cells and associated supporting cells
what surrounds the hair cells in otolith organs?
Overlying the hair cells and their hair bundles is a gelatinous layer; above this layer is a fibrous structure, the otolithic membrane, in which are embedded crystals of calcium carbonate called otoliths.
what happens when the head is tilted? what do the utricle and saccule each repond to?
• When the head tilts, gravity causes the membrane to shift relative to the sensory epithelium. The resulting shearing motion between the otolithic membrane and the macula displaces the hair bundles, which are embedded in the lower, gelatinous surface of the membrane.
• This displacement of the hair bundles generates a receptor potential in the hair cells.
• A shearing motion between the macula and the otolithic membrane also occurs when the head undergoes linear accelerations; the greater relative mass of the otolithic membrane causes it to lag behind the macula temporarily, leading to transient displacement of the hair bundle.
• The striola forms an axis of mirror symmetry such that hair cells on opposite sides of the striola have opposing morphological polarizations.
• A tilt along the axis of the striola will excite the hair cells on one side while inhibiting the hair cells on the other side.
The saccular macula is oriented vertically and the utricular macula horizontally.
• Inspection of the excitatory orientations in the maculae indicates that:
The utricle responds to movements of the head in the horizontal plane, such as sideways head tilts and rapid lateral displacements.
The saccule responds to movements in the vertical plane (up–down and forward–backward movements in the sagittal plane).
• Note that the saccular and utricular maculae on one side of the head are mirror images of those on the other side. Thus, a tilt of the head to one side has opposite effects on corresponding hair cells of the two utricular maculae.
how do otolith neurons sense linear forces?
The structure of the otolith organs enables them to sense both static displacements, as would be caused by tilting the head relative to the gravitational axis, and transient displacements caused by translational movements of the head.
The change in firing rate in response to a given movement can be either sustained or transient, thereby signalling either absolute head position or linear acceleration.
The range of orientations of hair bundles within the otolith organs enables them to transmit information about linear forces in every direction the body moves.
- The utricle, which is concerned with horizontal motion.
- The saccule, which is concerned with vertical motion.
These two combine to effectively gauge the linear forces acting on the head at any instant in three dimensions.
Tilts of the head off the horizontal plane and translational movements of the head in any direction stimulate a distinct subset of hair cells in the saccular and utricular maculae, while simultaneously suppressing the responses of other hair cells in these organs.
what planes do the semicircular canals lie in? what does this mean?
which is each one it?
they lie in orthogonal planes, which means that there is an angle of 90* between any pair of them
Horizontal semicircular canal = horizontal plane = rotation of head
Anterior/superior semicircular canal = sagittal plane = nodding of head
Posterior semicircular canal = coronal plane = head to shoulder
- Sensitive to pitch, roll and yaw (each canal sensitive to its own one – horizontal detects yaw, posterior detects pitch and superior detects roll) – essential for coordination of eye movement
what do the semicircular canals sense?
head rotations
what does each semicircular canal have at its base? what does this contain?
a bulbous expansion called the ampulla, which houses the crista, that contains the hair cells
the hair bundles extend out of the crista into a gelatinous mass called what? forming what?
the cupula, forming a fluid barrier through which endolymph cannot circulate
how does movement of endolymph cause changes in neuronal activity?
• The hair bundles extend out of the crista into a gelatinous mass, the cupula, forming a fluid barrier through which endolymph cannot circulate.
• As a result, the relatively compliant cupula is distorted by movements of the endolymphatic fluid that surrounds the cupula.
• When the head turns in the plane of one of the semicircular canals, the inertia of the endolymph produces a force across the cupula, distending it away from the direction of head movement and causing a displacement of the hair bundles within the crista.
• In contrast, linear accelerations of the head produce equal forces on the two sides of the cupula, so the hair bundles are not displaced.
• Unlike the saccular and utricular maculae, all of the hair cells in the crista within each semicircular canal are organized with their kinocilia pointing in the same direction.
• Thus, when the cupula moves in the appropriate direction, the entire population of hair cells is depolarized and activity in all of the innervating axons increases.
• When the cupula moves in the opposite direction, the population is hyperpolarized and neuronal activity decreases.
Deflections orthogonal to the excitatory–inhibitory direction produce little or no response.
• Each semicircular canal works in concert with the partner located on the other side of the head that has its hair cells aligned oppositely. There are three such pairs:
The two pairs of horizontal canals
The superior canal on each side working with the posterior canal on the other side.
• Head rotation deforms the cupula in opposing directions for the two partners, resulting in opposite changes in their firing rates.
• Thus, the hair cells in the canal towards which the head is turning are depolarized, while those on the other side are hyperpolarized.
how do semicircular canal neurones sense angular accelerations?
• If an experiment has three phases: an initial period of acceleration, then a period of several seconds at constant velocity, and finally a period of sudden deceleration to a stop.
The maximum firing rates observed corresponds to the period of acceleration.
The maximum inhibition corresponds to the period of deceleration.
During the constant-velocity phase, the response adapts so that the firing rate subsides to resting level.
After the movement stops, the neuronal activity decreases transiently before returning to the resting level.
• When rotation is stopped, the inertia of the endolymph causes the cupula to bend in the other direction, generating an opposite response from the hair cells and a temporary sensation of counterrotation.
what are the reflexes associated with vestibular system?
- Vestibulo-ocular reflex
- Vestibulo-cervical reflex
- Vestibulo-spinal reflex
vestibulo-ocular reflex
- what for
- what happens
- what are the three types
• The vestibulo-ocular reflex (VOR) in particular is a mechanism for producing eye movements that counter head movements, thus permitting the gaze to remain fixed on a particular point.
• These eye movements compensate for head movements to produce a stable image on the retina.
• There are three types of vestibulo-ocular reflexes:
1. Rotational VOR – rotational head movement – semicircular canals
2. Translational VOR – linear head movement – otolith organs
3. Ocular counter-rolling response – head tilt – otolith organs
- Prevents retinal slip
- Head rotates left, eyes rotate right!
- Vestibular apparatus detects the angular acceleration of the head to the left, and it compensates using this pathway to counter-rotate the eyes by the same number of degrees to the right
- Left eye: contract medial rectus, relax lateral rectus
- Right eye: contract lateral rectus, relax medial rectus
what happens with rotational VOR? what is this reflex eye movement pattern called?
- The semicircular canals in one ear sense rotation of the head in one direction.
- The eyes slowly rotate in the opposite direction – slow phase (vestibular).
- The eyes rapidly reset to centre of gaze – fast phase (brainstem).
- Reflex eye movement pattern = “nystagmus”
activity in the left horizontal canal induced by leftward rotary acceleration of the head results in compensatory eye movements to the right. explain the pathway
- This effect is due to excitatory projections from the vestibular nucleus to the contralateral nucleus abducens that, along with the oculomotor nucleus, help execute conjugate eye movements.
- Horizontal movement of the two eyes toward the right requires contraction of the left medial and right lateral rectus muscles.
- Vestibular nerve fibres originating in the left horizontal semicircular canal project to the medial and lateral vestibular nuclei.
• Excitatory fibres from the medial vestibular nucleus (MVN) cross to the contralateral abducens nucleus, which has two outputs.
Motor pathway - causes the lateral rectus of the right eye to contract.
Excitatory projection - decussates and ascends via the medial longitudinal fasciculus (MLF) 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 of these several connections is that excitatory input from the horizontal canal on one side produces eye movements toward the opposite side. Therefore, turning the head to the left causes eye movements to the right.
what is nystagmus? what does it consist of? what are the different types? what mediates/triggers each phase? test?
- This is defined as a pattern of reflex eye movements.
- It consists of two phases: fast phase and slow phase.
- Nystagmus can be of several types: optokinetic (visual), vestibular, post-alcoholic.
(constant uncontrolled movement of the eyes – the movements are usually side to side but can also be up and down in a circular motion)
- An element of the VOR involving alternating slow eye movement with rapid saccadic movement
- Slow phase movements mediated by vestibulo-ocular pathway, fast phase movements are triggered by the cerebral cortex
- Physiological nystagmus (e.g. optic kinetic)
- Can test clinically by introducing warm or cold water into the external auditory meatus
- Causes convection currents in the endolymph, stimulates hair cells as if the head was rotating leading to nystagmus
what are descending projections from the vestibular nuclei essential for?
Postural adjustments of the head, mediated by the vestibulo-cervical reflex (VCR).
Postural adjustments of the body, mediated by the vestibulo-spinal reflex (VSR).
vestibulo-cervical reflex
- what is pathway
- what does it regulate
- give an example
- This involves the medial vestibular nucleus.
- Axons descend in the medial longitudinal fasciculus to reach the upper cervical levels of the spinal cord.
- This pathway regulates head position by reflex activity of neck muscles in response to stimulation of the semicircular canals from rotational accelerations of the head.
For example:
• During a downward pitch of the body (e.g., tripping), the superior canals are activated and the head muscles reflexively pull the head up. The dorsal flexion of the head initiates other reflexes, such as forelimb extension and hindlimb flexion, to stabilize the body and protect against a fall.
vestibulo-spinal reflex
- what is pathway
- what does pathway mediate
- This involves the lateral vestibular nucleus.
- This also involves the lateral and medial vestibulospinal tracts and the reticulospinal tract.
- The inputs from the otolith organs project mainly to the lateral vestibular nucleus, which in turn sends axons in the lateral vestibulospinal tract (LVST) 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.
- When hair cells in the otolith organs are activated, signals reach the medial part of the ventral horn.
- By activating the ipsilateral pool of motor neurons innervating extensor muscles in the trunk and limbs, this pathway mediates balance and the maintenance of upright posture.
- Basic balance and postural control
- Axons from vestibular nuclei descend ipsilaterally
- Synapse on LMNs (lower motor neurones)
- Activity in the vestibular nuclei is modulated by the cerebellum
what are the vestibular pathways of the thalamus and cortex? what do these areas respond to?
• The superior and lateral vestibular nuclei send axons to the ventral posterior nuclear (VPN) complex of the thalamus, which in turn projects to two cortical areas relevant to vestibular sensations.
- Posterior to the primary somatosensory cortex, near the representation of the face.
- The transition between the somatic sensory cortex and the motor cortex (Brodmann’s area 3a).
- The relevant neurons in these areas respond to proprioceptive and visual stimuli as well as to vestibular stimuli.
- Many of these neurons are activated by moving visual stimuli as well as by rotation of the body (even with the eyes closed), suggesting that these cortical regions are involved in the perception of body orientation in extrapersonal space.
what is aphasia?
the inability to speak, write or understand the written or spoken word, which results from a lesion in the brain
which hemisphere is dominant for language?
The left hemisphere is dominant for language in over 95% of right-handers and in over 70% of left-handers.
where is the primary auditory cortex?
on the superior bank of the Sylvian fissure in the temporal lobe ??
where are the initial steps of language processing that enable particular sequences of sounds to be identified and comprehended performed?
in the adjacent association cortex = Wernicke’s area
- found on the superior temporal gyrus in the dominant hemisphere
what does articulation of the sounds that constitute speech depend on?
depends on the face area of the primary motor cortex, located in the inferior portion of the precentral gyrus.
where is the motor program that activates particular sequences of sounds to produce words and sentences formulated?
in the adjacent association cortex, which is called Broca’s area
- Broca’s area lies in the inferior frontal gyrus in the dominant hemisphere
where are neural representations for sounds converted into words and where are neural representations for words converted back into sounds?
Wernicke’s area
Broca’s area
what does the ability to hear a word and then repeat it aloud require? how does this happen?
it requires transfer of information across the Sylvian fissure from Wernicke’s area to Broca’s area
The two areas communicate via the arcuate fasciculus
how is aphasia classified? what are the classifications?
- what causes each
- what happens in each
according to the site of lesion:
- Sensory/Receptor Aphasia
Occurs form a lesion to the in Wernicke’s area.
There is fluency of language but words are muddled.
This varies from insertion of a few incorrect or non-existent words into speech to a profuse outpouring of jargon.
The reason this happens is because the patient is unable to understand their own speech due to the damage that has occurred in the Wernicke’s area. - Motor/Expressive Aphasia
Occurs form a lesion to the in Broca’s area.
There is reduced speech fluency with relatively preserved comprehension.
The patient makes great efforts to initiate language, which becomes reduced to a few disjointed words with failure to construct sentences.
Patients who recover say they knew what they wanted to say, but could not get the words out. - Conductive Aphasia
Occurs form a lesion to the in arcuate fasciculus. These are the association (white matter) fibres connecting the Wernicke’s area and the Broca’s area.
The output of speech is fluent but paraphrasic, comprehension of spoken language is intact, and repetition is severely impaired.
Naming and writing are also impaired.
Reading aloud is impaired, but reading comprehension is preserved. - Global/Central Aphasia
This means the combination of the expressive problems of Broca’s aphasia and the loss of comprehension of Wernicke’s with loss of both language production and understanding.
what is the basic circuit for understanding spoken language? and replying?
- When a person hears a sentence, this is transmitted via the auditory apparatus to the primary auditory cortex in the temporal lobe.
- This then connects to Wernicke’s area, which decodes the language into meaning.
- If the sentence is to be repeated, or replied to, the information has to be transmitted forwards to Broca’s area (expressive speech) in the frontal lobe (via the arcuate fasciculus).
- Broca’s area then produces speech via the motor programmes of the motor cortex, which activate the tongue and laryngeal muscles.
what is the basic circuit for understanding written language? and then speaking?
- Visual input is transmitted to the visual cortex in the occipital lobe.
- Input from the visual association area is sent to the left angular gyrus, where the objects are recognized and named.
- Input then goes to Wernicke’s area, where words are assembled into sentences, and the appropriate messages are sent via the arcuate and superior longitudinal fasciculi to Broca’s area.
- Broca’s area activates motor programmes in the primary motor cortex that elicit speech via appropriate brainstem centres and muscles of the tongue and larynx.
what is otitis media? what does it result from?
an inflammatory condition of the middle ear that results from dysfunction of the eustachian tube as a result of inflammation of the mucous membrane/adenoid tonsils in the nasopharynx, which in turn can be caused by a viral URI or possibly by allergies
what can the dysfunction of the Eustachain tube cause?
- Because of the dysfunction of the Eustachian tube, the gas volume in the middle ear is trapped and parts of it are slowly absorbed by the surrounding tissues, leading to negative pressure in the middle ear.
- Eventually the negative middle-ear pressure can reach a point where fluid from the surrounding tissues is sucked in to the middle ear’s cavity, causing a middle-ear effusion.
- This fluid is usually sterile but may become infected by bacteria or viruses from the nasopharynx producing an acute (or sometimes chronic) infection of the middle-ear.
what does acute otitis media result form?
when pathogens from the nasopharynx are introduced into the inflammatory fluid collected in the middle ear
- the proliferation of these pathogens in this space leads to the development of the typical signs and symptoms of acute middle-ear infection
how is acute otitis media diagnosed?
The diagnosis requires the demonstration of fluid in the middle ear (with tympanic membrane immobility) and the accompanying signs and symptoms of local or systemic illness.
Fluid in the middle ear is typically demonstrated or confirmed with pneumatic otoscopy.
In the absence of fluid, the tympanic membrane moves visibly with the application of positive and negative pressure, but this movement is dampened when fluid is present.
With bacterial infection, the tympanic membrane can also be erythematous (inverted), bulging, or retracted and occasionally can spontaneously perforate.
The signs and symptoms accompanying infection can be local or systemic, including diminished hearing, fever, malaise or irritability.
what is the aetiology of acute otitis media? most common bacterial cause?
Acute otitis media typically follows a viral URI.
The causative viruses can themselves cause subsequent acute otitis media; more often, they predispose the patient to bacterial otitis media.
- Streptococcus pneumoniae is the most common bacterial cause.
what is treatment for acute otitis media?
Amoxicillin is a first line drug if after 72 hours if the infection has not settled down.
recurrent acute otitis media
- what is it
- what due to
- treatment
- More than three episodes within 6 months or four episodes within 12 months.
- It is generally due to relapse or reinfection.
- In general, the same pathogens responsible for acute otitis media cause recurrent disease; even so, the recommended treatment consists of antibiotics active against β-lactamase-producing organisms.
- Antibiotic prophylaxis can reduce recurrences.
serous otitis media/otitis media with effusion/glue ear
- what is it
- pathophysiology
- how long effusions last
- what lead to
- In serous otitis media (otitis media with effusion), fluid is present in the middle ear for an extended period and in the absence of signs and symptoms of infection.
- This has the same pathophysiology as otitis media because most otitis media will result in effusion.
- In general, acute effusions are self-limited; most resolve in 2–4 weeks.
- However, effusions can persist and are associated with significant hearing loss in the affected ear. In younger children, persistent effusions and decreased hearing can be associated with impairment of language acquisition skills.
how is otitis media with effusion normally resolved? what if it’s not?
• The great majority of cases of otitis media with effusion resolve spontaneously within 3 months without antibiotic therapy.
• Antibiotic therapy or myringotomy with insertion of tympanostomy tubes (bilateral ventilation tube insertion) is typically reserved for patients in whom bilateral effusion;
1. Has persisted for at least 3 months.
2. Is associated with significant bilateral hearing loss.
what is a tympanostomy tube?
- A grommet (tympanostomy tube) is a tube that is inserted into the tympanic membrane and ventilates the middle ear cavity, i.e. it takes over the Eustachian tube’s function.
- Grommets are extruded from the tympanic membrane as it heals (lasting from 6 months to 2 years).
- However, developmental outcomes are not improved by grommet insertions.
chronic otitis media
- what is it
- what can it cause
- what used
- Chronic otitis media is characterized by persistent or recurrent purulent otorrhea in the setting of tympanic membrane perforation.
- Usually, there is also some degree of conductive hearing loss.
- This infection can spread to the mastoid bone or spread superiorly causing osteomyelitis of the tegmen tympani.
- Antibiotic drops are used during an episode of discharge.
Meniere’s disease
- what is it
- attacks
- what associated with
- treatment
increase in endolymph pressure – disrupts signal transduction and can result in tinnitus, nausea, spontaneous nystagmus
• This is a disease of the inner ear characterized by recurring episodes of rotatory vertigo, deafness and buzzing in the ears (tinnitus).
• Attacks are recurrent over months or years. Typically the attacks are preceded by a sensation of fullness in the ear.
• Classically it is associated with a low frequency sensorineural hearing loss, feeling of fullness in the affected ear, loss of balance, tinnitus and vomiting.
• There is a build-up of endolymphatic fluid in the inner ear.
• Treatment involves the use of vestibular sedatives. Preventative measures, such as a low-salt diet, and avoidance of caffeine are useful. If the disease cannot be controlled in this way, then a chemical labyrinthectomy, which involves perfusing the round window orifice with ototoxic drugs such as gentamicin, is possible.
Gentamicin destroys the vestibular epithelium; therefore the patient has severe vertigo for around 2 weeks until the body compensates for the lack of vestibular input on that side.
tinnitus
- what is it
- hearing loss?
- cause
- treatment
- This is a sensation of a sound (ringing/buzzing) when there is no auditory stimulus.
- It can occur without hearing loss.
- It usually does not have a serious cause but vascular malformation/ vascular tumours may be associated.
- A tinnitus masker (a mechanically produced continuous soft sound) can help.
what can hearing loss be associated with in terms of genes?
Recessive inheritance – in this case the hearing loss is congenital and profound.
Dominant genes – the onset is in adolescence or adulthood and varies in severity.
conductive hearing loss
- what is it
- what is conductive hearing ability mediated by
- common causes
- treatment
Conductive hearing loss – this is middle ear (or external ear) hearing loss.
It occurs when there is a problem with conducting sound waves anywhere along the route through the outer ear, tympanic membrane, or middle ear.
Conductive hearing ability is mediated by the middle ear composed of the ossicles: malleus, incus, stapes.
Common causes:
- External ear – earwax (cerumen) and otitis externa
- Tympanic membrane – TM perforation and TM retraction
- Middle ear – acute otitis media and serous otitis media
Treatment:
- Hearing aids
- Antibiotics
- Cochlear implants
sensorineural hearing loss
- what is it
- what is sensorineural hearing ability mediated by
- causes
- treatment
Sensorineural hearing loss – this is inner ear hearing loss.
Sensorineural hearing ability is meditated by the inner ear composed of the cochlea with its basilar membrane and attached vestibulocochlear nerve (VII).
Causes:
- Poor hair cell receptor growth
- External causes (acquired) – noise trauma and infection
- Intrinsic causes (congenital) – deafness genes
- Vast majority have this
- Occurs when problem with the sensory (hair cells) and/or neural structures (nerves) in the inner ear (cochlea)
- Most often, sensorineural hearing loss involved damage to the tiny hair cells that are activated by sound waves to vibrate and release chemical messengers that stimulate the auditory nerve (made up of many nerve fibres that then carry signals to the brain that are interpreted as sound)
- This hearing loss can also result from damage to the auditory nerve
- Intensity of sound is reduced, but sound can also be distorted even when the sounds are loud enough
- Most cannot be reversed with treatment and is typically described as an irreversible, permanent condition
- Most can benefit from hearing aids
noise-induced hearing loss
- what exposure causes hearing loss
- which frequencies
- Long or repeated exposure to sounds at or above 85 decibels (dB) can cause hearing loss.
- The louder the sound, the earlier the hearing loss will develop.
- Sounds of less than 75 dB, even after long exposure, are unlikely to cause hearing loss.
- Noise-induced hearing loss has an unusual pattern of hearing impairment in which the loss at 4000 Hz is greater than at higher frequencies.
what is nonsyndromic hearing loss and deafness? what caused by?
- Nonsyndromic hearing loss and deafness (DFNB1) is characterized by congenital, non-progressive, mild-to-profound sensorineural hearing impairment.
- No other associated medical findings are present.
- DNFB1 mutation is inherited in an autosomal recessive manner.
what is the Weber test? what does it show?
- In the Weber test a vibrating tuning fork (256 Hz) is placed in the middle of the forehead, above the upper lip under the nose over the teeth, or on top of the head equi-distant from the patient’s ears on top of thin skin in contact with the bone.
- The patient is asked to report in which ear the sound is heard louder.
- A normal weber test has a patient reporting the sound heard equally in both sides.
- In an affected patient, if the defective ear hears the Weber tuning fork louder, the finding indicates a conductive hearing loss in the defective ear.
- In an affected patient, if the normal ear hears the tuning fork sound better, there is sensorineural hearing loss on the other (defective) ear.
• Example – if the right ear is defective and the Weber test is conducted, the results will be as follows:
Sound heard in right (defective) ear louder – conductive loss in the right ear.
Sound hear in left (normal) ear louder – sensorineural loss in the right ear.
• Here, we assume we are aware of which ear is defective. In the case where the patient is unaware or has acclimated to their hearing loss, we use the Rinne’s test in conjunction with the Weber to characterize and localize any deficits.
what is Rinne’s test? what does it show?
- For the Rinne test, a vibrating tuning fork (typically 512 Hz) is placed initially on the mastoid process behind each ear until sound is no longer heard.
- Then, the fork is then immediately placed just outside the ear with the patient asked to report when the sound caused by the vibration is no longer heard.
- A normal or positive Rinne test is when the sound heard outside of the ear (air conduction or AC) is louder than that heard when the tuning fork end was placed against the skin on top of the mastoid process behind the ear (bone conduction or BC). “AC > BC”
- A negative Rinne (“BC > AC”) indicates conductive hearing loss of that ear.
when are Weber and Rinne’s tests used together?
• This is used when a patient walks in not knowing if they have a defective ear.
• First, the Weber test is conducted, to work out the possible combinations of hearing loss (i.e. potential conductive hearing loss of one ear OR the potential sensorineural hearing loss of the other ear).
• Next, the Rinne’s test is conducted to diagnose the hearing loss.
Example:
Patient walks in not knowing which ear is defective.
Weber test results show that the patient heard the noise louder in his right ear.
This could indicate conductive hearing loss of the right ear OR sensorineural hearing loss of the left ear.
Rinne’s test is carried out on the right ear, the results of which could show the following:
BC > AC = conductive loss of the right ear.
AC > BC = sensorineural loss of the left ear.
pure-tone audiogram
- how are air and bone conduction thresholds determined
- what happens in the presence of hearing loss
- what is response measured in
- what is an audiogram
- what is the air-bone gap, what does it indicate
• Air conduction thresholds are determined by presenting the stimulus in air with the use of headphones. Bone conduction thresholds are determined by placing the stem of a vibrating tuning fork or an oscillator of an audiometer in contact with the head. In the presence of a hearing loss, broad-spectrum noise is presented to the non-test ear for masking purposes so that responses are based on perception from the ear under test.
The responses are measured in decibels. An audiogram is a plot of intensity in decibels of hearing threshold versus frequency.
- The difference between these two lines plotted on your audiogram is the air- bone gap.
- An air-bone gap indicates problems somewhere in your outer or middle ears.
- sensorineural hearing loss = no air-bone gap
- conductive = >_ 15 dB air-bone gap
tympanometry
- what is it
- what does it measure
- what is it useful in detecting
- Tympanometry is a test of middle ear compliance.
- This test measures the stiffness of the eardrum and estimates middle ear pressure and the volume of the external canal.
- It is useful in detecting middle ear effusions in glue ear, underventilation of the middle ear space in eustachian tube dysfunction, and small perforations that are not seen on otoscopy.
otoacoustic emissions (OAE)
- what are they
- how measured
- what does their presence indicate
- what is it a standard test for
low-level sound emitted by the cochlea either spontaneously or evoked by an auditory stimulus
• These can be measured with microphones inserted into the external auditory canal.
• The emissions may be spontaneous or evoked with sound stimulation.
• The presence of OAEs indicates that the outer hair cells of the organ of Corti are intact and can be used to assess auditory thresholds and to distinguish sensory from neural hearing losses.
This test is now standard to test for new born sense of hearing.
- A present OAE tells us that the conductive mechanism of the ear is functioning properly
- This includes proper forward and reverse transmission, no blockage of the external auditory canal, normal tympanic membrane movement and a functioning impedance matching system
- Small probes are placed in the ear – one delivers sound and the other is a microphone
- If the cochlea is functioning properly it should echo in response to the sound
- There are four types of sounds that the cochlea produces
- The test picks up vibrations from the hair cells in the inner ear
what is the caloric test? what happens? what are the results?
- This is a test of the vestibulo-ocular reflex that involves irrigating cold or warm water into the external auditory canal.
- Ice cold or warm water or air is irrigated into the external auditory canal, usually using a syringe.
- The temperature difference between the body and the injected water creates a convective current in the endolymph of the nearby horizontal semicircular canal.
- Hot and cold water produce currents in opposite directions and therefore a horizontal nystagmus in opposite directions.
• “COWS”:
COLD water mimics a head turn to the contralateral side.
Both eyes turn to the same (ipsilateral) ear, with the horizontal nystagmus to the (quick horizontal eye movements) to the OPPOSITE (contralateral) ear.
WARM water mimics a head turn to the ipsilateral side.
Both eyes turn to the opposite (contralateral) ear, with the horizontal nystagmus to the (quick horizontal eye movements) to the SAME (ipsilateral) ear.
COWS refers to the nystagmus not the initial direction of movement of the eyes
it is possible to shift attention to objects imaged to some location on the retina outside the fovea - what are the ways in which this enhances visual processing?
Shifting attention to some location on the retina enhances visual processing in several ways:
Enhanced detection - A covert shift of attention in the retina makes it clear that attention makes things easier to detect, i.e. if the image on the fovea provides directions for a stimulus appearing somewhere outside the fovea, the brain is better prepared for directly recognising that stimulus.
Faster reaction times – A covert shift of attention makes reaction speed much faster to that space in the retina.
how do eye movement and attention relate?
attention can be moved independently of eye position
(When there are multiple visual stimuli (outside the field of the fovea), the areas of highest brain activity move away from the occipital pole as the attended sector moves out from the fovea. The pattern of brain activity shifts retinotopically.)
how is attention directed?
• Both cortical and subcortical structures may be involved in modulating the activity of neurons in areas of sensory cortex.
The pulvinar nucleus has reciprocal connections with most visual cortical areas of the occipital, parietal, and temporal lobes, giving it the potential to modulate widespread cortical activity.
People with pulvinar lesions respond abnormally slow to stimuli on the contralateral side, particularly when there are competing stimuli on the ipsilateral side. Such a deficit might reflect a reduced ability to focus attention on objects in the contralateral visual field.
• It is suggested that the brain circuitry responsible for directing the eyes to objects of interest might also play a critical role in guiding attention. There are direct connections between the frontal eye fields and numerous areas known to be influenced by attention, including areas V2, V3, V4, MT, and parietal cortex. Neurons in the FEF have motor fields, small areas in the visual field. If a sufficient electrical current is passed into the FEF, the eyes rapidly make a saccade to the motor field of the stimulated neurons.
what are the mechanisms that attention is mediated by?
Top-down mechanisms – This is to say we can “choose” to focus our attention.
Bottom-up mechanisms – Where we are alerted to a stimuli in our environment.
parietal lobe lesions
- what does it affect
- compensation
Parietal Lobe Lesions: Deficits of Attention
• The hallmark of contralateral neglect is an inability to attend to objects, or even one’s own body, in a portion of space.
• Affected individuals fail to report, respond to, or even orient to stimuli presented to the side of the body (or visual space) opposite the lesion.
• They may also have difficulty performing complex motor tasks on the neglected side, including dressing themselves, reaching for objects, writing, drawing, and, to a lesser extent, orienting to sounds.
• The parietal cortex, particularly the inferior parietal lobe, is the primary cortical region (but not the only region) governing attention.
- Importantly, contralateral neglect syndrome is specifically associated with damage to the right parietal cortex.
- The unequal distribution of this particular cognitive function between the hemispheres is thought to arise because the right parietal cortex mediates attention to both left and right halves of the body and extrapersonal space, whereas the left hemisphere mediates attention primarily to the right.
- Left parietal lesions tend to be compensated by the intact right hemisphere.
- When the right parietal cortex is damaged, there is little or no compensatory capacity in the left hemisphere to mediate attention to the left side of the body or extrapersonal space.
temporal lobe lesions
- what does it affect
Temporal Lobe Lesions: Deficits of Recognition
• Lesions of the visual association cortex in the temporal lobe result in difficulty recognizing, identifying, and naming different categories of objects (Agnosia).
• Patients with agnosia acknowledge the presence of a stimulus, but are unable to report what it is.
frontal lobe lesions
- what does it affect
Frontal Lobe Lesions: Deficits of Planning
• The particularly devastating nature of the behavioral deficits after frontal lobe damage reflects the role of this part of the brain in maintaining what is normally thought of as an individual’s “personality.”
what percentage of deaf children are born into hearing families?
90%
what are the four stages of thought characteristic of children’s views about illness?
- Sensorimotor – Birth to 2 years old.
- In the pre-operational stages 2-7 years explanations tend to focus around magic and superstition.
- In the concrete operational stage, children are able to distinguish between internal and external determinants of illness. This phase includes contamination, where children believe the cause of illness to be external to themselves but understand links between germs and possible effects on their body and internalisation. Children understand how the cause of an illness can be internal.
- By 11 years of age, children enter the formal operational stage and accept physiological explanations of illness that increasingly accommodate scientific theory.
describe language development in terms of discriminating between phonemes
• Children come into the world able to discriminate among different sounds that correspond to different phonemes in any language.
(Phoneme - any of the perceptually distinct units of sound in a specified language that distinguish one word from another, for example p, b, d, and t in the English words pad, pat, bad, and bat).
• What changes over the first year of life is that infants learn which phonemes are relevant to their language and lose their ability to discriminate between sounds that correspond to the same phoneme in their language.
when does the critical period for first language acquisition end? what happens if a child fails to get support as a language learner at this critical period?
ends somewhere between the ages of 4 and 12
the child can experience lifelong consequences (e.g. aggressive behaviours, withdrawn into silence and reading difficulties)
speech development
- when do children begin to speak
- what do children between 1 to 2 years talk mainly about
- when does syntax begin?
- At about 1 years of age, children begin to speak.
- One year olds have concepts for many things, and when they begin to speak, they are mapping these concepts onto words that adults use.
• Children 1 to 2 year olds talk mainly about people, animals, body parts and household implements.
- Between 1.5 and 2.5 years of age, the acquisition of phrase and well-formed sentences, or syntax begins.
- Children start to combine single words into two-word utterances such as “there cow”.
what are the theories of language development?
- B.F. Skinner emphasized the influence of the environment on language development.
- Piaget a cognitive developmental theorist, argued that thought comes before language.
- Vygotsky pointed out that social support from adults and especially from more competent peers can enable the child to advance to the next level.
- Nativist theory (Chomsky) – innate area in brain
- Empiricist theory – general brain processes are sufficient for language development
- Social interactionalist theory – learn by interaction
- Behaviourist theory – learn phrase, imitate and form habit, practice
- Cognitive theory – look for patterns, learn by themselves from mistakes – thought comes before word
describe language development - milestones
2 MONTHS
Pre-verbal
- Crying, gestures
- Hunger, tired, cold, hot, pain
- Coos and gurgles
- By 3 months fixes on sound
- Parents use melodic sounds and intonations
6 – 10 MONTHS
Babbling
- Child can distinguish sounds of any language and reproduce this: universal adaptability
- By age one this is lost! Begins to learn native language
- Communicates by sounds and intonations
6 – 12 MONTHS
- Begin by detecting very small differences between speech sounds (phonemes)
- As they get older they learn to ignore non-specific sounds
- By 6 months they can contract different vowel phonemes
- By 11-12 months they can recognise constants
1 YEAR
- One-word stage (morphemes)
- End of first year – should understand about 50 words and say about 5
- One word to describe actions – ‘ball’ = ‘get the ball’ – semantics (understanding) develops before word
- Learn words which produce effects: ‘again’, ‘more’
18 MONTHS
- Two-word phrases
- Should have about 20-50 words
- Naming
- Demanding
- Questioning
2.5 YEARS
- Simple sentences
- Lacks tenses
- Errors in syntax
- Recognition of rhyme and intonation
- 200-300 words
PRE-SCHOOL 2.5-5 YEARS
- Improvement in phonemes
- Development of pronunciation – articulation
PRIMARY SCHOOL 6-10 YEARS
- Master syllable stress to distinguish between similar words
what is behaviourism and cognitivism?
behaviourism = behaviour is learnt cognitivism = behaviour is a result of thoughts
what are the two types of otitis media? describe each one briefly
Two types:
- Acute otitis media (AOM)
- Otitis media with effusion (OME)
AOM:
- Comes on quickly and is accompanied by swelling and redness in the ear behind and around the ear drum
- Fever, ear pain, and hearing impairment often occur as a result of trapped fluid and/or mucous in the middle ear
OME:
- After an infection goes away, sometimes mucous and fluid will continue to build up in the middle ear
- This can cause the feeling of the ear being ‘full’ and affect your ability to hear clearly
what is apraxia of speech?
acquired oral motor speech disorder affecting an individual’s ability to translate conscious speech plans into motor plans, which results in limited and difficult speech ability
what is speech sound disorder?
some speech sounds (phonemes) in a child’s language are either not produced, not produced correctly, or are not used correctly
what is cluttering?
speech and communication disorder characterised by a rapid rate of speech, erratic rhythm and poor syntax or grammar, making speech difficult to understand
what does the pinna do?
it collects and amplifies sound - provides about 10-15 decibels of amplification
why do the tympanic membrane and following birds amplify the sound?
because of the ratio of the area of the tympanic membrane compared to the area of the oval window (much smaller)
how does the brain know the wavelength that the ear received?
- Lower wavelength waves have a higher frequency
- High frequency sounds cause maximum vibration of the basilar membrane in the cochlea near to the opening, where the oval and round windows are found
- Low frequency sounds cause maximum vibration of the basilar membrane at the apex of the cochlear duct
- Each area on the basilar membrane has a corresponding set of nerve cells
what frequency do you normally look at clinically?
8-125 Hz
what is presbyacusis?
- Relatively normal hearing in the lower frequencies
- Tails off much more into the higher frequencies
- Age-related hearing loss
what is the vocal tract like in consonants and vowels?
partially closed for consonants
open for vowels
what are formants?
- Chunks of energy clustered in certain frequency areas
- In the case of vowels the first two formants (F1 and F2) combined create a characteristic vowel and are most important for intelligibility (measure of how comprehensible speech is in given conditions)
- they determine the phonetic quality of a vowel
what is the name of certain sounds that if you can make means you should have normal speech?
ling sounds
what is:
- phonology
- morphology
- syntax
- semantics
- pragmatics
- orthography
- vocabulary
- Phonology: the basic sound units of language (phonemes)
- Morphology: units of meaning within words; the way words are formed (morphemes)
- Syntax: phrase and sentence structure – what makes sense (grammar)
- Semantics: the way language conveys meaning
- Pragmatics: appropriate word choice and use in context to communicate effective – social language use – using language for different purposes, changing language according to needs to listener or situation, following rules for story-telling and conversation
- Orthography: spelling patterns
- Vocabulary: knowledge of the meaning and pronunciation of words (lexicon)
what might delays in speech suggest?
a problem with hearing
cochlear implants
- what is it
- who suitable for
- what does it do
- Electrode sits within the cochlea
- Stimulater package under the skin
- Patient wears magnet/hearing aid on the outside
- Suitable for people who are deaf, for whom hearing aids wouldn’t work
- Directly activating the auditory nerves
who benefits from cochlear implantation? when no longer useful?
Post-lingually deafened adults
- Have sound memory
- Have used hearing aids to optimise hearing
- Already know how to speak and use language
Pre-lingually deaf children
- Prescribe hearing aids before the age 3 months
- Implant before age 3 years, ideally <1!
After the period of neuroplasticity, cochlear implantation does not improve hearing or speech
what is 0 decibels? how do decibels work?
- a reference level of sound
- you can get minus decibels
- you can’t have no sound
- change in 1 decibel you wouldn’t notice, change in 5 you would clearly notice and change in 10 would feel twice as loud
what is the range of speech in frequencies?
200-500 Hz
why do you need two ears?
to know the direction of sound
is there wax and hair all along the external ear canal?
none in the inner two thirds
describe and explain middle ear ventilation
- what happens at atmospheric pressure and at abnormal pressure?
- Middle ear is an air contained space
- Air inside the body is always dissolving into the skin
- So, if you didn’t swallow every two minutes and open your eustachian tube, your middle ear would steadily become more and more negative pressure – the ear drum would stretch and not vibrate as easily
- Middle ear gas = mixed venous blood
- Ventilation of ME:
- at atmospheric pressure: physiological gas exchange across mucosa
- at abnormal pressure: eustachian tube opening
are vibrations transferred more efficiently in water or air?
water as it’s denser
what is a single frequency triggered by? where in the basilar membrane are higher frequencies resonated?
a single neuron
in the basal turn
what does an increase in number of cochlear neurones triggered mean?
there has be an increase in the amplitude of the stimulus
what is the current theory of cochlea hearing?
- Rigid resonating structure:
- basilar membrane, tectorial membrane, OHCs
- Inner space fluid movement:
- IHCs
- Efferent nerve feedback to OHCs:
- contractile stiffening of organ of Corti
- fine tuning removed by OHC death
what is theory of mind?
being able to put yourself in other people’s shoes
what are the different ways in which you can identify yourself as a deaf person?
- Culturally hearing – ‘hearing identity’ i.e. viewing deafness as a disability to be surmounted
- Culturally marginal – identity lacking social embedding in either hearing or deaf culture
- Culturally deaf – positive acceptance of one’s deafness and pursuit of positive relationships with social deaf peer group
- Bicultural – identity that reflects comfort in both deaf & hearing environments
what is the saccule continuous with? what does it detect?
the cochlear duct anteriorly
it detects vertical acceleration (e.g. in a lift)
what is the utricle continuous with? what does it detect?
the semi-circular ducts posteriorly
it detects horizontal acceleration (e.g. in a car)
what do the otolith organs rely on to function?
- Rely on inertia (resistance of an object to any change in its velocity) to function by detecting changes in linear acceleration
in summary, how do the semi-circular canals detect movement and transfer this to brain?
- Fluid movement (endolymph) displaces a gelatinous mass known as the cupula
- This causes physical strain on ‘hair cells’
- Deflection towards the kinocilium increases firing (K+ ions move in), deflection away from the kinocilium decreases it (K+ doesn’t move in)
- Allows for very rapid detection of changes in angular acceleration of the head
- Signal transduction by mechanically-gated channels
- Glutamatergic transmission
what is the wiring for the vestibulo-ocular reflex? what modulates the reflex?
- Scarpa’s ganglion fibres (input from CNS into vestibular system) enter at the level of the rostral medulla and they synapse as the medial vestibular nucleus
- Then they ascend to the pons to the abducens nucleus
- Then entering the medial longitudinal fasciculus, crosses over the midline, ascending over the midbrain and synapsing in the oculomotor nucleus
The cerebellum modulates the VOR – cerebellum compares intended movement with actual movement
what is nystagmus like in a comatose patient?
slow phase is still present, but not the fast phase
what does a dysfunctional slow phase of nystagmus imply?
a lesion in the vestibulo-ocular pathway
