A person determines the horizontal direction from which sound comes by two principal means: (1) the time lag between the entry of sound into one ear and its entry into the opposite ear, and (2) the difference between the intensities of the sounds in the two ears.
The first mechanism functions best at frequencies below 3000 cycles/sec, and the second mechanism operates best at higher frequencies because the head is a greater sound barrier at these frequencies. The time lag mechanism discriminates direction much more exactly than the intensity mechanism because it does not depend on extraneous factors but only on the exact interval of time between two acoustical signals. If a person is looking straight toward the source of the sound, the sound reaches both ears at exactly the same instant, whereas if the right ear is closer to the sound than the left ear is, the sound signals from the right ear enter the brain ahead of those from the left ear.
The two aforementioned mechanisms cannot tell whether the sound is emanating from in front of or behind the person or from above or below. This discrimination is achieved mainly by the pinnae of the two ears. The shape of the pinna changes the quality of the sound entering the ear, depending on the direction from which the sound comes. It changes the quality by emphasizing specific sound frequencies from the different directions.
Neural Mechanisms for Detecting Sound Direction. Destruction of the auditory cortex on both sides of the brain, whether in human beings or in lower mammals, causes loss of almost all ability to detect the direction from which sound comes. Yet, the neural analyses for this detection process begin in the superior olivary nuclei in the brain stem, even though the neural pathways all the way from these nuclei to the cortex are required for interpretation of the signals. The mechanism is believed to be the following.
The superior olivary nucleus is divided into two sections: (1) the medial superior olivary nucleus and (2) the lateral superior olivary nucleus. The lateral nucleus is concerned with detecting the direction from which the sound is coming, presumably by simply comparing the difference in intensities of the sound reaching the two ears and sending an appropriate signal to the auditory cortex to estimate the direction.
The medial superior olivary nucleus, however, has a specific mechanism for detecting the time lag between acoustical signals entering the two ears. This nucleus contains large numbers of neurons that have two major dendrites, one projecting to the right and the other to the left. The acoustical signal from the right ear impinges on the right dendrite, and the signal from the left ear impinges on the left dendrite. The intensity of excitation of each neuron is highly sensitive to a specific time lag between the two acoustical signals from the two ears. The neurons near one border of the nucleus respond maximally to a short time lag, whereas those near the opposite border respond to a longtime lag; those in between respond to intermediate time lags.
Thus, a spatial pattern of neuronal stimulation devel ops in the medial superior olivary nucleus, with sound from directly in front of the head stimulating one set of olivary neurons maximally and sounds from different side angles stimulating other sets of neurons on opposite sides. This spatial orientation of signals is then transmitted to the auditory cortex, where sound direction is determined by the locus of the maximally stimulated neurons. It is believed that all these signals for determining sound direction are transmitted through a different pathway and excite a different locus in the cerebral cortex from the transmission pathway and termination locus for tonal patterns of sound.
This mechanism for detection of sound direction indicates again how specific information in sensory signals is dissected out as the signals pass through different levels of neuronal activity. In this case, the “quality” of sound direction is separated from the “quality” of sound tones at the level of the superior olivary nuclei.
Centrifugal Signals From the Central Nervous System to Lower Auditory Centers
Retrograde pathways have been demonstrated at each level of the auditory nervous system from the cortex to the cochlea in the ear. The final pathway is mainly from the superior olivary nucleus to the sound-receptor hair cells in the organ of Corti.
These retrograde fibers are inhibitory. Indeed, direct stimulation of discrete points in the olivary nucleus has been shown to inhibit specific areas of the organ of Corti, reducing their sound sensitivities 15 to 20 decibels. One can readily understand how this mechanism could allow a person to direct his or her attention to sounds of particular qualities while rejecting sounds of other qualities. This characteristic is readily demonstrated when one listens to a single instrument in a symphony orchestra.
Hearing Abnormalities
Types of Deafness
Deafness is usually divided into two types: (1) that caused by impairment of the cochlea, the auditory nerve, or the central nervous system circuits from the ear, which is usually classified as “nerve deafness,” and (2) that caused by impairment of the physical structures of the ear that conduct sound itself to the cochlea, which is usually called “conduction deafness.”
If either the cochlea or the auditory nerve is destroyed, the person becomes permanently deaf. However, if the cochlea and nerve are still intact but the tympanum ossicular system has been destroyed or ankylosed (“frozen” in place by fibrosis or calcification), sound waves can still be conducted into the cochlea by means of bone con duction from a sound generator applied to the skull over the ear.
Audiometer. To determine the nature of hearing dis abilities, an “audiometer” is used. This instrument is an earphone connected to an electronic oscillator capable of emitting pure tones ranging from low frequencies to high frequencies, and it is calibrated so that zero-intensity-level sound at each frequency is the loudness that can barely be heard by the normal ear. A calibrated volume control can increase the loudness above the zero level. If the loudness must be increased to 30 decibels above normal before it can be heard, the person is said to have a hearing loss of 30 decibels at that particular frequency.
In performing a hearing test using an audiometer, one tests about 8 to 10 frequencies covering the auditory spectrum, and the hearing loss is determined for each of these frequencies. Then the so-called audiogram is plotted, as shown in Figures 1 and 2, depicting hearing loss at each of the frequencies in the auditory spectrum. The audiometer, in addition to being equipped with an ear phone for testing air conduction by the ear, is equipped with a mechanical vibrator for testing bone conduction from the mastoid process of the skull into the cochlea.
Fig1. Audiogram of the old-age type of nerve deafness.
Fig2. Audiogram of air conduction deafness resulting from middle ear sclerosis.
Audiogram in Nerve Deafness. In nerve deafness, which includes damage to the cochlea, the auditory nerve, or the central nervous system circuits from the ear, the person has loss of ability to hear sound as tested by both air conduction and bone conduction. An audiogram depicting partial nerve deafness is shown in Figure 1. In this figure, the deafness is mainly for high-frequency sound. Such deafness could be caused by damage to the base of the cochlea. This type of deafness occurs to some extent in almost all older people.
Other patterns of nerve deafness frequently occur as follows: (1) deafness for low-frequency sounds caused by excessive and prolonged exposure to very loud sounds (e.g., a rock band or a jet airplane engine), because low-frequency sounds are usually louder and more damaging to the organ of Corti, and (2) deafness for all frequencies caused by drug sensitivity of the organ of Corti—in particular, sensitivity to some antibiotics such as streptomycin, gentamicin, kanamycin, and chloramphenicol.
Audiogram for Middle Ear Conduction Deafness. A common type of deafness is caused by fibrosis in the middle ear after repeated infection or by fibrosis that occurs in the hereditary disease called otosclerosis. In either case, the sound waves cannot be transmitted easily through the ossicles from the tympanic membrane to the oval window. Figure2 shows an audiogram from a person with “middle ear air conduction deafness.” In this case, bone conduction is essentially normal, but conduction through the ossicular system is greatly depressed at all frequencies, but more so at low frequencies. In some instances of con duction deafness, the faceplate of the stapes becomes “ankylosed” by bone overgrowth to the edges of the oval window. In this case, the person becomes totally deaf for ossicular conduction but can regain almost normal hearing by the surgical removal of the stapes and its replacement with a minute Teflon or metal prosthesis that transmits the sound from the incus to the oval window.
