Basic Operation of Cochlear Implants, Brief Introduction, Histor Flashcards

1
Q

What is the significance of the Military Medical Academy in Leningrad in the 1930s?

A
  • Stimulating electrodes inserted into the middle ear of patients with and without ME structures
  • Frequency of alternating current (AC) was varied and patients asked to describe the pitch (Gersuni & Volokhov, 1936)
  • Pitch was no different for patients with or without ME structures. so ME was ruled out as the site of electrical stim
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2
Q

What is electrophonic hearing?

A
  • Electrical stim of the organ of Corti causes mechanical response = release NTs from HCs onto nVIII
  • Tectorial membrane converts electrical signal into the acoustic resulting in tonal pitch but at double the signal frequency
  • Direct electric activation of nVIII with steep loudness growth and occasional activation of nVIII
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3
Q

What is the cochlear microphonic?

A
  • Electrical potentials measured primarily from OHCs in cochlea in response to stimulus
  • Closely mirrored the stimulus
  • Aka the Wever-Bray effect
  • Used to dismiss the “telephone theory” of hearing
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4
Q

What were conclusions about telephonic hearing?

A
  • Research from late 40s and 50s concluded that deafness could not be completely corrected with wide-field electrical stimulation
  • Instead, more localized summation of ANFs would be necessary
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5
Q

What is the significance of Djourno and Eyries?

A
  • Seminal work on direct auditory nerve stimulation with coil
  • Djourno was a physiologist/researcher interested in neural prosthesis and Eyries was an otolaryngologist
  • First subject was a 57-y/o man s/p bilateral cholesteatoma resection, which resulted in deafness and facial paralysis
  • Surgery performed on 2/25/57
  • Patient underwent extensive therapy and was able to discriminate intensity differences well (butt poor frequency perception and non-existent speech perception)
  • Implant subsequently malfunctioned (twice) and Eyries and Djourno stopped working together but still credited with the first CI
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6
Q

Who was William House, MD, DDS?

A
  • Dentist-turned-otologist
  • Patient brought in a French article about the work of Eyries and Djourno
  • House has previously experimented with electrical hearing in patients during stapes surgery by placing electrodes on/near the oval window
  • Collaborated with Doyle brother (a neurosurgeon and an electrical engineer) to create CI
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7
Q

Who was F. Blair Simmons?

A
  • Stanford research and otolaryngologist that conducted an intraoperative study in an 18 y/o patient (indicated bipolar stim of nVIII, yielded auditory sensations and discrimination of different stim frequencies)
  • Two years later (1964), he implanted an electrical hearing device into the modiolus of a 60 y/o man
  • F/up pyschological testing of the pt. was difficult and Simmons was pessimistic about future electrical stim of nVIII yielding useful speech information
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8
Q

Who developed the first single-channel device?

A
  • William House and electrical engineer Jack Urban
  • House was concerned with safety and efficacy of the device
  • One pt. became a long-term experimental subject
  • From research on Graser, House & Urban abandoned the idea of multiple-electrode system and instead, went for single-wire electrode
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9
Q

Who was Robin Michelson?

A
  • Otolaryngologist in private practice who implanted several deaf patients with single-channel CIs in the 60s
  • Found that pts. could discriminate among different stim rates up to 600 Hz and differentiate between square and sinusoid wave
  • Partnered with Merzenich, a neurophysiologist, who was interested in mapping the IC
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10
Q

What was the Bilger Report (1975)?

A
  • 13 adult single-channel CI users (11 by House, 2 by Michelson) were studied in Pittsburgh
  • First study that legitimized CI use
  • Found that speech-reading scores were improved in all adults and that quality of life was significantly improved with minimal risk (still no open set speech recognition, but improved voice production)
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11
Q

What is the House/3M device?

A
  • 1972: House & Urban developed speech processor to accompany their single channel device (3M)
  • Implanted approx. 1000 people with device between 1972 and 1980s
  • Age criteria lowered from 18 years to 2 years of age in 1980
  • Received FDA approval for commercial marketing of device in 1984
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12
Q

What are the effects of deafness on the cochlea?

A
  • Primary place of concern is SGNs
  • More SGNs associated with better CI performance
  • Survival of SGNs dependent on presence of sensory epithelium and support cells of OoC
  • After loss of epithelium and support cells: 1) unmyelinated parts of SGNs in OoC degenerate rapidly, 2) more gradually, myelinated portions w/in osseous spiral lamina atrophy, 3) cell bodies in Rosenthal’s canal degenerate
  • Finally, soma of SGNs demyelinate and perikaryon shrinks
  • NOTE: Degeneration is an ongoing process
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13
Q

Why does loss of HCs cause SGN degeneration?

A
  • HCs and support cells in OoC are lost in SNHL
  • HCs express neurotrophic factors
  • Support cells express nerve growth factors
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14
Q

What pathologies directly affect SGNS?

A
  • Viral and bacterial labyrinthitis
  • Mechanical traume
  • Disruption of cochlear vasculature

^All result in more rapid degeneration of SGNs

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15
Q

What etiologies result in most SGN loss?

A
  • Postnatal viral labyrinthitis
  • Congenital/genetic deafness
  • Bacterial meningitis
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16
Q

What etiologies result in least SGN loss?

A
  • Aminoglycoside antibiotics
  • Sudden, idiopathic loss
  • Meniere disease
17
Q

What is the good news/bad news with SGN degeneration?

A
  • SGNs retain ability to fire even with extensive peripheral loss (neural activity with less than 5% of normal neural population)
  • Increase firing threshold noted (fewer you have, the more power needed; reduced spatial selectivity)
  • Demyelination decreases transmission efficiency (temporal processing capabilities reduced in those with long term deafness)
18
Q

What are the effects of deafness on the cochlear nucleus?

A
  • Studies show that changes to cells in the CN secondary to deafness are largely atrophic, not cell loss
  • Cell volume and shrinkage in CN have been demonstrated in ototoxic animal studies
  • Interestingly, ongoing process seems to stop with onset of hearing loss (degeneration can be stopped)
  • Pathophysiological effects are same as those to SGNS: 1) increased threshold for activation, 2) smaller action potentials, 3) shorter membrane time constants, 4) smaller after-hyperpolarization
19
Q

What is the role of CIs in action potential generation?

A
  • Electrode arrays of CIs, electrically depolarize location populations of SGNs, initiating an action potential
  • The implant serves no role after the AP is initiated
  • Saltatory conduction along the central processes of the SGNs and its passage across synapses within the CN are performed via normal physiology processes
20
Q

What are the effects of deafness on the SOC?

A
  • Same effects as those seen in the CN
  • Neural soma and nuclei were 33-50% smaller than those of hearing cats
  • Decrease in # of synapses per soma
  • 20-30% reduction in neural soma in SOC of deaf humans
21
Q

What are the effects of deafness on the IC?

A
  • IIC is tonotopically organized and receives excitatory input from contralateral ear
  • Gets information from SOC (binaural) and CN (contralateral)
  • Studies of unilaterally deafened animals show strong projections from ipsilateral CN to IIC following onset of deafness
  • However, if we examine overall IIC structure, after one year of deafness, no difference found between unilateral HL and normally hearing
22
Q

What are the effects of deafness on the auditory cortex?

A
  • Changes are dependent on: severity of SNHL, unilateral or bilateral, developmental stage at time of HL
  • Studies of effects on AC are difficult because other effects previously noted effect quality and organization of input to AC
  • Good news = AC appears to be plastic, meaning that reintroduction of stimulus (through CI!) results in re-organization of AC
23
Q

What morphological changes to AC may result from deafness?

A
  • Limited data in this area
  • Rabbit model demonstrates no change in neuron soma area, number of dendritic branches or dendritic length
  • However, some loss of number of spines along dendrites and some reorganization of these dendrites without spines (those with spines stay put!)
  • Overall = loss of synapses with prolonged deprivation of auditory input
24
Q

What evidence supports the notion of primary auditory cortex plasticity?

A
  • Studies of adult onset unilateral hearing loss show that ipsilateral-contralateral differences in response on evoked potentials occur once deafness sets in and continues over two years
  • Evoked potential studies in long-term CI users shows that potentials measured in auditory cortex are near normal
  • Leads to “activation-induced maturation” theory of auditory cortex