The transmission of external sound into the human ear and its eventual perception by the auditory cortex depends on the following three links: first, the impedance matching of the middle ear sound transmission structures; second, the conversion of sound energy into nerve impulses by the inner ear auditory receptors; and third, the smooth neural conduction from the cochlear nucleus through the brainstem to the auditory cortex of the collaterals. Failure of any of these three links can produce otalgia. In terms of causes and anatomy, tinnitus can be divided into two categories: subjective tinnitus and objective tinnitus.
I. Subjective tinnitus
Subjective tinnitus means that only the patient himself can hear the tinnitus under the condition that there is no sound source, but the examiner cannot hear it, also called conscious tinnitus or non-pulsatile tinnitus.
(A) Organic factors
1.Outside ear canal obstruction lesion Acute or chronic inflammation of the middle ear, stapes fixation, etc., tinnitus is mostly low-pitched and inconsistent with the degree of deafness.
2. Inner ear receptor lesions and auditory nerve damage Abnormal auditory signals triggered by stimulation of auditory hair cells are probably the most important cause of tinnitus. An irritated state of the hair cells (depolarization) can be induced by transient hypoxia, with early or transient tinnitus. In case of hair cell degeneration and poor contact between the auditory cilia and the capsule, persistent, tinnitus can occur. In the case of limited hair cell injury, the nature of the tinnitus is close to pure tone.
If the cochlear nerve fibers are mechanically stimulated, they can act directly on the nerve cells and trigger abnormal nerve impulses, causing rhythmic tinnitus.
Under normal conditions, the efferent pathway of the cochlea has a role in regulating nerve conduction, and any disruption of this bundle may also cause tinnitus. It is commonly seen in ischemic diseases of the brainstem.
(ii) To the nerve reflex factors
1. Tympanic plexus reflex As the tympanic plexus belongs to the central plexus, it is connected through the sympathetic nerve fibers of the glossopharyngeal nerve, trigeminal nerve and carotid artery, and receives excitation stimulation and conducts to the central superior frontal gyrus, forming tinnitus.
2. Internal chronic disease of the eye
The vasomotor nerve fibers of the internal auditory artery come from the inferior cervical ganglion fused with the first ganglion to form the stellate ganglion, which is connected with the abdominal organs through the vagus nerve. Therefore, the nerve impulses generated by the viscera can cause spasmodic contraction or dilation of the inner ear vessels, which changes the blood supply to the inner ear and causes tinnitus.
3. Neuropsychiatric factors The mechanism of tinnitus caused by neurosis and autonomic dysfunction is not well understood.
Objective tinnitus
Objective tinnitus is vibratory tinnitus or fluttering tinnitus. Extrinsic tinnitus is caused by a sound source near the ear, such as muscle spasm. It is caused by vasoconstriction, etc. This type of tinnitus has the presence of real sound with acoustic energy rather than the sensation of sound, so it can be examined and recorded with instruments. The rhythmic opening of the cartilage of the eustachian tube caused by palatal muscle clonus and the occurrence of a rattling sound is one of the symptoms of objective tinnitus. The popping of the temporomandibular joint can also be a cause of objective tinnitus.
I. Subjective tinnitus
(A) Ear diseases
1.Disorder of vagus blood circulation.
2.Ototoxic drug poisoning.
3.Meniere’s disease.
4.Acute otitis media.
5.Chronic otitis media.
6.Otosclerosis.
7.Age-related deafness.
8.Auditory neuroma.
(II) Systemic diseases
1.High blood pressure.
2. Plant nerve dysfunction.
II. Objective tinnitus
(A) Vascular.
(II) Muscle contractile.