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Sensory Neuroscience 316 > Lecture 24; Inner ear disease part one > Flashcards

Lecture 24; Inner ear disease part one Flashcards

1
Q

What does data indicate about people under 25?

A

That 50% of people under 35 have experienced tinnitus which is representative of hearing loss / damage, after listening to loud music.

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2
Q

If sensory cells are damaged, can they repair?

A

No, they cant regenerate.

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3
Q

What percentage of the world population has a disabling hearing loss?

A

2%

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4
Q

What percent of the population have a hearing impairment?

A

10%

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5
Q

What percent of the population suffer from other hearing disorders?

A

20%

  • Tinnitus
  • Menieres disease.
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6
Q

What are the types of hearing loss?

A

1) Conductive hearing loss
2) Sensorneural hearing loss
3) Auditory Processing Disorders

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7
Q

What are the causes of sensorneural hearing loss?

A
  • Genetic disorders
  • Infection / Inflammation
  • Trauma
  • Ageing
  • Intense sounds (temp or perm)
  • Ototoxic drugs
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8
Q

Describe the incidence of congenital hearing loss and its consequences?

A
  • 2-3 per 100 children

Consequences;

  • Poor language and behavioural development
  • Lower literacy and academic achievements
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9
Q

What is the main cause of congenital hearing loss?

A
  • Genetic factors are thought to cause more than 50% of congenital hearing loss
  • 100+ genes identified as underlying cause of deafness.

Otherwise intrauterine infections; Cytomeagly virus, herpes simplex virus, hypoxia, maternal drug / alcohol use

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10
Q

How can the inner ear become infected?

A
  • Spread of bacteria/virus (infection) from the middle ear (otitis media) to the inner ear.
  • Can cause direct tissue injury to the inner ear or nerve as a consequence of infection / inflammation
  • Meningitis is also a source of inner ear inflammation and results from infection through the CSF
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11
Q

Describe how inflammation/ infection can cause acquired hearing loss;

A

The inner ear can rapidly mount an inflammatory response which can cause bystander tissue injury

The inflammatory response can damage delicate structures of the inner ear and cause permanent hearing loss

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12
Q

What are the most common causes of acquired hearing loss?

A
  • Presbyacusis
  • Noise Trauma
  • Ototoxic drugs
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13
Q

What is the common feature of pathology in acquired hearing loss?

A

The loss of sensory cells

  • Particular OHC are sensitive to damage
  • Once lost are replaced by scar tissue formed by supporting cells

Auditory nerves degenerate

  • Loss of afferent neurons
  • takes time
  • Once lost the picture of sensorneural hearing loss is complete.
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14
Q

What are the common functional features of drug, noise and age related hearing loss?

A
  • Initial loss of basal cells and high frequencies (especially for drug and age)
  • Noise related hearing loss depends on the frequency of noise trauma.
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15
Q

Whats the incidence of noise induced hearing loss;

A
  • Most common occupational disease in industry and military
  • Leisure activites i.e clubbing will cause this in young people
  • Predicted to affect 25% of people by 2050
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16
Q

Describe the types of noise induced hearing loss on the cochlea

A

Depending on the db and duration it can cause temporary or permanent hearing loss

Temporary recovers within 24 hrs to 7 days

Permanent hearing loss is associated with sensory cell and nerve damage.

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17
Q

Describe the impact of noise trauma on the OHC?

A
  • First likely place of damage is the stereocilia of the OHC
  • Mechanical forces on these stereocilia from the tectorali membrane can cause tip links / stereocilia to damage, can lead to upregulation of apoptotic pathways in the OHC and thus permanent damage
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18
Q

Describe the impact of noise trauma on the IHC?

A

IHC auditory synapse is susceptible to excitotoxicity from glutamate. Can also cause damage to spiral ganglion neurons, resulting in swelling etc

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19
Q

Describe the impact of noise trauma on the supporting cells?

A

Pillar cells can buckle and pressure and the organ of corti can collapse

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20
Q

Describe the impact of noise trauma on the stria vasulcaris / lateral wall?

A

Important for K secretion and maintenance of the endocochlear potential.

Can swell after noise exposure and then can be followed by atrophy. Reducing its functions.

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21
Q

Describe glutamte excitotoxicity?

A

Glutamate is released by IHC and with excessive noise trauma a lot of glutamate can be released

Acting on NMDA receptors can lead to cell swelling, resulting in the condition called sudden onset hearing loss. Due to the plasticity of neurons it can recover

Repeated exposure/ noise trauma can lead to excessive Ca influx to the type one neuron that can result in upregulation of necrotic/apoptotic pathways and cell death. = permanent hearing loss

22
Q

Describe inflammation in the cochlea

A

Excessive noise trauma can lead to inflammation in the cochlea

This involves the recruitment of leukocytes / inflammatory cells from an external source

They mop of damaged cells, but they can release pro-inflammatory cytokines that can lead to cell damage.

23
Q

What is the most established cause of noise induced hearing loss?

A

Oxidative stress

In the cochlea may be common factor for hearing loss from noise, aminoglycosides antibiotics, ototoxic anticancer drugs and ageing.

24
Q

How can oxidative stress contribute to hearing loss?

A

Free radicals are capable of breaking down lipid and protein molecules, damaging DNA and triggering cell death, all of witch contribute to the loss of function after noise exposure.

25
Q

How are free radicals formed as a result of noise?

A

During noise exposure, the ETC of the mitochondira uses large amounts of oxygen, which can create large amounts of superoxide as an unwanted bi-product.

Superoxide can then react with other molcules (as increased levels can be handled) to generate higher levels of ROS in the cochlea.

26
Q

Summerise what happens in noise induced hearing loss;

A

Overdriving the mitochondria
Excitotoxicity
Ischemia/Reperfusion
Inflammation

All these processes lead to ROS

Which damages the components of the cells;

  • Lipid peroxidation
  • DNA damage
  • Protein damage

Leading to apoptosis and necrosis.

27
Q

Describe the incidence of age related hearing loss;

A

Onset 45-54

  • 44% population by 69
  • 66% population by 79
  • 90+% population over 80
28
Q

Where does age related hearing loss start?

A

At high Hz

AS you age you start to lose the lower hz

29
Q

Describe how presbyacusis occurs?

A

A mixture of aquired auditory stresses, trauma and ontological diseases superimposed on intrinsic, genetically controlled, ageing process.

30
Q

What does intreated presbyacusis lead to?

A

Social isolation, depression and loss of self esteem

31
Q

What is presbyacusis characterised by?

A
  • Reduced hearing sensitivity and speech understanding in noisy environments
  • Slowed central processing of acoustic information
  • Impaired isolation of sound sources.
32
Q

What is the age related pathology?

A

Similar to that in noise trauma but over a longer period of time.

  • Stria vascularis cells are particularly affected because of loss of vasculature in the cochlear.
  • Sensory hair cells damaged
  • Spiral ganglions damaged
  • Central auditory pathways are damaged
33
Q

What are the classifications of prysbyacusos pathology?

A

Classified based on their pathology

  • Senosory (OHC)
  • Neural
  • Metabolic (Strail atrophy)
  • Mixed and indetermined

Sensory and neural are related to environmental factors while strial is highly hereditary.

34
Q

How is cochlear ageing studied in gerbils?

A

Gerbils raised in noisy and quite environments have the same hearing loss.

  • Predominately degeneration of the strial vascularis
  • Thus loss of Na/K ATPase needed to K secretion and EP
  • Declining EP and loss of stria vascularis gives rise to the dead battery theory of presbyacusis
35
Q

What are the types of animal models to study hearing loss?

A
  • Early onset hearing loss mouse
  • Late onset hearing loss mouse

These two models address genetic factors in hearing loss as early late onset of AHL resistant gene.

36
Q

What are some animal models that address sensory hearing loss?

A
  • Albino mouse

- Gerbil

37
Q

What is special about the gerbils?

A

Damaged cochlear vasculature with age.

38
Q

What are the causes of presbyacusis?

A
  • Reduction of vasculature in the stria vascularis
  • Oxidative stress
  • Apoptosis
  • Collagen damage (fibroblasts in spiral ligaments, K recycling)
  • Accumulative noise exposure

Combination of genetic and envionrmental

39
Q

Describe ototoxicity;

A

Major drugs to cause this;

  • Aminoglycoside antibiotics
  • Platinum based chemotherapeutic agents
40
Q

What is the pathology of ototoxicity?

A

Both damage the hair cells at the basal tunr of the organ of corti, spiral ganglion neurons, and the lateral wall tissues resulting in functional deficits.

41
Q

Describe how aminoglycosides enter the hair cells

A

Through the tip links and leads to the production of ROS and lead to apoptosis.

42
Q

How can apoptosis occur?

A

ROS can trigger apoptosis by;

  • Extrensic death receptor-mediated apoptosis
  • Intrinsic mitochondria mediated cascade. (major pathway supported by literature)
43
Q

Describe apoptosis via ROS and intrinsic pathway;

A
  • Stress activation of JNK
  • Increased intracellular Ca and release of cytochrome C from the mitochondria.
  • Leads to activation of caspases, 8,9,3 which are key to apoptosis.
44
Q

What are some platinum containing anticancer drugs?

A

Cisplantin and carboplatin

45
Q

Describe cisplatin ototoxicity;

A

Tinitus and bilateral high frequency sensorineural hearing loss

High incidence (up to 80%)

46
Q

How does cisplantin cause hearing loss

A
  • Involves the production of ROS and depletion of glutathione and antioxidant enzymes (SOD, catalase, glutathione peroxidase) in the cochlea
  • Excessive ROS production activates primarily caspase-dependent apoptotic pathways
  • Ototoxicity can be ameliorated by protective agents targeting oxidative stress and apoptosis (often interferes with cisplantin activity)
47
Q

Describe noise management in the prevention of hearing loss;

A
  • legislation framework
  • noise management and monitoring
  • use of protection devices
  • hearing monitoring
  • education on the causes of NIHL and ways to prevent it
48
Q

Describe some pharmacogical stratageies to reduce earing loss

A

Pharmacological interventions to reduce hearing loss

(1) restoring the normal balance of free radicals with antioxidants(2) reducing glutamate excitotoxicity with NMDA receptor antagonists
(3) maintaining adequate cochlear blood flow during and after noise
(4) suppressing inflammation
(5) inhibiting pathways to apoptotic cell death to preserve hair cells

49
Q

How can antioxidants be increased in the cochlea?

A

Increasing cochlear antioxidant supplies can substantially prevent hair cell damage and hearing loss.

Antioxidant levels can be increased in two ways:

  • Application of exogenous antioxidant molecules locally or systemically into the body
  • Endogenously by using sound conditioning
50
Q

What are antioxidants?

A

Antioxidants are molecules that scavenge ROS and convert them to less dangerous molecules.

Mammals maintain complex systems of multiple types of antioxidants, such as glutathione, vitamins A, C and E, magnesium, as well as enzymes such as catalase, superoxide dismutase and various peroxidases.

51
Q

What is sound conditioning?

A

A method of increasing antioxidant supply to the ear.

I.e being exposed to non-traumatic noise can lead to protection from traumatic noise

52
Q

Whats an experimental therapy for hair cell replacement?

A

Experimental therapies: Hair cell regeneration
• Gene transfer technology (change supporting cells)
• Replacement of hair cells by stem cells

Sensory Neuroscience 316 (32 decks)

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