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Brain Plasticity and Perceptual Learning
The brain—young as well as adult—has the capacity to adapt in response to changes in the external environment, to changes in the sensory input due to peripheral injury such as hearing loss, and as a result of training (perceptual learning). Brain plasticity is a determining aspect of the potential success of hearing aids and cochlear implants (CIs). It basically allows the user to adjust to the more or less deformed way the environment and speech are presented to the hard of hearing or completely deaf persons. This learning may often be enhanced by training. Here, I will not present exhaustive details about human developmental plasticity, this is discussed in Chapter 8 , Early Diagnosis and Prevention of Hearing Loss, and its relation to CI use is reviewed in Chapter 11 , Cochlear Implants.
2.1
The External Environment
Simply plugging the ears or exposing humans to low-level sound for 2 weeks is sufficient to induce reversible changes in loudness perception ( ). In this study, normal hearing (NH) human volunteers were asked to wear either earplugs or a set of open-canal, in-the-ear speakers producing a low-level noise between 1 and 8 kHz with a peak level of 50 dB SPL at approximately 6 kHz. Earplugs or earphones were worn for at least 23 h/day for 2 weeks, and subjects performed loudness judgments on 500 and 2000 Hz tones before and after treatment. The noise-exposed subjects needed an additional 4–8 dB of sound level to match their pre-exposure loudness judgments. Conversely, subjects who wore earplugs needed up to 5–9 dB less sound level compared with their baseline judgments. Hearing thresholds were not affected by either treatment. The noise-exposed subjects showed no difference in posttreatment loudness judgments between 500 and 2000 Hz, despite the fact that the noise spectrum did not extend to 500 Hz. Two possible explanations for the loudness changes are that the auditory system undergoes physiological changes or that the listeners simply recalibrate their behavioral criteria ( ). These physiological changes could occur in auditory cortex, and subsequently by cortical modulation of processing at the brainstem level ( ) could change the gain of the brainstem mechanisms ( ).
An interesting variant on the procedures is monaural ear plugging, which as expected affects sound localization in azimuth. However, found that the effect was minimal for low-level sound presented to the unplugged ear side. In contrast, they observed that at higher sound levels azimuth localization was highly perturbed. The plug thus creates interaural level differences (see chapter: Hearing Basics ) that far exceed the normal physiological range provided by the head shadow. Yet, these erroneous cues were incorporated in forming the azimuth percept, giving rise to larger localization errors than for low-intensity stimuli for which the binaural cues were absent. Thus, listeners rely on monaural spectral cues for sound-source azimuth localization as soon as the binaural difference cues break down. had provided another interesting variant on plastic phenomena in sound localization by changing the pinnae with molds. Localizing sounds in elevation was dramatically degraded immediately after pinna modification, however, accurate performance improved again over a time period of 6 weeks, after which the learning process stabilized. Immediately, after removing the molds, the subject’s localization accuracy with undisturbed ears was still as high as before the start of the experiment. Apparently, the auditory system had acquired a new representation of the pinna transfer functions, without interfering with the old set.
2.1.1
Critical and Sensitive Periods
The human cochlea is fully developed by 24 weeks of gestation. A blink startle response can first be elicited (acoustically) at 24–25 weeks and is constantly present at 28 weeks. Hearing thresholds are 40 dB SPL at 27–28 weeks and reach the adult threshold of 13.5 dB SPL by 42 weeks of gestation ( ). Early born preterm children often end up in the neonatal intensive care unit (NICU). Quite often they show signs of auditory neuropathy and sensorineural hearing loss; however, even in case they do not, they may have other neurological problems from which they only very slowly recover ( ).
In an NICU, noise is continuously present in the confines of an incubator. A big issue is the so far largely unknown effect of such prolonged noise exposure in the NICU on the neonatal brain. Whereas it has been established that this does not cause audiometric hearing loss, it may still have profound effects on hearing, as animal studies suggest ( ). In neonatal and adult animals, band-pass noise exposure leads to contracting tonotopic regions surrounded by expanding tonotopic regions ( ). Potential extrapolations can be drawn that pertain to human auditory development. Several studies of long-term outcomes in NICU graduates mention speech and language problems ( ). However, few studies have specifically linked speech and language problems with noise type and levels.
Both adult and critical period (CP) animals show plastic changes, i.e., a capacity for change in the structure and/or function of the nervous system, as a result of sensory experience following passive exposure to tonal or noise stimuli. A sensitive period is one, typically developmental, where brain plasticity results as a function of sensory experience. The CP, in general, is considered a time period within a sensitive period when the best neural representation of the environment is selected from among the many competing inputs that affect the maturing nervous system. The growth and function of lateral inhibitory circuits may be important for terminating the CP. The difficulty of this problem is highlighted by the fact that the closure of the early CP may be dependent on the input received ( ). Note that in adult rats exposed to continuous noise found a complete disappearance of tonotopic order, i.e., as if the rats had reentered a condition similar to the CP rats. Tonotopy, also called cochleotopy, an ordered spatial representation of frequency, is found along the so-called lemniscal pathway (see chapter: Hearing Basics ; Fig. 2.1 ) from brainstem to auditory cortex. Only 5 of the 13 auditory cortical areas in cats or primates (including humans) are tonotopically organized (see chapter: Hearing Basics ).
In neonatal animals pulsed noise stimulation, at a level not causing hearing loss, disrupts the tonotopic map and broadens frequency tuning ( ), whereas in adult animals ( ) map changes do not occur but behavioral effects related to broader frequency tuning are evident. Depending on the precise CP day, tonal stimulation in CP animals either expands the region of single frequency stimulation ( ) and up to an octave-wide region on either side, or contacts the region of multitone stimulation and expands the surrounding frequencies ( ). In adult animals, the stimulated region contracts regardless being stimulated with band-pass tonal or noise stimuli, whereas the bordering regions dramatically expand ( ). These changes in adults spontaneously recover, those in CP animals only in the case of continuous noise ( ), which delayed closure of the CP. For the pulsed noise or tonal stimulation in CP animals spontaneous recovery does not occur. The relationship between map changes in A1 and behavior remains unclear ( ).
It is not exactly known whether there are similar CPs in human auditory development ( ), but from the CI literature one may derive CPs for the necessity of auditory stimulation for binaural hearing (<2 years of unilateral hearing, i.e., in single-sided deafness ( ), or using one CI ( )). Support for this plasticity and the positive effects of early intervention in congenitally unilaterally deaf white cats is provided in the work of . Also the development of certain auditory evoked response components, i.e., N 1 does not develop after more than 3 years of deafness under the age of 6 ( ) suggests a CP. Normal language development in CI patients also suggests a CP ( ). Conductive hearing loss in children is a major determinant of language delay and may potentially cause long-lasting deficits (see chapter: Causes of Acquired Hearing Loss ).
2.2
Learning Paradigms
The main point of including animal data in the context of this chapter is to elucidate the various mechanisms underlying brain plasticity. grouped these mechanisms in the following categories: habituation, sensitization, and conditioning. The first two are considered nonassociative learning; conditioning, including classical conditioning and operant conditioning, is a form of associative learning ( Fig. 2.2 ). The following is also extensively discussed in the work of .
2.2.1
Nonassociative Learning
Nonassociative learning is a change in a response to a stimulus that does not involve associating the presented stimulus with another stimulus or event such as reward or punishment. There are two forms: habituation and sensitization.
2.2.1.1
Habituation
Repeated stimulus presentation, without any other consequences, results in loss of attention and behavioral responses, and usually, in a reduction of the neural responses within relevant sensory cortex. This process of learning not to attend to such a stimulus is termed habituation. It differs from sensory adaptation and fatigue as habituation can occur at long interstimulus intervals, develops more rapidly with weaker stimulus intensity, and is highly specific to the parameters of the repeated stimulus ( Fig. 2.2 ). Repeated sensory stimulation is widely used in studies of sensory cortex where both respond to decrements and increments, with modification of receptive field (RF) properties, have been reported. Thus, habituation is a form of adaptive behavior (or neuroplasticity) that is classified as nonassociative learning.
In the last few decades a phenomenon of relative decrease in neural activity of a frequently presented stimulus relative to the much larger activity produced by an infrequent stimulus was discovered ( ). Under passive listening conditions the difference waveform between the long-latency auditory evoked potential (AEP) to the unexpected (also called deviant or odd-ball) sound and the AEP to the frequent sound was called the mismatch negativity (MMN). The MMN was interpreted as a reflection of neural information processing in the brain that would allow behavioral detection of a difference in, or discrimination of, the two sounds. At the single-unit level this phenomenon was later named “stimulus-specific adaptation” (SSA) and proposed as “a neural correlate of the MMN” ( ). An extensive discussion on SSA can be found in the work of .
2.2.1.2
Sensitization
Sensitization refers to the process by which a synapse becomes more efficient in its response to a stimulus. An example of sensitization is that of kindling ( ), where repeated stimulation of hippocampal or amygdala neurons (even when induced by repeated stimulation of primary auditory cortex) eventually leads to seizures in laboratory animals. Having been sensitized, very little stimulation is required to produce the seizures. Sensitization is also a nonassociative learning process because it involves increased responses with repeated presentations to a single stimulus. The increase of responsiveness can be more generalized than to the presented stimulus ( Fig. 2.2 ).
2.2.2
Classical Conditioning
Classical conditioning involves two sequential stimuli, where the second stimulus is strong and biologically significant, e.g., food or a noxious stimulus. The first stimulus is referred to as the conditioned stimulus (CS), and the second stimulus as the unconditioned stimulus (US). It was thought that repeated pairings of the CS and US were necessary for conditioning to emerge; however, many conditioned responses (CRs) can be learned with a single trial as in fear conditioning and taste aversion learning ( ). Fear conditioning, for example, using a tone paired with a shock, is the most commonly used model. A behaviorally neutral CS is followed by a nociceptive US. After a few pairings, animals and humans react to the CS with autonomic (change in heart rate, interruption of respiratory rhythm, increase in blood pressure) as well as somatic (e.g., freezing) fear-related CRs.
2.2.3
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