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Panayiota Lalaki, MD, Ph.D. Introduction
In 1946, Grant Rasmussen reported his discovery of the
olivocochlear (OC) system. Warr and Guinan (1979)
anatomically outlined the two separate segments of the OC system, the lateral
and the medial. An efferent
auditory pathway can be found in all cases of vertebrates. In human, the
efferent auditory pathway is completely mature by 40 weeks after gestation (Ryan και Piron,1994). Morlet et al., (1993) have reported abnormal function
of the OC bundle in a study of 42 premature infants (33-39 weeks). Its
functional role remains largely unknown. The two efferent divisions
differ with respect to a number of morphological features, including (Sahley et al., 1997a): 1.
pattern
of development, 2.
the
size of cell bodies, 3.
brainstem
locus of origin, 4.
preferred
side of projection to the periphery, 5.
postsynaptic
targets within the auditory periphery The descending (efferent) OC
system is known to have cell bodies and axons originating from nuclei within
the superior olivary region in the upper pons (superior olivary complex-SOC).
The descending fiber bundles provide direct, bilateral input to the cochlea via
anatomically segregated medial and lateral efferent divisions (Warr 1992). All available evidence indicates that the
dynamic properties of the Outer Hair Cells (OHCs) fall under the modulatory control
of the medial efferent auditory system (Kujawa et al.,
1993,1994; Collet et al. 1992; Gifford & Guinan 1987). Clinical interest in the medial
efferent system has been awakened by the advances made in the field of
Otoacoustic Emissions (OAEs). Since the micromechanical properties of the OHCs
are directly under the control of the medial efferent bundle, it sounds logical
that stimulating this neural pathway, OHCs motility and, hence, OAEs should be
affected. It is well established that the amplitude of both types of Evoked
Otoacoustic Emissions (TEOAEs as well as the Distortion Product Otoacoustic
Emissions-DPOAEs) can be suppressed when simultaneous contralateral sound
stimulation is applied (Williams et al., 1994; Moulin
et al., 1993; Ryan et al., 1991). This phenomenon is considered to be
mediated through the medial efferent system (Williams
et al., 1994). Overview of the efferent auditory system neuroanatomy
The efferent auditory system is a descending
bundle, which originates from the auditory cortex and terminates at the sensory
cells of the organ of Corti. Throughout its descending course the efferent
auditory pathway interacts with the afferent auditory pathway through feedback
loops. The olivocochlear
bundle In 1946, G.
Rasmussen reported his discovery of the OC bundle. Warr (1992) and Warr &
Guinan (1979) outlined two separate anatomic segments of the efferent
auditory system, the lateral and medial. The lateral OC bundle arises from
neurons within the Lateral Superior Olivary (LSO) nucleus complex in the upper
pons and its unmyelinated axons terminate to the inner hair cells (ICHs) mainly
(89%-91%) of the ipsilateral cochlea. They do not synapse directly at the basal
surface of the IHCs but at specialized postsynaptic regions on afferent type I
dendrites (Pujol & Lenoir 1986). The medial OC
bundle arises
from the neurons of the Medial Superior Olivary (MSO) nucleus complex and the Medial
Nucleus of the Trapezoid Body (MNTB) and comprises of thick myelinated nerve
fibers. About 75% of the fibers cross at the floor of the 4th
ventricle and terminate at the OHCs of the contralateral cochlea, while the
rest of them remain uncrossed and terminate to the OHCs of the ipsilateral
cochlea. The fibers of the medial OC bundle synapse directly at the basal
surface of the OHCs. Figure 1
schematically illustrates the olivocochlear bundle and its connections with the
cochlear nucleus and hair cells within the cochlea.
Figure 1: Schematic presentation of the
efferent auditory system and its connections to the afferent auditory system
and the hair cells of the organ of Corti. Both the lateral
and medial fibers of the OC bundle pass dorsally from their cell bodies through
the reticular formation to the floor of the 4th ventricle (Warr 1992). Together with the crossed vestibular
efferents, descending auditory efferent axons form a compact bundle within the
vestibular nerve root, the fibers pass the cochlear nuclei and send collateral
projections into this structure before exiting the brainstem as a ventral
component of the inferior division of the vestibular nerve (Warr 1992). Efferent fibers travel within the
vestibular nerve, then enter the cochlea between the basal and second turn and
enter the spiral ganglion, via the vestibulocochlear anastomosis of Oort in the
fundus of the internal auditory meatus (Warr 1992;
Iurato 1974). Descending
pathways to the superior olivary complex Descending
auditory pathways arise from within the auditory cortex -the primary (AI) and
secondary (AII) auditory field as well as the anterior auditory field (AAF)-
through which the cortex may exert control over the superior olivary neurons of
the efferent OC bundle. This descending control is indirect, via connections
mostly with the ipsilateral inferior colliculi (IC). Limited amount of existing
evidence suggests that descending fibers from the IC terminate on the cells of
the SOC and MNTB. Furthermore, the descending collicular input to the SOC and
MNTB is found to be tonotopic, which supports electrophysiological evidence (Rajan 1990) that descending collicular input is very
capable of modulating levels of excitability within medial efferent OC neurons
(Kimiskidis et al., 2004; Sahley et al., 1997b). SOC
interactions with the cochlear nucleus Descending
fiber projections arise from the SOC bilaterally, travel within the
intermediate and dorsal acoustic stria and terminate within the cochlear
nuclei. Fibers from LSO complex mainly terminate to the ipsilateral ventral
cochlear nucleus (VCN) and, vice versa, afferent fibers from the VCN project to
the ipsilateral LSO complex. A dense plexus from the MSO complex send fibers
that terminate to the ipsilateral and mainly to the contralateral dorsal and
ventral cochlear nuclei. Furthermore, afferent auditory fibers from the
cochlear nuclei project mainly to the contralateral MSO nuclei (Sahley et al., 1997b). Thus, most medial OC nuclei
are activated by the contralateral cochlea they innervate, and most lateral OC
nuclei are excited by ipsilateral cochlear output. There exists, therefore, a
neural pathway from one cochlea via the afferent auditory system to the MSO
nuclei, and from there to the other cochlea via the medial efferent auditory
system (fig. 2). 
Figure 2:Schematic
presentation of contralateral
suppression emission test and the neural pathways (afferent and efferent
auditory system) being activated. Overall TEOAE amplitude without contralateral
noise is at 16.3 dB SPL; when white noise is presented to the contralateral ear
the overall amplitude is suppressed to 8.3 dB SPL. (MSO:
medial superior olivary, CN: cochlear nucleus, SL: sensation level). The role and clinical
relevance of the efferent auditory system
The role of the
efferent auditory system remains largely unknown. In view of the preferential
innervation of the OHCs by MSO fibers, it has been hypothesized that the
stimulation of the medial efferents alters IHCs sensitivity indirectly by
altering the micromechanical properties of the OHCs. It is well established
that the length, tension and the stiffness of the OHCs along their longitudinal
axis are under the control of the MOC bundle, thus enhancing the auditory
sensitivity, especially for low level stimuli at 30-40 dB SL (Brownell 1990; Guinan 1986; Kim 1986; Siegel & Kim, 1982).
There is some
evidence suggesting that the medial efferent system enhances the frequency
resolving capacity (Micheyl & Collet, 1996;
Igarashi et al., 1979) and the vowel discrimination, especially in a
background of noisy environment (Muchnik et al., 2004;
Sahley et al., 1997c). Furthermore, Tolbert et
al. (1982) support the idea that the OC bundle optimizes the detection
of interaural intensity differences for higher frequency signals by increasing,
within the cochlea, the interaural disparity reaching the LSO. Therefore,
better understanding of the significance of the medial efferent system and its
pharmacological manipulation may prove beneficial for children and adults who
have difficulties in speech discrimination in noisy environment (classroom
etc), despite normal pure tone audiometric thresholds, as well as for subjects
exposed to intense occupational noise. Several studies
have provided evidence suggesting that activation of the medial efferents
serves a protective function in the mammalian auditory periphery against
high-level auditory stimuli (Canlon 1996; Subramanian
et al., 1993; Liberman 1991). Since the medial olivocochlear
bundle is mainly inhibitory, there has been already suggestions that
dysfunction of the efferent auditory system, at any level from auditory cortex
to cochlea, may be a basis for tinnitus generation, especially in noise-induced
tinnitus cases (Prasher et al., 2001; Attias et al.,
1996) and in tinnitus after head injury (Ceranic
et al, 1998). It has been also suggested that
hyperacusis might be associated with dysfunction of the efferent system, as
estimated by the abnormal OAEs suppression and the extreme high prevalence of
recordable multiple SOAEs (Ceranic et al., 1998). Suppression
of OAEs Because
descending medial efferent fibers preferentially terminate on OHCs, the
prevailing view is that the micromechanical properties of the OHCs are in
direct control of the efferent innervation. Since OAEs is thought to reflect
these dynamic properties, it has been hypothesized that activating the medial
efferents would produce alterations to cochlear micromechanics and, hence, to
OAEs. Indeed, there is now great body of evidence that auditory sound
stimulation, presented ipsilaterally (Tavartkilage et
al., 1997) or contralaterally, results in reduction of the amplitude of
both types of Evoked OAEs (TEOAEs and DPOAEs) (Moulin
et al., 1993; Ryan et al., 1991; Collet et al., 1990). This phenomenon
is called suppression of OAEs and it is proved that is mediated through the
medial efferent system (Williams et al., 1994; Kujawa
et al., 1993; Veuillet et al., 1991; Warren & Liberman 1989). Thus, it has
been suggested that the contralateral suppression of OAEs could serve as an
objective, non-invasive clinical test for the exploration of the non-linear
micromechanics of OHCs and the clinical neurologic evaluation of the auditory
brainstem in general and descending efferent bundle, specifically. How
to perform the suppression test? As mentioned
before, both types of evoked OAEs (TEOAEs and DPOAEs), can be suppressed when
auditory stimulus is applied either to the ipsilateral or the contralateral
ear. Contralateral suppression is more commonly used in both clinical and
experimental projects. Ipsilateral suppression of TEOAEs has been studied by G. Tavartkiladge et al., (1997), but special equipment
(probe) is needed and, as stated by the authors, suppression of TEOAEs could
not be attributed only to the medial OC bundle but to intracochlear processes,
as well. The optimum
parameters for performing the contralateral TEOAEs suppression test were found
to be as follows (fig. 2): 1. stimulus for
TEOAEs generation: linear-clicks at approximately 60 dB SPL (±3 dB peak SPL), duration 80 μs and
repetition rate of 50s-1. 2. contralateral
sound stimulation: white noise at low intensity (30-50 dB SL) (Berlin et al, 1994; Ryan et al, 1991), so that any
crossover phenomenon and contraction of the contralateral stapedius muscle is
avoided. Some authors suggest that
the contralateral sound stimulus should be presented at intensities of 10-15 dB
lower than the threshold of contralateral acoustic reflex, elicited by white
noise (Williams et al, 1994). 3. collection
and analysis of data: Ten runs of 60 sweeps each are averaged alternately with
and without contralateral white noise stimulus. Thus, 5 alternate buffers were
combined to give an average of 300 sweeps each. The difference between the
amplitude in dB SPL of the total response without contralateral noise and that
with contralateral noise is measured as the degree of suppression of TEOAEs (Prasher et al, 1994). The
suppression of TEOAEs in normal hearing adults shows a great intra-individual
variability, but, according to several studies, 1 dB SPL is considered to be
the “cut-off” point for normal medial OC bundle function (Prasher et al., 1994; Collet, 1993). Considering 1 dB
SPL as the lowest “normal” level, the method shows a false positive rate of 6%
(Prasher et al, 1994) in normal hearing
subjects, and a false negative rate of 17% and 0% in cerebellopontine angle
tumors and intrinsic pontine lesions, respectively. The
suppression of DPOAEs has been studied mainly in experimental animal projects. Moulin et al (1993) propose the following parameters
as optimal for this test: 1. stimulus for
DPOAEs generation: primary tones at low level (L1=L2=50-60
dB SPL). 2. contralateral
sound stimulation: white noise at a minimum intensity of 30 db SL. DPOAEs are suppressed throughout
their frequency range, the maximum suppression being at frequencies from 0.5 to
2 kHz (Moulin et al., 1993). DPOAEs suppression
shows frequency specificity if narrow-band noise is used as a contralateral
stimulus (Chery-Croze et al., 1993). In conclusion, simultaneous
contralateral sound stimulation results in the following changes in OAEs
(SOAEs, TEOAEs and DPOAEs) (Collet 1993): 1. Reduction of
the overall amplitude of at least 1 dB SPL. 2. Phase shift. 3. The
suppression effect becomes greater when the intensity of contralateral noise
increases (greater suppression is reported at an intensity of 50 dB SPL). 4. The degree of
TEOAE and DPOAE suppression becomes greater as the level of the ipsilateral
stimulation decreases (greater TEOAEs suppression is reported with clicks at an
intensity of 60 ± 3 dB SPL and greater DPOAEs
suppression with low-level primary tones). Influence
of maturation and ageing In preterm
babies (up to 40 weeks of gestation) no suppressive effect has been evidenced (Morlet et al., 1993), due to immaturity of the
efferent auditory pathway. In fullterm babies a slight effect has been shown (Ryan et al., 1994). In the elderly, the suppressive
effect is present but smaller than in young adults (Castor
et al., 1994). Influence of sleep
OAEs suppression occur during
sleep whatever the stages, but in almost half of the subjects no effect is seen
at the onset of sleep during 15 minutes (Froehlich et
al., 1993). OAEs
suppression in clinical applications OAEs is the
only objective and non-invasive method for the evaluation of the functional
integrity of the medial efferent system, and, therefore, for the evaluation of
the structures lying along its course, at least up to the level of inferior
colliculi (VIII nerve, cerebellopontine angle and pons). Diagnosis
of extrinsic and intrinsic pontine lesions Although,
literature data are rather poor, there is evidence that the efferent test could
be useful in the diagnosis of pontine lesions either extrinsic (acoustic
neuromas, meninigiomas, congenital cholesteatomas) or intrinsic (multiple
sclerosis, ischemic infarcts, tumors). Prasher et al. (1994) conducted a
study in 18 patients suffering cerebellopontine angle (CPA) tumors and 11
patients with intrinsic pontine lesions. According to their results, 15 out of
18 patients with CPA tumors demonstrated abnormal TEOAE suppression ipsilateral
to the lesion. The suppression was abnormal in all patients suffering intrinsic
pontine lesions. The author
performed the TEOAE suppression test in a group of 11 patients with CPA tumors
(6 with acoustic neuroma, 1 congenital cholesteatoma, 3 meningioma, 1 lipoma)
and a second group comprised of 21 patients suffering intrinsic pontine lesions
(10 with multiple sclerosis, 7 ischemic infarct, 1 pontine hemorrhage and 3
tumors). A third group of 20 young healthy, normal hearing volunteers served as
the control group for the TEOAE suppression test. Normal suppression (³1 dB SPL) demonstrated 18 out of the
20 controls (false positive rate 6.7%). All patients with CPA tumors showed
abnormal suppression (<1 dB SPL), either ipsilaterally to the lesion or bilaterally
(sensitivity 100%). Bilateral abnormal suppression was found whenever pressure
was exerted on the pons due to the size of the tumor. Abnormal suppression was
recorded in 17 out of 21 patients of the intrinsic pontine lesions (sensitivity
81%). Figures 3 and 4 illustrate characteristic cases of abnormal
TEOAE suppression in pontine demyelinating disease and CPA tumor, respectively. 
    
Figure 4: TEOAEs suppression test in a case
of a 51 year-old woman suffering a CPA meningioma on the right (MRI). She had
a mild to moderate sensorineural hearing loss, normal OAEs and abnormal
suppression bilaterally, presumably due to the pressure exerted on the
brainstem by the tumor.
Auditory
neuropathy Auditory
neuropathy is a clinical entity that has drawn the interest of audiologists the
last few years. It is characterized by sensorineural hearing loss in pure tone
audiometry, speech discrimination difficulty, absence of acoustic reflexes,
normal OAEs and absent or severely abnormal auditory brainstem responses (ABR)
without any radiologically evident retrocochlear lesion. The age of patients
range from infancy to adulthood and it could present as a neuropathy of the
VIII nerve alone or, most frequently, as a part of hereditary motor sensory
neuropathies (i.e. Charcot-Marie-Tooth syndrome, Freidreich’s ataxia syndrome)
(Doyle et al., 1998; Starr et al., 1996) Auditory neuropathy patients lack suppression of
OAEs (Hood et al., 2003; Lalaki 2003; Abdala et al,.
2000). In conclusion, there exists evidence
that the assessment of the medial olivocochlear system by recording OAEs under
contralateral acoustic stimulation in a suspected lesion of the CNS could
contribute to neuro-otological topographic diagnostics. It could be performed
complementary to Auditory Evoked Brainstem Responses (ABR) or in cases with
mean hearing threshold worse than 60 dB HL where the ABR test is of limited
sensitivity (provided that TEOAEs could be recorded due to the retrocochlear
nature of the hearing loss).
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