Chapter 161:Tinnitus and Hyperacus s

Figure 161.1Axial contrast""nhanoed MRI shows le vestf

bu lar schwannoma (white arrowhead) that was causing
nonpulsatlle tinnitus.

which increase neural firing, such as aspirin, nomteroi

dal anti-inflammatory medication, nicotine, ethanol, and
caffeine, can cause or exacerbate nonpulsatile tinnitus
(Table 161.2).
The underlying mechanism of nonpulsatile subjective
tinnitus, including the generator of the noise, has not yet
been described. Advances in experimental and imaging
techniques have revealed significant imights into the
etiol ogy of this disorder. These insights may ultimately
guide rational treatment of this form of tinnitus.

CN
Vlll/CNS

Dietary

Charcot-Marie-Tooth
Meningi1is
Meningioma
Multiple sclerosis
Vestibular sdlwannoma
Caffeine
EUlanol

Initial theories of the generation of nonpulsatile tinni

tus forused on the role of the cochlea, specifically the
role of certain cochlear structures such as outer hair
cells.1hese 1heoriea flowed logically from observations
1hat subjective nonpulsatile tinnitus is frequently seen in
individuals with measurable hearing loss or following
known ototoxic inju ries (such as ototoxic medication
exposure, noise exposure, head injwy). However, later
findings, such as the persis tence of tinnitus following
truncation of the auditory nerve or ablation of the
cochlea, disproved these exclusively cochleogenic
etiologies for 1hemajority of sufferers of sub jectiv1!
nonpulsatile tinnitus (6-8).
More recently, imaging studies on humans with tin
nitus and animal studies have revealed changes in
neural activity and connectivity throughout the
auditory system following loss of hearing. 1he
spontaneous firing rate of auditory neurons increases
during tinnitus, a phenomenon 1hat may generate the
tinnitus sound (9,10). Another pos sibility is that
increased synchrony of firing wi1hin audi tory
pathway neurons may be perceived as tinnitus (9,11).
Many studies have noted a decrease in inhibitory neural
input at multiple sites along the central auditory
pa1hway!, including the dorsal cochlear nucleus (1215). 'Ibis leads to a net increase in excitatory signaling
in the auditor:y pathway and has been proposed as the
neurophysiologic basis for subjective tinnitus.
Others have proposed that neuronal plasticity may
lead to tinnitus. Following hearing loss, studies in
animals and humans have demonstrated a change in
the tonotopic map 1hroughout 1heauditory system.
Some have proposed that these plastic changes in the
frequency representa tion in areas of the brain and
brainstem are the origin of tinnitus, while oth have
suggested that 1hese changes in the tonotopic map are
merely epiphenomena of that hearing loss (16). Many
other plastic changes also follow

EAC pathology

Acquired stenosis
Cerumen
Foreign body

IHCdamage

Genetic HL
HZO

Labyrinthitis
Meniere disease
NIHL

Drugs

Antibiotics
Antidepreuanu
Immune modulators
Nicotine

2599

Middle ur disease

Ototoxicity
Prasbyacusis
Cholesteatoma
Chronic otitis media
Otosclero5is

CN. c:ranial nerve;CNS,Cl9ntral nervous system; EAC. extemal auditory canal; HL. hearing loss; HZO. her
pes zoster oticus; I HC. inner hair Cl911; NIHL, noise-induc:ad hearing loss.

2600

Section IX:Otology

MEDICATIONS lHAT CAN CAUSE NONPULSATILE TINNITUS

Antfbfotfcs

Aminoglycosides
Macrolides
Vaneomycin

Immune

lnfergen

modulators

Mycophenolate
Sirolimus
Soriatane
Tacrolimus
Ibuprofen

Antidepreaants

TCAs

NSAIDs

Antimalarial
Chemotherapeutics

SSRls
SNRls
Quinine
Cisphrtinin

Salicyfates
Mile.

Loop dfurwtfcs

Aspirin
Caffeine
Nicotine
Pravacid

Edlacrynic acid
Lasix

Misc., miscellaneous; NSAIDs, non-steroidal anti-inflammatory drugs; SNRls,serotonin-norepinephrine

reuptake inhibitors; SSRls,selective serotoninrptake inhibitors; TCAs, tricyclic antideprnsanu.

deafferentation of areas of the auditory system,

including changes in synaptic structure and firing
patterns,formation of new synapses and elimination of
othen, and dendrltic branching. All of these changes
may underlie the com plaint of nonpulsatile tinniws
(16).
None of these etiologies address patients with com
plaints of tinnitus who fall into two categories encowi
tered in clinical practice. One is the patient who has
had hearing loss for years and yet awakens suddenly
with tin nitus. The other is the rare patient who has
normal hear ing, even in the ultra-high frequencies, no
other dietary or toxic risk factors, and no psychiatric
comorbidities who complains of tinnitus. For these
patients, careful history taking may wicaver a
traumatic or emotional event that was coincident with
the onset of their tinnitus. Similarities between tinniws
and phantom limb pain have fueled the

hypothesis that both are "aversive memoi:y networks.

.According to this theory, the phantom awareness (tinni
tus) only becomes conscious when linked to other brain
networks, and then becomes bothenome when linked by
learned associations with unpleasant emotions (17).

Risk Factors
The most prevalent risk factor for subjective, nonpulsa
tile tinniws is hearing loss. As discussed above, hearing
loss may be the initial instigating factor underlying non
pulsatile tinnitus. Frequently this hearing loss includes
significant sensorineural losses at higher frequencies;
occasionally, the hearing loss can only be detected using a
high-frequency audiogram. (Fig. 161.2). Of note, not
every patient with hearing loss will have complaints of
tinniws,
Frequency,HZ (CPS)

Frequency,HZ (CPS)

125
0

250

500

:
\

I
I

750

1000 1500

f-E

2000

I
I
I

--0-

10
0
0
0

30

--

lI

SRT:S dB
SDS:100% @
45HL

Left Ear

SRT: SdB
SOS; 100%
@if5HL

3 0
20

" "'

40

40

-50
60
-

,,.

i
I
I

70

--

80

80

14,000

18,000

I
I

I
I

1 ......--(

I
I

16,000

.l.-( Y i
I

-I

I
I
I

I
I
I

I
I
I

90
=
00

110

10

Figure 161.2 Normal {A) and high-frequency (B) audiogram' of a patient with nonpul,atile
tinni tus, demonstrating normal hearing from 250 to 8,000 Hz and a very-high-frequency
bilateral hearing lo9,.

50

--6
7
8

-100

I
I

!/' 3

/1

I
I

70

12,50()

10,000 111,200

'\.

Right Ear

10

90

10 0
110

9000

3000 4000 6000 8000

0

I
I

100

-110

20.000