Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys. Updating… Please wait. Unable to process the form. Check for errors and try again. Thank you for updating your details. Log In. Sign Up. Become a Gold Supporter and see no ads. Log in Sign up. The tensor tympani also plays a role in sound modulation by tensing the tympanic membrane to prevent loud sounds from damaging the inner ear. The tensor tympani originates in the cartilaginous portion of the Eustachian tube that connects the pharynx to the middle ear.
The muscle inserts on the medial portion of the malleus. It gets innervated by the mandibular division of the trigeminal nerve CN V. The tensor tympani is activated during talking, chewing, coughing, and laughing. Middle ear myoclonus MEM , one of many causes of pulsatile tinnitus, is due to dysfunction of either the tensor tympani or stapedius muscle. It is often characterized as a clicking sound with the involvement of the tensor tympani and as a buzzing sound when due to the dysfunctional movement of the stapedius.
It has also been described as a tapping, throbbing, fluttering, or whooshing sound. The tinnitus is usually objective and, therefore, can be heard by the examiner. MEM has been treated successfully in the past with surgical removal of the involved tendon.
However, there is still some controversy over what the best approach to treatment is, warranting more prospective controlled trials. Cochlear implantation is a surgery whereby an electrode is inserted into the cochlea to bypass the cochlear function and provide a direct electrical stimulus to the cochlear nerve, thereby allowing for patients with complete or partial hearing loss to regain the ability to hear.
Cochlear implantation is reserved for patients with sensorineural hearing loss that will not improve with the use of hearing aids. Two weeks after successful implantation of the internal device, the patient is ready to have the external device, which the patient wears over the ear, activated. A microphone in the external device captures sound and encodes it into an electric impulse using a speech processor.
The information transmits via a radio-frequency link to the internal receiver and then travels to the cochlea, where it electrically stimulates the auditory nerve. Patients with severe vertigo unresponsive to medical therapy can elect to undergo a labyrinthectomy whereby the organs that make up the labyrinth are surgically removed.
The pathophysiology of BPPV involves the displacement of otoconia that rests atop the otolithic membrane of the macule located in the utricle. Otoconia become displaced from the utricle to the semicircular canals, which leads to the unwanted perception of angular rotation of the head. BPPV is diagnosable with the Dix-Hallpike maneuver, which involves quickly moving a patient from an upright position to a horizontal position, with the head hanging over the side of the table and turned at a degree angle.
Reproduction of symptoms and the presence of nystagmus indicates a positive exam. Vestibular neuritis also referred to as vestibular neuronitis, is a self-limiting form of vertigo that occurs due to a viral infection or due to residual inflammation following viral infection of the vestibular nerve. Patients may also experience disequilibrium, sweating, nausea, vomiting, and imbalance. Recovery can take many weeks and may require balance physical therapy. Meniere disease characteristically demonstrates episodic vertigo, hearing loss, tinnitus, and aural fullness.
Episodes of vertigo last from minutes to hours. Presbycusis refers to age-related hearing loss due to the loss of hair cells. Presbycusis categorizes into either sensory and neural. Sensory refers to hair cell dysfunction that begins at the basal end of the cochlea, leading to loss of high-frequency sounds. Neural refers to cochlear nerve cell atrophy, leading to a defect in speech discrimination.
Sudden sensorineural hearing loss SSHL is the sudden loss of hearing due to pathology within the cochlea or vestibulocochlear nerve that cannot be explained by some other disease related to the outer or middle ear. The criteria for diagnosing SSHL include the sudden hearing loss within 72 hours of 30 dB in at least three sequential frequencies.
The current treatments for SSHL are oral or intratympanic steroids, with the possible addition of hyperbaric oxygen if diagnosed early. Tinnitus is the unwanted perception of sound, often in the absence of external stimuli. Tinnitus can be either objective or subjective. Objective tinnitus is audible by both the patient and clinician and is due to sound created by the flow of blood within vessels or of the contraction of a muscle in nearby structures. Causes include dural arteriovenous malformation, carotid bruits, venous bruits, carotid sinus fistulas, carotid dissections, and stapedial myoclonus.
Presbycusis and otosclerosis seen in elderly patients can lead to the perception of subjective tinnitus. Another cause of subjective tinnitus is damage to the hair cells within the cochlea secondary to noise trauma or ototoxic medications. Treatment for tinnitus varies based upon its underlying cause. When there is an identifiable cause of tinnitus, treatment focuses on the specific underlying etiology.
However, with idiopathic tinnitus, treatment is aimed at mitigating triggers known to be associated with tinnitus. In the author's experience, this frequently presents as a slowly progressive sensorineural hearing loss. When considering the clinical syndromes of pressure sensitivity , such as found in superior canal dehiscence , perilymph fistula , and Meniere's disease , one naturally must also think about the various interfaces that the inner ear has to other compartments -- spinal fluid and the air pressure in the middle ear.
Between the middle ear and the perilymph of the inner ear there are two moveable structures -- the oval and round windows. The oval window is coupled to external ear pressure via the tympanic membrane. The round window is coupled to middle ear pressure through it's membranous interface. Perilymph is connected fairly directly to spinal fluid pathways via the cochlear canaliculus aqueduct. When spinal fluid pressure changes, perilymph pressure changes within about 10 seconds.
In some people, there may be also a more direct connection around the vestibular nerve accounting for the so-called "gusher" found on fistula surgery.
In perilymph fistula , there should be a generally lower perilymph pressure than normal as well as an increased "compliance" of the perilymphatic compartment i. Rapid changes in CSF pressure should be transmitted more easily to perilymph.
Endolymph is coupled more indirectly to CSF pressure and air pressure, through membranes. One pathway is via the endolymphatic duct, to the sac, and the dural membrane. Another is via the membranes that separate the endolymphatic and perilymphatic compartments. Curiously, there are many narrow tubes in the endolymphatic system - -the endolymphatic duct, and two tiny ducts between the vestibular system and the cochlea. It would seem from this design that there is something to be gained by isolating these structures from each other.
Another way to think about interfaces and coupling is to consider the frequency response of the compartments. Perilymph is the most directly coupled to spinal fluid -- and therefore has the highest frequency response. A rough estimate of the time constant is 10 seconds. Perilymph is also coupled to air via the oval and round windows. This task is carried out by Na, K-ATPase, which is expressed in the membrane of intermediate and marginal cells.
Furthermore, the co-transporter NKCC1, expressed in the membrane of marginal cells, is also involved in this regulation by using the sodium gradient generated by the Na, K-ATPase to cause the ingression of potassium into the marginal cell.
Finally, chlorine ions, which enter the cell at the same time as sodium and potassium ions via the co-transporter NKCC1, are expelled by CIC-K chlorine channels associated with their regulating beta-subunit, barttine.
Mutations in these two genes give rise to Jervell and Lange-Nielsen syndrome, causing bilateral hearing loss and a long cardiac QT. Connexion Powered by eZPublish - Ligams. Contact Credits. Menu Students and professionals. General audience. Cochlear fluids.
0コメント