HIPERAKUSIS

hiperakusis adalah kondisi dimana berkurangnya toleransi terhadap

suara biasa di lingkungannnya. Orang dengan hiperakusis mendengar
suara dengan intensitas kecil menjadi sangat keras dan sangat nyeri
untuk didengarkan. Hal ini harus dibedakan dengan phonophobia,
yang disebabkan dengan migraine dimana pada orang phonophobia
adanya sensitivitas terhadap suara yang keras.
Stapedial reflex, atau dikenal juga sebagai attenuation reflex
diinervasi oleh facial nerve dan berfungsi untuk meredam intensitas
suara. Jika adanya gangguan terhadap reflex ini dapat menyebabkan
hiperakusis.
(Tanya Singh MS, Michael D. Seidman MD, FACS, in Neurosensory
Disorders in Mild Traumatic Brain Injury, 2019)
Hyperacusis is occasionally associated with facial nerve
palsies (D.M. Baguley, ... D.J. McFerran, in Handbook of Clinical
Neurology, 2016)
Secara anatomis, facial nerve terdiri dari komponen motoris dan
sensoris dimana komponen motoris mensupply muskulatur untuk
tersenyum, stapedius, stylohyoid dan posterior belly digastric.
Paralisis otot stapedius juga dapat menyebabkan keluhan hiperakusis
(baca lebih lanjut : https://neupsykey.com/cranial-nerve-vii-the-facial-nerve/)
If there is hyperacusis (increased
auditory volume in an affected ear),
this is due the stapedius muscle in
the middle ear being affected. The
stapedius muscle functions to
dampen ossicle movements, which
normally decreases volume. If there
is cranial nerve VII nerve damage,
this muscle is paralyzed. Because
the branch of the seventh cranial
nerve that goes to the stapedius
muscle begins very proximally,
hyperacusis due to seventh cranial
nerve lesions indicates a lesion close
to the nerve’s origin in the
brainstem rather than more
peripheral. Nevertheless, it is still a
lower motor neuron lesion, because
the lesion is not affecting the
corticbulbar tract. *(the trigeminal and facial nerve, paulette marie gillig,
(yang gambar diatas ini buat tambahan aja ya)
--

Tinnitus
Tinnitus is defined as the perception of sound without an external
acoustic source commonly referred to as “ringing in the ears” (Bauer
et al., 2008).

Robert A. Levine, Yahav Oron, in Handbook of Clinical Neurology,

2015
Abstract
Tinnitus, the perception of sound in the absence of an external sound, usually results from a
disorder of: (1) the auditory system(usually peripheral, rarely central); (2) the somatosensory
system(head and neck); or (3) a combination of the two. Its cause can be determined through its
characteristics. The history must include the tinnitus’: (1) quality (including whether it can ever
be pulsatile or have a clicking component); (2) location; (3) variability; (4) predominant pitch
(low or high); and (5) whether the patient can do something to modulate the percept. In addition
to the standard neuro-otologic examination, the exam should include inspection of the teeth for
evidence of wear, listening around the ear and neck for sounds similar to
the tinnitus, palpation of the craniocervical musculature for trigger points, and probing whether
the tinnitus percept can be modulated with “somatic testing.” All subjects should have a
recent audiogram.

Presently the most compelling tinnitus theory is

the dorsal cochlearnucleus (DCN) hypothesis: both the auditory and
somatosensory systems converge upon and interact within the DCN. If
the activity of the DCN's somatosensory-interacting fusiform cells
exceeds an individual's tinnitus threshold, then tinnitus results.
Tambahan info buat pengetahuan (gausah ditulis hehe) :
Tinnitus is a perceived sound that is not related to an external source.
It usually is described by patients as a ringing, clicking, humming, or
blowing sound. Most patients with tinnitus have an underlying otologic
problem, most commonly hearing loss. It is postulated that tinnitus is
the result of an imbalance between excitation and inhibition of auditory
pathways. The imbalance may occur at any level, including cochlear
hair cells, midbrain, and cortical central auditory pathways.
A.
Diagnosing the cause of tinnitus requires a detailed history.
Onset, duration, frequency, and localization are helpful in the
evaluation for the underlying cause. Tinnitus may be caused by
systemic disease, infection, metabolic abnormalities, medication
exposure, or inflammatory conditions. Review exposure to
aminoglycosides, loop diuretics, salicylates, quinine,
antimalarials, NSAIDs, and any history of toxic exposure to
heavy metals with the patient.
B.
The physical examination should include a check of the blood
pressure, a head and neck examination, and an auscultation for
vascular bruits and heart murmurs.
C.
If tinnitus is diffuse and not localized to either ear, consider
encephalitis of the temporal lobe and psychiatric illnesses.
Auditory hallucinations are noted primarily in patients with
psychosis.
D.
It occurs in objective (perceived by the examiner and patient)
and subjective (heard only by the patient) forms.
E.
Subjective tinnitus is more common than objective tinnitus, but
diagnosis of the underlying cause is more difficult. The
differential diagnoses of subjective tinnitus are medication and
toxic exposure, metabolic abnormalities, pathologic condition in
the peripheral (cochlear) or central (retrocochlear) pathways,
anxiety, depression, and dental disorders. Metabolic
abnormalities include hypothyroidism, hyperthyroidism,
hyperlipidemia, anemia, and zinc deficiency. The initial workup of
a patient should include a CBC, fasting glucose, triglycerides,
cholesterol, and thyroid-stimulating hormone. Pathologic
conditions of the ear associated with subjective tinnitus
include otosclerosis, chronic suppurative otitis media, Meniere's
disease, presbycusis, and noise-induced hearing loss.
F.
Objective tinnitus is rare. Causes include acquired and
congenital vascular malformations, neuromuscular disorders
(palatal myoclonus, stapedius muscle spasm, and
temporomandibular disorders), intracranial tumors, and structural
defects of the ear. Objective tinnitus is of two types: vascular and
mechanical.
G.
Pulsatile tinnitus refers to nonexternal sounds that are amplified
and synchronous with the patient's pulse. Benign intracranial
hypertension, jugular bulb abnormalities, and aberrant carotid
artery are included in the differential diagnoses. High-resolution
CT of the temporal bones is needed when a retrotympanic mass
is noted on examination. MRI and angiography are indicated for
patients with normal otoscopic examination to evaluate for dural
venous thromboses and to look for the empty sella and
small ventricles associated with benign intracranial hypertension.
Angiography is used when atherosclerotic carotid artery
disease, fibromuscular dysplasia, and small dural arteriovenous
(AV) malformations are suspected and the patient is a surgical
candidate.
H.
Stapedial muscle spasm–induced tinnitus is amplified with
external noise and is intermittent. Stapedial muscle spasm is
associated with facial nerve palsies, although it can occur
without them. Division of the stapedius muscle and tensor
tympani tendons is reserved for severe cases. Long-term use of
benzodiazepines for stapedial muscle spasm is not
recommended.
I.
Palatal myoclonus is apparent on examination of the oral cavity.
The tinnitus is thought to be generated from the opening and
closing of the eustachian tube and the rubbing of mucosal
surfaces. Electromyography (EMG) of the palatal muscles
confirms the diagnosis. Treatment with benzodiazepines results
in a decrease in anxiety.
J.
Tinnitus associated with the patulous eustachian tube is
synchronous with breathing. The patient may experience
autophony (hearing of his or her own voice or breathing). Rapid
weight loss and high estrogen states (e.g., use of birth control
pills, postpartum) are associated with patulous eustachian tubes.
Hearing evaluations include assessment of sensorineural
hearing impedance testing and speech discrimination. These
tests assist in localizing the otologic deficit. Nonvibratory tinnitus
lesions can be attributed to defects in the cochlea (75%), CNS
(18%), and middle ear (4%).
L.
Peripheral tinnitus is associated with symmetric hearing loss,
usually gradual in onset. Presbycusis is common with this
condition. As hearing loss increases, tinnitus increases. Treating
the hearing loss may result in a decrease in tinnitus because
ambient background noise is amplified. In patients with hearing
loss that is not treatable by a surgical procedure, a hearing aid
may improve the tinnitus. Hearing aids and masking devices may
be used together in patients who do not respond to hearing aids
alone. Medications should be given to patients with severe
disability.
M.
Central tinnitus requires an evaluation for posterior fossa
problems, including cerebellopontine angle tumors. The most
common cerebellopontine tumor is the acoustic neuroma.
Symptoms of an acoustic neuroma include unilateral hearing
loss, tinnitus, and disequilibrium. Distinguishing Meniere's
disease from acoustic neuromas is difficult clinically. Meniere's
tinnitus is intermittent, whereas the tinnitus of acoustic neuroma
is constant. Meniere's disease is associated with vertigo as
distinguished from the disequilibrium of an acoustic neuroma.
MRI with gadolinium contrast to assess for posterior masses is
indicated for abnormal auditory brainstem response (ABR) tests.
The sensitivity for acoustic neuromas <15 mm is greater with
MRI with gadolinium contrast than with high-resolution CT. In
patients with unilateral hearing loss and normal ABR tests,
surveillance is required at 6 months and 1 year to assess for
progression of symptoms. ENT referrals are indicated for all
patients with asymmetric hearing loss. Treatment for tumors
depends on the size, location, and the patient's preoperative
state.
N.
Conductive hearing loss requires evaluation for a pathologic
condition of the external and middle ear, malignancy, glomus
tumor, and cholesteatoma. Early referral to ENT is
recommended.