OTITIS MEDIA -
Acute (Infectious)
or Chronic
(Non-infectious)
Can be drained
(although not
cured) by grommits
Children have small
flat tube, more prone
to block if inflamed –
more adult like after 6
years)
More than 7 in 10
children have at
least one episode
of glue ear before
they are four years
old.
Only the 5-8%
severe/persistent
minority are cases
for treatment
Fluid builds up in
middle ear and
eustacian tube,
prevents the ear
drum vibrating
properly
Eustachian tube is the 'vent' to help maintain
same pressure as other side of TM. Air in middle
ear passes into nearby cells over time. If it is not
replaced by air coming up the tube a vacuum
will form, sucking the TM inwards and fluid out
from the cells giving glue like consistency
Most important
question: How long
have they had it? Fluctuating?
May need
temporary
hearing aids
Otosclerosis
(fusion of the
bones) e.g. after
pregnancy /
genetic
Perforation of
T.M. (trauma,
infection /
operation)
Ossicular
discontinuity
(trauma / birth
defect)
People w conductive
HL will still have good
bone conduction
Note raised AC
thresholds
Then note the BC thresholds
WNL, as skipping middle
ear...
SENSORINEURAL
Congenital~1.5/1000
Maternal infection -
particularly CMV, also
rubella, HSV
CMV - usually
progressive
H.L.
Birth complications -
premature, asphyxia
etc...
Genetic about 50% of
HL in children, but
most (90%) born to hearing
parents
Acquired
e.g. of
Presbycusis
(getting old)
Inner hair cells
become less
sensitive
Noise damage
- hair cells can
be sheared off
Typically shows notch
/ raised thresholds
on audiogram at
3-4kHz
Can be more
genetically
predisposed to
this
Losses up to 50dB will be due
to outer hair cell losses.
Hearing losses above 50dB will be due to
inner hair cell losses.
Infection - e.g.
Meningitis, mumps
/ measles
Meningitis, cochlea
can become ossified
(turn to bone) so
tend to put a
cochlea implant in
sooner rather than
later
Ototoxic drugs
e.g. Antimalarials
4. Chemotherapy
Also general toxins
e.g. viruses,
bacteria,
environmental,
alcohol
Trauma to
the ear
Fracture of
the temporal
bone lead to
HL in 70-80%
cases
Outer hair cells typicaly the
ones to go - provide
descrimination
Inner hair cells are the
big workers - send signal
off to the brain, less likely
to falter
Inner Ear or
hearing nerve
Usually
permanent in
nature
Bone Conduction
thresholds and
Air Conduction
are the same -
there is no air
bone gap
This loss is where the low
powered/high freq sibilants
and consonants lie and these
are the most important
components of speech
"Everyone mumbles
nowerdays."
FACTORS AFFECTING SPEECH: Severity,
frequency and relevant speech sounds,
cause (temp/permanent), progressive,
aided, aided thresholds and
descrimination
Find out if children
are wearing their
hearing aids
TEMPORARY / PERMANENT
MIXED H.L.
'NON ORGANIC' / Faking it
Person displays a
deficit, where no
true hearing loss
exists
Typified by lack of
co-operation / difficulty
concentrating on listening
tasks
Scale anything
from
phsycosematic -
attention
seeking
Variable,
unreliable
results
AUDITORY NEUROPATHY
Outer hair cell function of
inner ear preserved,
damage to inner hair cells,
or some part of the pathway
that relays signals to the
brain
Damage to
inner hair
cells
Connection
between inner
hair cell and
nerve
Damage to
auditory
nerve
Functional
deficit varies
greatly
Lots of SLT
CENTRAL AUDITORY PROCESSING DISORDER
Hearing is normal but child
has difficulty differentiating,
locating and recognising
sounds
Really tricky to
diagnose - may be
highlighted by SALT
Struggle with hearing,
particularly in
background noise
Difficulty
following
oral
instructions
Diff understanding
rapid / degraded
speech
Is it possible this
could relate to
SLI?
AUDIOGRAM CONFIGURATIONS:
Presbycusis
Conductive - e.g.
glue ear /
Meniere’s
Congenital -
long term
'cookie bite'
(may be hard to
aid)