Auditory Brainstem Response - Cochlear Implantation and Central Auditory Development

Cochlear Implantation and Central Auditory Development

There are about 188,000 people around the world who have received cochlear implants. In the United States alone, there are about 30,000 adults and over 30,000 children who are recipients of cochlear implants. This number continues to grow as cochlear implantation is becoming more and more accepted. In 1961, Dr. William House began work on the predecessor for today’s cochlear implant. William House is an Otologist and is the founder of House ear institute in Los Angeles, California. This groundbreaking device, which was manufactured by 3M company was approved by the FDA in 1984. Although this was a single channel device, it paved the way for future multi channel cochlear implants. Currently, as of 2007, the three cochlear implant devices approved for use in the U.S. are manufactured by Cochlear, Med El, and Advanced Bionics. The way a cochlear implant works is sound is received by the cochlear implant’s microphone, which picks up input that needs to be processed to determine how the electrodes will receive the signal. This is done on the external component of the cochlear implant called the sound processor. The transmitting coil, also an external component transmits the information from the speech processor through the skin using frequency modulated radio waves. The signal is never turned back into an acoustic stimulus, unlike a hearing aid. This information is then received by the cochlear implant’s internal components. The receiver stimulator delivers the correct amount of electrical stimulation to the appropriate electrodes on the array to represent the sound signal that was detected. The electrode array stimulates the remaining auditory nerve fibers in the cochlea, which carry the signal on to the brain, where it is processed.

One way to measure the developmental status and limits of plasticity of the auditory cortical pathways is to study the latency of cortical auditory evoked potentials (CAEP). In particular, the latency of the first positive peak (P1) of the CAEP is of interest to researchers. P1 in children is considered a marker for maturation of the auditory cortical areas (Eggermont & Ponton, 2003; Sharma & Dorman, 2006; Sharma, Gilley, Dorman, & Baldwin, 2007). The P1 is a robust positive wave occurring at around 100 to 300 ms in children. P1 latency represents the synaptic delays throughout the peripheral and central auditory pathways (Eggermont, Ponton, Don, Waring, & Kwong, 1997).

P1 latency changes as a function of age, and is considered an index of cortical auditory maturation (Ceponiene, Cheour, & Naatanen, 1998). P1 latency and age has a strong negative correlation, decrease in P1 latency with increasing age. This is most likely due to more efficient synaptic transmission over time. The P1 waveform also becomes broader as we age. The P1 neural generators are thought to originate from the thalamo-cortical portion of the auditory cortex. Researchers believe that P1 may be the first recurrent activity in the auditory cortex (Kral & Eggermont, 2007) . The negative component following P1 is called N1. N1 is not consistently seen in children until 12 years or age.

In 2006 Sharma & Dorman measured the P1 response in deaf children who received cochlear implants at different ages to examine the limits of plasticity in the central auditory system. Those who received cochlear implant stimulation in early childhood (younger than 3.5 years) had normal P1 latencies. Children who received cochlear implant stimulation late in childhood (younger than seven years) had abnormal cortical responses latencies. However, children who received cochlear implant stimulation between the ages 3.5 and 7 years revealed variable latencies of the P1. Sharma also studied the waveform morphology of the P1 response in 2005 and 2007. She found that in early implanted children the P1 waveform morphology was normal. For late implanted children, the P1 waveforms were abnormal and had lower amplitudes when compared to normal waveform morphology. In 2008 Gilley and colleagues used source reconstruction and dipole source analysis derived from high density EEG recordings to estimate generators for the P1 in three groups of children: normal hearing children, children receiving a cochlear implant before the age of four, and children receiving a cochlear implant after the age of seven. Findings concluded that the waveform morphology of normal hearing children and early implanted children were very similar. Late implanted children have smaller amplitudes and poorer morphology. Only the late implanted children differed in latency difference that was statistically significant.

The take home message is that auditory evoked potentials is a valid clinical tool when assessing individuals pre and post cochlear implantation. Done by determining the need for a cochlear implant and assessing if the cochlear implant is working post implantation by measuring the benefit to the user. Children implanted prior to age 3.5 years showed P1 latencies within the normal developmental limits. Children who are implanted after the age of seven years almost always show evidence of abnormal central auditory maturation when examining the latency of the P1 response. The critical window is when the child is younger than 3.5 years of age. Implantation done before this age will improve the success of their cochlear implant.