Case 16- ears Flashcards

1
Q

Common bacterial causes of acute otitis media

A
  • Streptococcus pneumoniae (30-35%)
  • Haemophilus influenza (20-25%)
  • Moraxella catarrhalis (10-15)
  • Up to 30% of AOM cases are viral, viral infections make bacterial infections more likely as they reduce mucocillary clearance
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2
Q

Otitis media and measles

A

Otitis media occurs in about 8% of measles cases, more common in children as there eustacian tube has less of an angle also due to immature immune system.

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2
Q

Otitis media with effusion

A

Fluid behind the tympanic membrane, appears dull, the cone of light is ill defined. Can occur after acute otits media but there may be no known cause. Often sterile with no surrounding bacteria. Fluid forms behind the tympanic membrane causing pressure changes, may mean the tympanic membrane does not vibrate correctly causing hearing loss. Can have a significant effect if the child is first learning speech.

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3
Q

Treatment for Otitis media effusion

A

No particular treatment tends to resolve. May use a grommet which is a tube that goes through the tympanic membrane and causes the pressure to equilibrate.

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4
Q

Perforation of the tympanic membrane

A

Can occur if there is a severe infection or from barrow trauma (big difference in pressure between inside and outside). Tend to be small and resolve spontaneously but occasionally need to be repaired in an operation called a tympanic plasty.

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5
Q

Oto-acoustic emission (OAE)

A

The faint echo that occurs when you play a sound in the ear. This emission shows that the cochlea is healthy i.e. the biological amplifies is working. Easy way to screen for hearing in babies. Used in the NHS neonatal screening programme

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6
Q

Key processing stages in the auditory pathway

A

• Auditory nerve connects the cochlea to the brain
• First synapse in the auditory pathway is the Cochlear nucleus
• Superior olivary complex- the information from the two ears interact, this is important for localising sound
• Inferior colliculus- midbrain auditory centre
• Medial geniculate body- thalamic auditory nucleus
• Auditory cortex- in the temporal lobe
Connections are mirrored in both ears

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7
Q

The auditory pathway- lots of information

A

1) The auditory nerve fibre enters the brain at the Ventral and Dorsal cochlear nucleus.
2) This is at the junction between the medulla and the pons.
3) Information travels to the right and left Superior olive complex.
4) Information then travels up a bundle of fibres known as the Lateral lemniscus and synapses in the midbrain at the Inferior colliculus.
5) From here fibres go to the Medial Geniculate body in the Thalamus of the forebrain.
6) Fibres then go to the Auditory cortex in the temporal lobe of the Cerebral cortex.

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8
Q

Location of the auditory complex

A

The auditory cortex is in the superior surface of the temporal lobe. The Sylvian fissure runs between the temporal and parietal lobes. The primary auditory cortex is in Heschel’s gyrus, Planum temporale is also part of the primary auditory complex, receives the strongest input from the primary auditory thalamus.

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9
Q

How brain damage can cause speech defecits

A

Dysphasias are deficits in speech

1) Receptive dysphasia- problems in speech comprehension. Associated with the back of the temporal lobe in Wernicke’s area
2) Expressive dysphasia- problems in speech production. Associated with Broca’s area

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10
Q

Cues for sound localisation

A
  • The position of sound is not represented on the basilar membrane in the cochlea
  • You compare the inputs from the two ears and contrast with eyes
  • Because the ears are separate, sounds can cause differences in timing and intensity (loudness) between the ears. The left ear hears differently from the right ear
  • these are termed intra-aural (between the ears differences)
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11
Q

Method of sound localisation- path difference

A

The extra distance and time that the sound has to travel in order for the same point in the sound wave to reach the opposite ear. Causes a continuous difference in the timing between the ears. At any given point the phase of the sound will be different between the two ears. The path difference changes as the source of the sound changes location. This only works for low frequency sounds <1500 Hz.

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12
Q

Localising high frequency sounds >1500 Hz

A
  • Because the waves are close together the head casts a sound shadow for high frequencies, this can block how much sound gets to the other ear. Less sound will get to the ear away from the sound source
  • The brain detects differences in sound levels between the ears
  • This difference changes as the sound source changes position
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13
Q

Benefits of Binaural hearing- having two ear

A

Improves speech detection in noisy environments i.e. the ability to listen selectively to one person in a noisy room. Speech is easier to detect when the competing noise comes from a different location, Binaural hearing aids are better then just one. We can do this due to our ability to separate sound sources spatially.

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14
Q

Sound

A

Longitudinal pressure waves travelling through air or another medium

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15
Q

What is sound defined by

A
  • Frequency- pitch of sound, measured in Hertz (Hz) cycles per second
  • Amplitude (intensity)- loudness, measured in a log scale (because the ear can detect a wide range of sound pressure). Its measured in dB (deciBels).
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16
Q

Pressure wave- sound

A

Alternating compression (closer together) and rarefraction (further apart) of air molecules causing sound

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17
Q

Frequency, Intensity and T

A

T= period (s), the time between the peak of one wave and the next.
Frequency= 1/t Hertz (s-1)
A high frequency means the peaks are closer together. Intensity measures the pressure fluctuations i.e. the height and how loud it is

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18
Q

How is intensity measured

A

How loud it is, its measured using the log of the ratio of sound pressures, one of them being the reference level (20) which is the quietest sound humans can hear
20*log (measured pressure / reference pressure).
A dB of 0 doesn’t mean there is no sound but that it is at the reference level

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19
Q

Frequency range

A

20Hz to 21kHz (for a young person)
At a really high or low frequency you need a louder sound in order to hear it. Frequenzy is measured on a log scale, as you age the upper frequency limit decreases

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20
Q

Nerve fibres and hair

A

The nerve fibres are from the 8th cranial nerve, 30,000 fibres 95% of nerve fibres are type 1 and go to the inner hair cells. Each inner hair cell receives up to ten type 1 fibres. Each nerve fibre only goes to one hair cell. Type 1 nerve fibres carry the most amount of information. Type 2 nerve cells are associated with the outer hair cells. Each type 2 nerve fibre makes contact with a number of outer hair cells. Unclear role. Most of the information we use to analyse sound comes from the type 1 nerve fibres.

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21
Q

How many inner and outer hair cells are there

A

There are 12,000 outer hair cells in 3-5 rows and 3,500 inner hair cells

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22
Q

Type 1 nerve fibres- frequency

A

Each auditory nerve fibres responds to a limited range of frequencies. There is one frequency in which its most sensitive to, which requires the least sound level to cause the firing of the nerve (Best frequency). As you increase the sound level (loudness) the range of frequencies it can respond to increases, however, this range is still narrow. Each nerve fibre is selective for a limited frequency range but together they cover a wide range of frequencies

23
Q

What happens when you damage the outer hair cell amplifiers

A

The fibres become less sensitive with poorer tuning. This can affect speech intelligibility especially in noisy situations. Sounds are more blurred and difficult to distinguish

24
Q

Place code

A
  • One way in which we analyse sound, how sound frequency is represented in the brain
  • The auditory system keeps track of where information originated on the basilar membrane (beginning with the nerve fibre)
  • Throughout the auditory pathway sound frequency is mapped within the processing centres and on the surface of the auditory cortex
  • Called Tonotopic organisation
25
Q

Tonotopic organisation

A

The nerve fibres nearest the base are tuned to a higher frequency and the ones near the apex to a lower frequency. When the nerve fibres leave the cochlear they enter the brain, the first place they synapse is at the Cochlea nucleus. Low frequency sounds synapse at the anterior end of the Cochlea nucleus and high frequency sounds synapse at the posterior end. So the neurons are programmed to progressively higher frequencies, this mapping of frequency in the Tonotopic organisation.

26
Q

Time code

A
  • One way in which we analyse sound, how sound frequency is represented in the brain
  • The firing of action potentials in the auditory nerve fibres synchronise with peaks in the sound waveform
  • Phase locking- the synchronising of firing to the wave form of the sound
  • The time between action potentials tells us about the frequency of the sound
  • Only occurs for low frequency sounds below 3-5 kHz, as its only then that the nerve fibres can fire fast enough to synchronise with the wave form of the sound
  • Probably the basis for musical pitch
27
Q

More explanation of time coding

A

1) The action potentials synchronise with the peaks of the waveform
2) The time between action potentials is the period and the reciprocal of the period is the frequency of the sound. Frequency= 1/T
3) You don’t get an action potential at every cycle of the sound but every time you do get an action potential it is at the peak of the wave form. Because there are multiple nerve fibres associated with the hair cell, if one nerve fibre misses a waveform another one will pick it up.
4) For high frequency sounds you rely entirely on place coding

28
Q

Types of hearing loss

A

Can be genetic and Acquired. Acquired damage might have a genetic component if they are more susceptible to damage

29
Q

Conductive hearing loss

A

Middle ear e.g. infection - otitis media or otitis media with effusion. Can be caused by Otosclerosis (ossicular chain stiffens and becomes less efficient at transferring sound; can be treated by replacing the Stapes in a stapedectomy)

30
Q

Sensorineural hearing loss

A

Cochlea- damage to hair cells and synapses and auditory nerve fibres (synaptopathy). Not just a loss of volume, but also resolution - sound also becomes ‘blurred’, there is less selectivity as the hair cells can only respond to selective frequencies and some of these are damaged. Hearing aids don’t compensate for loss of resolution. Much more difficult in crowded places with many talkers – social isolation. Most common cause of hearing loss

31
Q

Central hearing loss

A

I.E. following a stroke. Word deafness (rare- no deficit for simple sounds). Normally due to damage in the cortex of the brain. Problems with following speech, but are fine with simple sounds, known as auditory verbal agnosia.

32
Q

Tinnitus

A

1) Ringing in the ear, often accompanied by hearing loss
2) Can be a high frequency tone or a rushing sound like the sea
3) Incicence- 15% of the population
4) In 3% of the population it has a major effect on quality of life distress, depression etc
5) No effective treatment but you can manage it

33
Q

Causes of sensorineural hearing loss

A

1) Genetic- 80% are nonsyndromic (autosomal dominant or recessive gene). 20% syndromic (with other symptoms). Usher’s syndrome, Waardenburg syndrome, mitochondrial disorders
2) Noice induced hearing loss
3) Disease i.e. measles, meningitis. Measles encephalitis is 1 in 1000-2000 cases of measles. Brain damage can damage the inner ear and cause deafness
4) Presbycusis= age-related hearing loss, gradual loss of sensitivity to high pitched sounds
5) Drug damage i.e. aminoglycoside antibiotics, cisplatinum, furosemide. Due to ototoxicity

34
Q

Sensorineural hearing loss- noise induced

A

1) Temporary threshold shift (recovers in hrs/days)- temporarily lose your hearing.
2) Permanent threshold shift (4k Hz notch). Hair cells damaged or lost; the synapse between the hair cell and the auditory nerve fibre is lost. Leisure noise is the major contributor - not work-place noise. Can be damaged by one instance of very loud noise, or repeated exposure to slightly less intense loud noise. At 80dbs employers need to take action to prevent hearing loss.

35
Q

Audiogram

A

Measures the ability of the patient to hear sounds over a number of frequencies. Normally measures from 250Hz to 8000Hz

36
Q

Levels of hearing loss

A
  • 0-20 dB normal hearing levels
  • 20-40 dB mild hearing loss- normal speech
  • 40-70 dB moderate hearing loss- dog barking, loud shouts
  • 70-90 dB severe hearing loss- telephone ring
  • > 90 dB profound hearing loss- gun shots, jack hammer
37
Q

The cochlear ear (bionic implant)

A

Given to patients with little or no cochlear function. The cochlear nerve fibres are activated by an electrode array. arranged from high to low frequency. The induction coil transmits signals across the scalp and skull to the implant receiver. The microphone and processor converts sound to electrical pulses. The electrode sites stimulate the auditory nerve fibres positioned in the cochlea, these nerve fibres will be associated with different frequencies. At the base it will be high pitched, at the apex low pitched. The implant and induction coil is internal, the microphone and processor is external. There are 32 electrodes in a cochlea implant array. Not the same as normal acoustic hearing. Best when implanted early

38
Q

Where is the vestibular system

A

It is within the inner ear. The inner ear is within the bony otic capsule, buried in the lateral part of the petrous bone. The membranous labyrinth contains endolymph and is suspended in the side bony labyrinth which contains perilymph, this is then surrounded by the temporal bone.

39
Q

Composition of the vestibular system

A

1) The 8th Cranial nerve divides into the vestibular and auditory nerve
2) The cell bodies of the vestibular nerves are found in the Scarpa’s ganglion
3) The vestibular organs are made of the Urticle and Saccule, together the Otolith organs
4) There are 3 semi-circular canals
5) The semi-circular canals are at 90 degrees to each other- so you can sense movement in different planes of space
6) The Lateral (horizontal) canal is parallel to the base of the skull, you also have the Posterior and Superior semicircular canal which are verticle.
7) The ampulla is a bulge at the base of each semicircular canal

40
Q

The vestibular apparatus

A

There are two divisions, the otolith organs (vestibule) and the semi-circular canals. The vestibule contains the Urticle and Saccule which are connected by the urticulo-saccular duct. The Semi-circular canals originate from the urticle.

41
Q

Structure of the Urticle and Saccule

A

Both the Utricle and the Saccule work in similar ways. Within the Utricle you have a surface called the Macula which is covered in hair cells, they have Stereocilia and large Kinocilium. Kinocilium is different from Stereocilia because it has a club like ending at the top. Overlying the Stereocilia and Kinocilium is a gelatinous cap. Over the gelatinous cap is the Otoliths which are fragments of calcium carbonate.

42
Q

What do the Otoliths respond to

A

1) Changes in the angle of the head

2) Linear acceleration and deceleration

43
Q

How the Otoliths respond to changes in the angle of the head

A

1) Gravity acts on the Otoliths pulling the stereocilia, so if you raise your chin they will point towards the back of the head
2) The vestibular hair cells are associated with nerve fibres which signal the change in angle
3) When the Stereocilia points towards the smallest Stereocilia, the hair cell hyperpolarises.
4) It depolarises when it points towards the tallest Stereocilia.

44
Q

How the Otoliths respond to linear acceleration and deceleration

A

1) When a person is moving forwards in a straight line and suddenly stops, there is a tendency for the Otoliths to keep moving and bend the Stereocilia towards the tallest one, depolarising the hair cells.
2) If someone begins to move from a stationary position the hair cells will bend towards the smallest one and hyperpolarise the hair cells. So the Otoliths can respond to gravity when the head is tilting or linear movement.

45
Q

The hair cells are orientated to cover different directions

A

1) The nerve cells in the Utricle are orientated horizontally (Urticular macula) and the Saccules are orientated vertically (Saccular macula).
2) Some of the Stereocilia depolarise if they bend in one direction but there are other Stereocilia that depolarise if they bend in the opposite direction.
3) This is because half of the Stereocilia face backwards and the other half face forwards.
4) The sensory epithelium is called the macula and the hair cells are arranged to cover different directions

46
Q

Semicircular canals

A

1) Detect rotational acceleration
2) The superior, posterior and lateral canals are sensitive to rotation in different planes
3) Hair cells are embedded in the gelatinous cupula in the ampulla.
4) Projecting into the Ampulla is this gelatinous structure called the Cupulla. The Stereocilia of the hair cells are embedded within the cupulla. At rest the Cupulla stands vertically upwards. The fluid is endolymph.
5) The firing rate in the two ears will be opposite
6) The vestibular axons are spontaneously active so can signal both an increase and a decrease in firing

47
Q

How the semicircular canals detect acceleration

A

1) When the head rotates in the appropriate plane, the canal rotates but initially fluid remains stationary owing to its inertia.
2) It bends the cupola and stereocilia of hair cells.
3) Initially, if you rotate your head clockwise it appears like the fluid is moving anticlockwise, this causes the cupula to bend to the right.
4) This causes depolarisation of the hair cells.
5) Eventually the fluid catches up with the canal and rotates at the same velocity, the cupola are dragged back to the upright position and the bending of the Stereocilia is eliminated.
6) The reverse occurs when rotations stop, as the semi-circular canal is still but the endolymph is moving in the opposite direction (same direction as rotation).
7) The Stereocilia are now bent to the left and there is Hyperpolarisation.

48
Q

Vestibular system- nerve pathway

A

1) Fibres from the Otolith organs go to the lateral vestibular nucleus. Projections from the lateral vestibular nucleus go to the Cerebellum and the Limb motor neurons
2) Fibres from the semi-circular canals go to the medial vestibular nucleus. Projections from the medial vestibular nucleus go to the Extraocular motor neurons (3,4,5) and the neck motor neurons.

49
Q

Roles of the central vestibular system

A
  • Important in controlling head, eye and body position- this ensures the world appears stationary as we move. Helps the eyes to remain fixed on a object as the head moves. Maintains equilibrium and balance
  • The lateral vestibular nucleus projects to the spinal cord via the vestibulospinal tract, controls limbs to maintain balance i.e. when you lose balance on a slippery floor
  • The semi-circular canals project to the medial vestibular nucleus, the medial vestibular nucleus which projects to the motor neurons of the neck and trunk, the extraocular motor neurons (cranial nerves 3,4,5) and via the thalamus to the cerebral cortex.
50
Q

Vestibulo-ocular reflex

A
  • Stabilises eyes- keeps them pointing in the same direction despite head movement
  • Compensates for head movement with counter rotation of the eyes i.e. the head rotates to the right, eyes rotate to the left
  • Don’t need vision- works in the dark
  • Appropriate contraction and relaxation of eye muscles (lateral and medial rectus) to give appropriate movement.
51
Q

Mechanism of vestibulo-ocular reflex

A

1) When your head rotates to the left, the eyes rotate to the right.
2) You contract the lateral rectus of the right eyes and relax the medial recti.
3) In the left eye you contract the medial recti and relax the lateral rectus muscle.
4) The signals the semi-circular canals provide make these movements happen.
5) The horizontal semicircular canal connects to the vestibular nucleus, then the abducens nucelus (VI) and the Oculomotor nucleus (III).

52
Q

Nystagmus

A
  • Physiological response to rotation or external movement
  • The slow movement of eyes in the opposite direction to rotation followed by a rapid flick back
  • Also seen when rotation stops- in the opposite direction
  • When the person rotates to the left, the slow eye movement goes to the subjects right, the fast eye movement goes to the subjects left. The direction of nystagmus is specified by the fast phase, here to the left. It’s a sawtooth waveform
  • Physiological nystagmus, jerky eye movement without rotation. It impairs vision, can be due to vestibular problems or brainstem lesions.
53
Q

Dizziness and other vestibular problems

A
  • Motion sickness- the vestibular system and vision giving conflicting signals
  • Vertigo from factors affecting the vestibular system- infection may lead to dizziness or vertigo and the sensation the world is moving around you. Could be due to damage to the vestibular system, vestibular nerves or nuclei. May make walking or standing difficult. Sometimes there is a gradual recovery over weeks or months as visual and proprioceptive system takes over. Brain appears to adapt to the signals from the vestibular system and ignore them in favour of visual signals
  • Dizziness and vestibular problems can be caused by Menieres disease
54
Q

Symptoms of Meniere’s disease

A

5-7.5 per 1000 people
• Intermittent rotatory vertigo- sensation of spinning (patient or world spins)
• Nausea, sweating, vomiting
• Fluctuating hearing loss- usually low frequency
• Distorted hearing
• Tinnitus (ringing in ears)
• Sensation of fullness- pressure in the ear

55
Q

Meniere’s disease

A

There is varying severity and duration of attacks. The cause is uncertain but leads to an imbalance in endolymph production and clearance. Often incapacitated. Also knows an endolymphatic hydrops. Sensorieural hearing loss