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Audiology Online
Identifying “Neuro-reflexes” of the External Ear Canal.
Max
Stanley Chartrand
Abstract:
This study addresses
measures and methods for identifying three
under-recognized neuroreflexes of the external ear
canal. These three neuro-reflexes are related to
hearing instrument dispensing practice, as they often
complicate and may cause failure to fit hearing
instruments. By using an External Ear Neuro-reflex
Checklist (EENC) clinical tasks such as video-otoscopy,
cerumen management, otoblock insertion, ear-impression
taking, and hearing aid adaptation can be more
effectively managed. The EENC is a significant
measurement tool and helps expose potential fitting
problems during the evaluative process. Increased
awareness of little-known ear dynamics can help reduce
negative incidences and unnecessary remakes,
modification and returns for credit.
Introduction:
The physiology of the human external ear
canal poses significant challenges with respect to
wearing and fitting hearing aids, wearing and fitting
ear protection devices, using stethoscopes, and the
application of various inserts for hearing and ear
measurement techniques and many other functions. Modern
ear and hearing devices require cooperation and
accommodation of “pre-modern” natural defensive
mechanisms designed to protect the external ear from
foreign objects, infection, injury, invasion, and
environmental exposure (Durrant and Lovrinic, 1984).
Disregard of these same defensive mechanisms can cause
discomfort or rejection of an otherwise beneficial or
necessary auditory task.
The percentage of people who experience
negative or perhaps unsatisfactory events or experiences
during hearing loss evaluation and hearing aid
exploration is significant. The Hearing Industries
Association (HIA) statistics revealed a high rate of
“return for credit” for hearing aids, hovering around
20% (Ross, 2002). Further evidence of dissatisfaction is
apparent in the number of hearing aids “in the dresser
drawer” (Kochkin, 2000). Additionally, shell and earmold
remakes at hearing aid factories and earmold
laboratories and countless in-office modifications made
every day, indicate the presence of an underlying
problem (Chartrand, 1999).
As a result of extensive clinical
observation and a review of the current literature,
three neuro-reflex mechanisms have been identified.
These three neuro-reflexes affect hearing health
practice procedures and hearing instrument success (Chartrand,
2004a). For the purposes of this paper, these neuro-reflexes
are referred to as:
·
The
Vagus Reflex-
This reflex may be evoked during insertion of the
otoblock, cerumen removal, and rarely, with hearing aid
use. This reflex is evidenced by cough, gag, and/or
watering eyes during any of these activities.
·
The
Trigeminal Reflex
is sometimes called the “red reflex,” can cause
excessive vascularization and thickening of the tympanic
membrane (TM) during otoscopy, otoblock insertion, and
during hearing aid wearing.
·
The
Lymphatic Reflex
is a slower reflex which may result from over-wearing of
hearing aids during the early adaptation period. This
reflex is evidenced by excessive swelling of tissues and
soreness while wearing a custom fitted earmold or
hearing aid. Sometimes, even a perfectly fitted device (earmold
or hearing aid) causes this reflex. The lymphatic
response may appear to be due to an allergic reaction,
or the result of a poor fit. Physical modification
(buffing, drilling, grinding etc.) during the lymphatic
response period potentially results in loose fittings,
acoustic feedback and a compromise of the integrity of
the amplification system -- acoustically and physically.
Physiologically what we
find is an elaborate, interconnected reflex system. The
reflex system consists of somatic afferent sensory
fibers and sympathetic and parasympathetic efferent
motor fibers, which respond to external stimuli on the
mechanoreceptors (Pacinian Corpuscles and, to a lesser
extent, Meissner’s Corpuscles) and hair follicle
receptors (Grenness, 1999; Kress and Zeilhofer, 1999;
Spray, 1986). When movement or occupation occurs in the
external ear canal, it is perceived as a “threat” and
the mission of these mechanoreceptors is to maintain
chemical, thermal, bacteriological, and ionic
homeostasis within the external ear, thus -- eliminating
the threat.
Neurologically, cranial, cervical and
auxiliary nerves are implicated in the neurocomplex
which innervates the external canal region. Although
most of these have nothing to do with hearing, they
impact the ear and surrounding tissue. The tympanic
branch of the glossopharyngeal nerve (CN IX), the
mandibular and maxillary branches of the trigeminal
nerve (CN V), the mandibular, submandibular, chorda
tympani, greater petrosal and tympanic plexus of the
facial nerve (CN VII), Arnold’s branch of the vagus
nerve (CN X), and others, interconnect in a complex and
difficult to predict (with regard to their impact on
hearing prosthetics) manner (UC-Davis, 2005).
One perplexing challenge is adaptation to
tactile pressure in the external ear canal. Elsewhere in
the human body, adaptation to tactile pressure on a
cutaneous sensory organ occurs only a short while after
movement ceases, such as wearing a wristwatch or jewelry
(Nafe and Wagoner, 1941). However, regarding
prosthetics in the external ear canal, movement never
ceases because of mandibular, facial, and other dynamics
of the head and neck region. In fact, at the aperture of
the ear, dimensional changes of 10% (or more) occur with
the simple opening and closing of the mouth (Oliviera et
al., 2005; Oliviera et al., 1992). Therefore, it is
almost impossible for sensory receptors in the external
ear to stop firing while a rigidly fixed object (i.e.,
hearing aid or earmold) is placed in an excessively
movable ear canal (Kolpe and Oliviera, 2003). Aging
ears can be even more adversely affected by these
factors (Willott, 1981).
The degree of sensitivity varies widely in
individuals, often depending upon the thickness of
epithelium and the corneum stratum (keratin layer) over
the surface of the external ear canal and tympanic
membrane (Chartrand, 2004b; Kolpe and Oliviera, 2003;
Naiberg, Proops, and Hawke, 1984). The most important
factor regarding whether an individual will adapt
comfortably to aural prosthetics may hinge on whether
the keratin layer of their external ear tissue—which
shields otherwise sensitive neuroreflexes as well as
maintain physical homeostasis—is healthy and intact (Chartrand,
2004a).
To help organize these
autonomic mechanisms into practical models that can be
observed, understood, and accommodated (where possible)
in the course of hearing health practice, each neuro-reflex
has been defined in behavioral terms in Table 1 (below).
Table 1.
Description of external ear neuro-reflexes affecting
hearing instrument dispensing procedures and activities.
Neuroreflex Causal/Action Neural
Attribution Symptoms
|
Vagus Reflex |
Sympathetic motor reflex caused by light touch upon
the superior-inferior (and anterior metal wall) of
the ear canal. |
1) Pacinian corpuscles, 2) Arnold’s branch, vagus,
30 Internal acoustic meatus, facial, 4)
Glossopharyngeal (no parasympathetic activity in
this reflex) |
Cough, gag, and/or eyes watering upon insertion of
otoscopy, otoblock & impression-taking, and, in some
cases, while wearing hearing aid or other device.
Also causes non-acoustic occlusion while wearing
hearing aids in some cases. |
|
Lymphatic Reflex |
Sympathetic response to pressure on the surface of
the skin, as well as on deeper structures |
Facial, interneural cross-connections, involving
mechanoreceptors Pacinian corpuscles (fast action),
Meissner’s corpuscles (slow action), and hair
follicles |
Swelling, soreness after wearing device for a time.
Later causes increased feedback and acoustic
detriment when earmold modifications are made during
swelling. |
|
Trigeminal Reflex (also known as “Red Reflex”) |
Sympathetic and parasympathetic vascularization at
TM, when pressure applied in outer 1/3 of ear canal
|
1) Mechanoreceptors Pacinian and Meissner’s
corpuscles and hair follicles, 2) Facial sensory and
motor neurons for sympathetic and parasympathetic
response to stimuli. |
Vasodilation at the TM during otoscopy or hearing
aid wear. Can cause need for more gain/output to
overcome TM impedance. |
Method:
Participants-
Twenty-seven hearing impaired individuals (18 male, 9
female) between the ages of 49 and 87, with a mean age
of 68.3 years, were studied during the course of the
hearing aid fitting process. No attempt was made to
randomize participants. Participants were recruited by
informed consent as they presented at three dispensing
offices in southern Colorado and Northern New Mexico
over a two-month period.
In many respects this subject population (n
= 27) was representative of that found in the typical
hearing health practice. For instance, there is a much
higher concentration of serious hearing impairment in
the older population, and the incidence of hearing
impairment in males over sixty years of age is roughly
twice that of females in the same age-group when
comparing age and degree of hearing impairment (Staab,
1990).
Measures/Apparatus:
Equipment and materials used to make our observations
consisted of the following:
American Electromedic AE-105 Tympanometer
Qualitone CD-3 Acoustic Appraiser
MedRx Video Otoscope
Welch-Allyn Hand-held Fiber-optic Otoscope
Fiber Ear Vision Ear Light Set
Westone Labs open-cell foam otoblocks
Dreve impression syringe
Dreve Oto-Form A/k silicone impression material
Cerumen management implements and solutions
Miracell Botanical Solution
A
standardized checklist, the External Ear Neuro-reflex
Checklist (EENC) with rating scale, was used to make
qualitative measurements and observations of each task
and their resulting reflexes (the EENC can be found in
Appendix A).
Procedure:
Clinical
tasks relative to assessing and evaluating hearing, and
the hearing aid fitting process were performed. Careful
observations (EENC) were recorded during; Video otoscopy,
cerumen management, Oto-block insertion, impression
material insertion & removal, earmold insertion, and
post-fitting adaptation.
Subject verbal
responses and experimenter observations were considered
in the rating scale for degree of effect during each
task. Table 2 (below) summarizes reflex indications
relative to a rating scale of 0-3 (i.e., 0 =
non-existent, 1 = weak, 2 = moderate, and 3 = strong):
Table 2. EENC rating
scale key.
\
Neuroreflex
Non-existent Weak
Moderate Strong
|
Vagus Reflex
|
No response
|
Verbal report of
tickle in throat |
Stifled cough |
Cough, gag
sensation |
|
Trigeminal Reflex |
No vascular change
at TM |
Mild dilation at TM |
Moderate dilation
at TM |
TM turns red, need
for increased gain |
|
Lymphatic Reflex |
No report or
behavioral response |
Mild discomfort
after >2 hours wear |
Moderate discomfort
after approx. >1 hour wear |
Immediate, marked
discomfort upon insertion |
The Vagus Reflex (involving mostly Arnold’s Branch) was
rated according to patient reports and involuntary
coughing, gagging, and/or eyes watering during any of
the targeted clinical tasks. Trigeminal Reflex
observations were made during and after certain tasks
with a hand-held fiber-optic otoscope. Most of the
responses for the Lymphatic Reflex were elicited during
adaptation of new hearing aids or earmolds.
Data
Analysis:
Two sets of data were
calculated from this study:
a-The Pearson Product
Moment Correlation co-efficient between
keratin status and an
elicited Vagus Reflex during otoblock insertion
b- Quantification of
how often any of the targeted reflexes occur
at any point in the
process.
To determine an
association between “keratin status” and vagus
sensitivity during otoblock insertion, we designated
keratin status by number. Normal appearance was
designated “0,” thin or granulated appearance was
assigned “1,” a “peeling” or “peeled” appearance was
assigned a value of “2’” and an appearance that was
absent/swabbed was assigned a value of “3.” Vagus
sensitivity was quantified in reverse order (0 =
non-existent, 1 = weak, 2 = moderate and 3 = strong).
Table 3.
Ordered arrangement of subjects (n=27) re keratin status
vs vagus reflex sensitivity
Subject Keratin Vagus Reflex
(N) Status
Sensitivity
|
01 |
0 |
0 |
|
02 |
0 |
0 |
|
03 |
0 |
0 |
|
04 |
0 |
0 |
|
05 |
0 |
1 |
|
06 |
0 |
1 |
|
07 |
0 |
3 |
|
08 |
1 |
1 |
|
09 |
1 |
1 |
|
10 |
1 |
1 |
|
11 |
1 |
2 |
|
12 |
1 |
2 |
|
13 |
1 |
2 |
|
14 |
1 |
2 |
|
15 |
1 |
2 |
|
16 |
1 |
2 |
|
17 |
2 |
2 |
|
18 |
2 |
2 |
|
19 |
2 |
2 |
|
20 |
2 |
3 |
|
21 |
2 |
3 |
|
22 |
2 |
3 |
|
23 |
2 |
3 |
|
24 |
3 |
2 |
|
25 |
3 |
3 |
|
26 |
3 |
3 |
|
27 |
3 |
3 |
Exhibit B shows
calculations for inferential and descriptive statistics
from the above data. For a visual correlational
representation of the data, a scatterplot with line of
regression (r = .735) is shown in Figure 1:

Figure 1.
Relationship between keratin status and vagus
oversensitivity during otoblock insertion.
The
second set of data concerned how often any of the three
reflexes occurred in the subject (n = 27) population at
any point in the evaluation, fitting, and post-fitting
process. An “X” represents reflexes were observed
(moderate or strong only), an “0” represents no
significant reflex was observed.
Pass/fail decisions were based on the following
criteria: Vagus if a cough reflex was evoked in at least
two procedures, Trigeminal if a visible and rapid
vascular dilation occurred during two or more
procedures, and Lymphatic upon discomfort or soreness
during the adaptation period. Data is tabulated in
Table 4 as follows:
Table 4.
Incidence of significant neuroreflex activity within the
subject (n = 27) population.
Subject Vagus
Trigeminal Lymphatic
(N = 27) Reflex
Reflex Reflex
|
01 |
0 |
0 |
0 |
|
02 |
0 |
0 |
0 |
|
03 |
0 |
0 |
0 |
|
04 |
0 |
0 |
X |
|
05 |
0 |
0 |
0 |
|
06 |
0 |
X |
0 |
|
07 |
0 |
0 |
0 |
|
08 |
0 |
X |
0 |
|
09 |
0 |
0 |
0 |
|
10 |
0 |
X |
0 |
|
11 |
0 |
X |
X |
|
12 |
X |
0 |
0 |
|
13 |
0 |
X |
X |
|
14 |
X |
X |
0 |
|
15 |
X |
X |
0 |
|
16 |
0 |
X |
0 |
|
17 |
0 |
X |
X |
|
18 |
X |
X |
0 |
|
19 |
0 |
X |
X |
|
20 |
X |
X |
0 |
|
21 |
0 |
X |
X |
|
22 |
X |
X |
0 |
|
23 |
X |
| |