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342 Disorders of the Auditory System
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system more than the peripheral nervous
system (Dublin, 1986; Shapiro, 2003).
number of central nervous system
A
structures can be involved, including the
globus pallidus, the subthalamic nuclei,
the brainstem nuclei (especially the auditory nuclei), the cerebellum, and the hippocampus. In regard to auditory pathology, the cochlear nuclei, the superior
olivary complex, the nuclei of the lateral
lemniscus, and the inferior colliculus have
all shown pathology. Involvement of the
auditory nerve or cochlea is seldom noted
(although retrograde degeneration is possible) (Dublin, 1976, 1986).
Medical Diagnosis
A complete history of the course of the
disorder with special attention to the duration of the disease and the serum levels
of bilirubin are critical components of the
medical evaluation. Important are blood
tests for bilirubin levels and Rh-incompatibility. Bilirubin levels of 40 mg/dL are
definitely too high and 30 mg/dL are of
concern, but many infants with this level
are fine, and levels of 20 to 25 mg/dL are
within the alerting range. There have been
some data indicating that tissue assays
of (unbound) bilirubin may be useful in
diagnosis. Also helping in the diagnosis of
HB can be the ABR, gaze testing (for nystagmus), tests of muscle tone, and a dental
exam to document any dental abnormalities (Shapiro, 2003).
Medical Management
It is important to diagnose the problem
early. The main treatment is the use of various forms of phototherapy. Blue spectrum
lights work well to degrade bilirubin and
fiberoptic blankets allow long duration of
light exposure. Of course, in Rh-incom-
patibility situations, transfusions may be
necessary as these drive up the red blood
cell count and reduce the bilirubin levels.
It also is important to treat any underlying problems such as infections, and often
it may be necessary to stop breastfeeding
(Lauer & Spector, 2011).
audiology and
neuRotoxins
A wide variety of neurotoxic substances
can compromise the CANS. It is beyond
the scope of this section to discuss all
of them. It is possible, however, to mention the audiologic correlates to some
of the key neurotoxic substances for which
there exists a reasonable amount of data.
Therefore, we focus on heavy metals (lead
and mercury), solvents (styrene), and the
organic toxin, bilirubin. It is reasonable
to assume that other neurotoxins would
likely have similar effects on higher auditory function, although there is not clear
evidence of this.
Audiology: Heavy
Metals and Solvents
Behavioral Test Procedures
Dichotic Listening Tests. Dichotic digit
results have been found to be depressed
for workers exposed daily to a mixture of
xylene, toluene, ketone, and methylethyl
compared to a nonexposed group of subjects (Fuente & McPherson, 2007a, 2007b).
The exposed groups of subjects, however, presented with essentially normal
pure-tone thresholds. Similar results for
dichotic listening tasks were reported by
Varney, Kubu, and Morrow (1998) in their
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study of workers also exposed to mixed
neurotoxic solvents.
Temporal Processing Tests. In a recent
study, temporal processing ability was
tested using the frequency and duration
pattern tests as well as the Gaps-in-Noise
(GIN) test on workers exposed to styrene on a daily basis. Other workers not
exposed to any solvents served as a control group. The frequency and duration
pattern results were found to be reduced
for the styrene-exposed group, but the
GIN measures were not when pure-tone
hearing loss was accounted for by using
statistical procedures (ZamyslowskaSzmytke et al., 2009). Fuente and McPherson (2007a, 2007b) also found significantly
lower scores for frequency patterns as well
as for random gap detection in workers
exposed to solvents compared to a control
group of workers.
Monaural Low Redundancy Speech
Tests. The Hearing in Noise Test (HINT),
filtered speech, and interrupted speech
tests have all shown lower scores for solvent-exposed groups compared to controls (Dietrich, Succop, Berger, & Keith,
1992; Fuente & McPherson, 2006, 2007a,
2007b). These results and the results mentioned earlier indicate the possible use of
behavioral central tests to assess central
auditory function in these populations.
Electrophysiologic Tests
Auditory Brainstem Response. Per-
haps the central auditory test most commonly utilized for heavy metal and solvent exposure has been the ABR. Studies
have shown abnormal ABRs, primarily
extended central conduction latencies (I–
III, III–V, and/or I–V intervals), for individuals exposed to solvents compared to
control groups (see Fuente & McPherson,
2006, for review). Individuals with exposure to lead or mercury also have shown
ABRs with abnormal latencies and morphology compared to control subjects
(Araki et al., 2000; Murata, Weihe, BudtzJørgenson, Jørgenson, & Grandjean, 2004;
Musiek & Hanlon, 1999). However, there
are data demonstrating that abnormal
central conduction times on the ABR may
be related to the lead blood levels only for
higher lead levels (40 ug/dL) (Araki et al.,
2000). There are also reports of ABR waves
I, III, and V all shifted in latency, consistent with peripheral hearing loss (see Castellanos & Fuente, 2016). Of interest is the
research of Allen Counter (Counter, 2002),
which measured the ABR in lead-glaze
workers in South America. The workers
in Counter’s study had been exposed to
lead on a daily basis for years and generations; however, this population showed
few, if any, abnormalities on ABRs. Some
individuals did show extended central
conduction times, but regression analysis
showed no correlation between lead blood
levels and the wave latencies obtained.
Could this study show adaptive effects of
the nervous system from constant exposure, or do the findings simply represent
variability in the neural mechanism measured via ABR? Additional studies would
be needed to answer this question.
Late Potentials (N1, P2, P300). The
P300 event-related potential seems to
dominate the literature in regard to late
potential data on heavy metal and solvent-exposed individuals. In regard to
solvent exposure, the P300 latency has
been shown to be prolonged for those
having solvent exposure versus control
subjects (see Fuente & McPherson, 2006,
for review). The P300 was also shown
to be extended in latency for workers
344 Disorders of the Auditory System
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exposed to lead and to be correlated with
lead levels in the studies reviewed by
Araki et al. (2000). In this review, there
was evidence to show that, unlike findings for the ABR, even relatively low
lead blood levels yielded delayed P300s.
Because the P300 data on heavy metal and
solvent exposure appear to be compelling,
this test should be given serious consideration for inclusion in the evaluation of
individuals with these types of exposures.
Currently, there is a paucity of data for the
N1, P2, and middle latency potentials in
exposed populations. Additional data are
needed before an informed recommendation regarding the applicability of these
potentials in the assessment of patients
exposed to toxic substances can be made.
Case 7–5: Mercury Poisoning
History
This case received national media attention when a college professor became ill
from mercury poisoning during an accident in a research lab. One of the first
symptoms reported following the accident was hearing difficulty, specifically
difficulty understanding speech. The
patient subsequently began to experience
a high-pitched tinnitus in both ears, balance problems, and slurred speech. When
we saw this middle-aged patient, her
ability to understand speech was diminished to the point where it was necessary
for individuals to resort to writing things
down to communicate with her.
Audiology
Interestingly, the patient’s audiogram
showed only a mild high-frequency hearing loss bilaterally; however, speech test-
ing could not be completed as the patient
could not understand spondees or monosyllabic words at any intensity level presented in either ear (Figure 7–5A). The
ABR showed poor waveform morphology
for both ears with what appeared to be
severe latency delays for the right ear and
essentially a loss of waveform integrity at
high-repetition rates bilaterally (Figure
7–5B). DPOAEs were essentially normal
for frequencies 1000 to 4000 Hz bilaterally (Figures 7–5C and 7–5D). Clearly, this
case demonstrated a greater central than
peripheral effect of the mercury poisoning on the patient’s auditory system (see
Musiek & Hanlon, 1999, for an in-depth
discussion of this case).
Impression
Central auditory involvement likely secondary due to mercury poisoning. Secondary findings include a mild high-frequency
sensorineural hearing loss.
Medical Management
The patient was acutely treated for mercury poisoning, but unfortunately, this
patient passed away due to complications
from her exposure.
Audiology:
Hyperbilirubinemia
Introduction
Excess of bilirubin in the brain can be neurotoxic as mentioned earlier in this chapter. Audiologic considerations are many.
One is that, most of the time, this condition occurs early in life; therefore, only
limited testing can be completed. In some
cases, the effect on auditory function
A
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Figure 7–5. Pure-tone thresholds and speech audiometry test results (A), ABR tracings (B), and
DPOAEs (C and D) for a patient diagnosed with mercury poisoning (Case 7–5). continues Note:
the dark lines on (C) and (D) represent the normative criteria used to differentiate normal versus abnormal DPOAE amplitude measures. (From “Neuroaudiological Effects in a Case of Fatal
Dimethylmercury Poisoning,” by F. E. Musiek and D. P. Hanlon, 1999, Ear and Hearing, 20(3),
271–275. Reproduced with permission.)
345
B
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C
D
Figure 7–5. continued
346
7. Disorders of the Central Auditory Nervous System 347
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remains and can manifest itself as an auditory processing disorder. An important
consideration is that, as shown earlier, HB
compromises primarily the CANS and not
the auditory nerve or the cochlea (Dublin,
1986). Therefore, with HB as an etiology,
the term auditory neuropathy spectrum
disorder (ANSD) should be used restrictively even though many of the reports
in the literature on ANSD include children with HB (see Rapin & Gravel, 2003).
Because the primary effects of high bilirubin levels are on brain nuclei, it is and
should be classified as a central auditory
disorder. As Dublin (1986) relates, HB
has a particular affinity for damaging the
cochlear nucleus.
Electroacoustic and
Electrophysiologic Tests
Auditory Brainstem Response. The
ABR should be abnormal in patients
with HB. Given that the main effect is
on auditory nuclei in the brainstem, the
early waves of the ABR may be present
(if peripheral hearing is adequate) and the
later waves (III, IV, V) may be delayed,
absent, or reduced in amplitude (Shapiro
& Hecox, 1988). It is possible that even
the early ABR waves (I and II) could be
absent if there is considerable hearing loss,
or if there is retrograde degeneration of the
auditory nerve from the cochlear nucleus.
Therefore, it is possible that HB could yield
a “no response” ABR (and as a result, be
difficult to discern from ANSD). It is important to realize that not all infants with high
bilirubin levels will yield abnormal ABRs
as even some with severe involvement
have been shown to have normal ABRs
(Rhee, Park, & Jang, 1999).
Electrocochleography (ECochG). In
cases of HB, the cochlear microphonic
(CM) should be recordable unless there is
coexisting severe damage to the cochlea.
By changing polarity, the CM, if present,
should reverse polarity, which is a procedure that can be used to help define the
CM (Akman et al., 2004).
Acoustic Reflexes and Otoacoustic
Emissions. Acoustic reflex thresholds
generally are absent or elevated in HB due
to the brainstem involvement. Otoacoustic emissions should be normal unless
there is coexisting cochlear involvement.
tRauma, head
injuRy (tRaumatic
BRain injuRy)
Introduction
Earlier in this book, there were sections
devoted to trauma to the peripheral auditory system. In this chapter, the focus is
on trauma that may affect the CANS. The
Centers for Disease Control and Prevention (2019) relates that head injury or traumatic brain injury (TBI) is caused by a jolt,
blow, or bump to the head that causes a
disruption of normal brain function. It also
can result from a penetrating head injury
(i.e., a bullet wound). These injuries can
result in mild to severe symptoms, which
occur along a continuum with symptoms
ranging from mild, brief changes in mental status to a severe alteration in mental
functions where the affected individuals
may experience a period of unconsciousness or amnesia. Along with these alterations are other dysfunctions that involve
motor and sensory systems. Synonyms
often used for head injury are head trauma,
traumatic brain injury, and intracranial
injury. Concussion is not the focus of
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the discussion here although much attention has recently been directed towards
this entity. A comprehensive discussion of
the literature in this area would be beyond
the scope of this chapter. However, we do
relate some selected information on concussion in certain contexts where relevant
to the ongoing discussion. Concussion is
less severe than TBI. It often has an abrupt
onset of a brief neurologic impairment
with imaging (CT and/or MRI) typically
found to be normal. Cognitive, physical,
and emotional symptoms can vary significantly. Unlike TBI, concussions typically
resolve within the first 2 weeks following
the injury (Iverson et al., 2017).
Symptoms
As noted previously, the symptoms related to head injury can range from subtle
to severe. In some cases, the symptoms
will not appear until days or even weeks
after the injury. Some of the more common
symptoms are headaches and a neck pain
that does not subside after a reasonable
period of time. Also, difficulty remembering and/or concentrating; slowness in
speaking, thinking, acting, and reading;
and general confusion are symptoms of
concern following a head injury. After hitting one’s head, extreme tiredness, mood
changes, and poor sleep patterns also may
emerge, and sensory symptoms such as
dizziness, poor balance, hypersensitivity
to sounds and light, and decreased sensitivity for smell and taste can occur secondary to head injury. In addition, difficulty
hearing in background noise and tinnitus
can be symptoms related to head injury
(Centers for Disease Control and Prevention, 2019). Of course, the nature of these
symptoms is related to the specific locus
of the head injury’s effects on the brain.
One has to consider that in most cases of
head injury, it is possible that more than
one system may be involved and therefore multiple symptoms often appear.
Incidence and Prevalence
Head injury is a common disorder. It is
estimated that 2.8 million TBI-related
emergency department visits, hospitalizations, and deaths occurred in the United
States in 2013 (Taylor, Bell, Breiding, &
Xu, 2017). The same source relates that
approximately 50,000 individuals per
year die from head injury in the United
States. A population that is at high risk
for head injury is our service men and
women who are deployed in the Middle East where blast injuries are unfortunately all too common. In regard to
the general population, head injury is a
result of falls in about 47% of the cases,
disproportionately affecting infants/toddlers and older adults. Events that result
in a person being struck by or thrown
against something or someone, such as in
sports, have a 15% incidence and motor
vehicle accidents make up 14% of all
head injuries in the United States (Taylor
et al., 2017).
Etiology and Pathology
In head injuries, several stages of pathologic activity can unfold after the incident.
The immediate insult is one that is
mechanical, that is, direct tissue damage
as a result of the brain being accelerated
and decelerated quickly, which means the
tissue can be expanded. These mechanical
mechanisms can cause tearing and/or
stretching of neural tissue and may contribute to tissue displacement and shearing
7. Disorders of the Central Auditory Nervous System 349
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forces, which can result in hemorrhage.
Impaired cerebral blood flow (CBF) and
altered tissue metabolism are likely actions
in head injury. From a vascular perspective, there can be a series of events that
can create problems. There can be hemorrhage and hyperfusion or hypofusion to
involved tissue. Often, CBF autoregulation is impaired and cerebral vasospasm
can occur. Additionally, oxygen and glucose metabolism can be affected by head
injury, which can result in a host of problems. Soon after the injury, edema and
inflammation can evolve causing serious
symptoms. If these conditions are not
ameliorated, necrosis and apoptosis (cell
death) ensues (Werner & Engelhard, 2007).
Analysis of head injuries resulting
from blasts has revealed that diffuse axonal injury often occurs in the frontotemporal areas, the internal capsule, the deep
gray matter, the upper brainstem, and the
corpus callosum. Contusions of the brain
commonly happen in the superficial gray
matter, and can affect the inferior, lateral,
and anterior frontal and temporal lobes.
Subdural hematomas seem to occur at
the convexities of the frontal and parietal
lobes (Taber, Warden, & Hurley, 2006).
From the information just presented, it is
obvious that, from an anatomic perspective, the auditory system often is involved
and therefore requires careful assessment.
level of consciousness on scale ranging
from 3 to 15 using verbal, motor, and eye
opening responses to stimuli as an index
(13–15 = mild, 9–12 = moderate, 3–8 =
severe). There also are classifications for
posttraumatic amnesia from less than an
hour to more than a day and for loss of
consciousness related to the duration of
unconsciousness from less than 30 min
to more than 24 hr (Saatman et al., 2008;
Valadka, 2004). Use of evoked potentials
can also contribute to diagnosis (see the
following discussion).
Medical Management
Medical management of patients with
head injuries can be highly varied depending on the type and severity of the injury,
making it difficult to cover in a concise
fashion. Acutely, neurosurgical procedures
to release intracranial pressure, arrest
bleeding, and repair tissue are all possibilities. Less acute management may include
management of symptoms (i.e., seizure,
pain, etc.). Rest is often key as well as
specialized therapies of all types. Also
important is patient and family education
for overall optimum management and
accommodation (Martin, Lu, Helmick,
French, & Warden, 2008).
Medical Diagnosis
Medical diagnosis is dependent on report
of the actual incident, quick assessment
of mental status, and whether or not consciousness was lost and for how long. For
more involved cases, such measures as
the Glasgow Coma Scale (GCS), which
yields mild, moderate, or severe classifications, may be used. The GCS grades the
Audiology
Head injury or TBI are terms that by their
core meaning indicate possible damage
to the central nervous system. The CANS
therefore must be considered a potential
site of involvement in patients presenting
with head injuries, a fact that often seems
to be overlooked. Head injury — like other
disorders that affect the CANS such as
strokes, tumors, and degenerative and
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developmental disorders — is more likely
to compromise the higher auditory system, although involvement of the lower
CANS can result. Although head injury
has its own unique set of circumstances
in the onset and evolution of the problem,
it has many similarities to other CANS
disorders. Disruption of appropriate neural function in the CANS in head injury
is secondary to pathophysiologic factors
such as immediate mechanical displacement and torqueing of tissue, stretching
and tearing of neurons and blood vessels,
and, later, edema, reduced circulation,
demyelination, and overall degeneration of affected neural substrate (Musiek
et al., 1994). The degree of involvement
depends on the severity and nature of the
blow or insult, the areas affected, and the
subsequent care received.
There has been a recent increase in
the interest in head injury because of its
incidence in veterans returning with such
injuries from the Middle East. Gallun and
his colleagues have been studying hearing status and central auditory function in
soldiers involved in the Middle East conflict who experienced blast injuries during
their deployments (Gallun, Diedesch, et
al., 2012; Gallun, Lewis, et al., 2012; Gallun et al., 2016; Gallun, Papesh, & Lewis,
2017). The hearing deficits noted in this
population of soldiers seem somewhat
different than those documented for previous conflicts where hearing losses were
noted, but central deficits were not discussed (likely due to the fact that central
testing was not conducted at the time of
these earlier conflicts). In a high percentage of the soldiers included in the Gallun
et al. studies there are indications of hearing difficulties (centrally based) but normal audiograms.
The degree of central auditory involvement associated with head injury depends
on whether or not the auditory tracts are
involved. There are data showing a relatively high incidence of either peripheral
or central deficits (68%) in head injury
populations (Bergemalm & Borg, 2001).
It must be realized that many individuals with head injury can have a number
of other nonauditory problems such as
attention, memory, and emotional deficits
that can influence auditory assessment.
Therefore, it will be important to consider
the potential impact of any cognitive and
emotional deficits that may exist on audiologic test results.
Behavioral Test Procedures
Dichotic Listening Tests. There is a
reasonable amount of data on dichotic listening and head injury. It appears that left
ear deficits on dichotic listening tests are
common among patients with head injury.
This is likely related to the stress placed on
the corpus callosum during head trauma
(Levin et al., 1989). Meyers and associates
(Meyers et al., 2002) reported a 60% sensitivity and a 100% specificity for a population with mild brain injury using a dichotic word test. Significant ear asymmetry
with left ear performance poorer than
right ear performance was also reported
for school-age children with head injury
compared to normal data (Benavidez
et al., 1999). In the normal population, the
difference between ears yielded a modest right ear advantage, whereas the head
injury population revealed nearly a 40%
performance advantage for the right ear
(Benavidez et al., 1999). Ear asymmetry appears to be related to the severity
of the injury as noted on imaging (Levin
et al., 1989). It appears that both cortical and brainstem damage from trauma
can yield abnormal dichotic listening
results; however, only a few cases of brain-
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stem involvement have been reported
(Musiek et al., 1994; Pinheiro, Jacobson, &
Boller, 1982). Gallun et al. (2016) showed
an abnormal performance rate for veterans with histories of long-term blast
injury on both the dichotic digits and
SSW tests. In this study, these central tests
were among the top performers among
the various central tests administered in
separating blast-injured individuals from
controls.
Temporal Processing Tests. There is a
paucity of reports on various temporal
processing tests and head injury. Pinheiro
et al. (1982) showed deficits for brainstem involvement on auditory patterns,
and deficits have been shown for cortical injury (Musiek et al., 1994, Musiek,
Baran, & Shinn, 2004). However, normal findings have also been reported for
patients with head injury on an auditory
pattern perception test (Musiek et al.,
2004). The results reported previously
were essentially based on the assessment
of individual cases; therefore, the findings must be interpreted with caution.
With timing being critical for temporal
tests, logically, it would be appealing to
utilize these procedures for patients with
head injury; however, more investigation
is required before a recommendation of
routine application of these procedures in
the head injury population can be made.
Referring again to blast injury data from
Gallun et al. (2016), the gaps-in-noise test
(GIN) showed nearly a 45% abnormal rate,
which was the best of the tests administered in this study in terms of test sensitivity. Nearly 35% of veterans demonstrated
reduced performance on frequency patterns. These data would indicate probable problems in temporal resolution (GIN)
and sequencing (frequency patterns) in
this clinical population.
Binaural Interaction Tests. Limited
data are available on head injury and binaural interaction tests. However, a critically important study completed many
years ago may provide some insights
in terms of the kinds of procedures that
may be useful. Lackner and Teuber (1973)
employed a binaural click fusion task with
subjects with head injury. Two clicks, with
one presented to the right ear and one to
the left ear, were separated by a varying
interstimulus interval. When the clicks
were perceived as one stimulus, the result
was considered as the subject’s fusion
threshold. Click fusion thresholds were
significantly higher for the head injury
group than for the control group. This
group difference was especially noted for
individuals with left hemisphere involvement. Based on the available evidence, this
procedure seems both valid and powerful and should be reintroduced in clinical
audiology. Masking level differences have
been used with blast injury patients (Gallun, Diedesch, et al., 2012). Performance
measured shortly after injury showed deficits but testing long term did not (while
other central auditory tests did). Clearly,
more research is needed regarding TBI
and MLDs.
Electrophysiologic Tests
Auditory Brainstem Response. The
ABR has been a key test for individuals
with head injury. The generators of the
ABR are the auditory nerve and brainstem
tracts. Therefore, these anatomic loci are
best evaluated by this test. The brainstem
is commonly involved in head trauma
from blast injuries (Taber et al., 2006).
Three key investigations have shown
approximately a 50% hit rate for ABR
and head injury of a mild degree (Bergemalm & Borg, 2001; Gaetz & Bernstein,
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