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Benign Neurogenic Tumors of the Ear

Benign neurogenic ear tumors include a glomus tumor and auditory nerve neuroma.

Glomus tumor (chemodectoma, nonchromaffin middle ear paraganglioma or glomerulocytoma) ranks first in frequency among benign tumors of the middle ear. It develops from glomuses (glomeruli), frequently occurring formations along the tympanic nerve, the auricular branch of the vagus nerve, and the superior stony nerve, located in the mucous membrane of the tympanic cavity, adventitia of the jugular vein bulb. Glomuses ranging in size from 0.5 mm (most often) to 2.5 mm have a capsule, they consist of numerous intertwined capillaries and precapillaries (arteriovenous anastomoses) and special epithelioid or glomus cells. Innervated by parasympathetic nerves (glossopharyngeal and vagus).

The middle ear glomuses from which tumors develop are nonchromaphine, apparently chemo- and baroreceptors. Tumors do not differ in structure from ordinary glomuses. They are of various sizes, very vascularized. A tumor emanating from the tympanic cavity gradually protrudes the eardrum and grows into the external auditory canal. It causes destruction in the tympanic cavity, leading to hearing loss and paralysis of the facial nerve, can grow into the jugular fossa, causing its destruction and paralysis of the IX, X, and XI cranial nerves (Garins posterior opening syndrome), sometimes grows into the cranial cavity, the posterior cranial fossa relevant symptoms. The tumor grows slowly, but has an infiltrative nature, often causing bleeding. Malignancy and metastasis are very rare.

Clinic. Glomus tumor occurs 5 times more often in women aged 30-50 years. The tumor of the middle ear (tympanic cavity) is manifested by a pulsating ear noise, hearing loss (usually conductive), a reddish neoplasm, visible through the eardrum. Then there is hyperemia, protrusion of the eardrum, smoothing of the identification points, the increase in hearing loss up to deafness. There are pains in the ear. When breaking into the external auditory canal, the tumor looks like a gray, gray-red or dark purple polyp, bleeding when touched. Sometimes there is peripheral paralysis of the YII nerve, a taste disorder in the anterior two-thirds of the tongue. It spreads more often to the mastoid process, the temporal bone pyramid, the cranial cavity, the jugular fossa with the defeat of the IX-XII cranial nerves and rarely to the labyrinth, auditory tube. When germinating in the cranial cavity, hypertensive syndrome joins. The jugular glomus tumor (from the jugular vein bulb) often destroys the jugular vein dome and grows into the tympanic cavity, through the jugular opening into the posterior cranial fossa, and sometimes into the lumen of the internal jugular vein. The IX-XII cranial nerves are affected, as well as V and VII. When spreading into the tympanum, the above symptoms are noted. The first symptoms of a pyramid tumor are damage to the V and VII nerves. Ear symptoms (otoscopic, cochleo-vestibular) join later, as are symptoms of damage to the middle cranial fossa (IX-XII cranial nerves) with increased cranial pressure.

Diagnosis at an early stage is difficult. Attention is drawn to conductive hearing loss and a pulsating noise in the ear, a change in the color of the eardrum, and its protrusion. Valuable information is obtained with impedance audiometry. A tympanogram of type B indicates a lack of mobility of the eardrum. The pressure in the tympanic cavity is not determined, the tympanogram peak is low, and the shape is flat. The acoustic reflex is not recorded. Pulse vibrations of the tympanic membrane synchronously to the pulse are observed. Before the tumor breaks into the ear canal, X-ray studies of the temporal bones according to Schuller, Mayer, Stenvers, Highway II, IV, tomography in direct and axial projections are of great importance. Computer or magnetic resonance imaging, retrograde jugulography are shown. In the pictures, bone destruction and tumor spread are determined. Diagnosis is facilitated by digital subtraction carotid angiography. A bleeding biopsy is often performed during surgery. The differential diagnosis is carried out with chronic purulent otitis media complicated by polyp, other tumors (especially vascular, malignant of the middle ear and base of the skull, neuroma of the VIII nerve, aneurysm of the branches of the external carotid artery, etc.).

Treatment. With small tumors of the tympanic cavity, tympanotomy is performed with removal of the neoplasm. If a tumor of the tympanic cavity grows into the ear canal, antrum, mastoid process, then an endaural mastoid operation is performed, and, if necessary, a radical operation. When the tumor spreads to the area of ​​the jugular vein bulb, it is removed using hypothermia after ligation of the external carotid artery, internal jugular vein, and exposure of the hypothympanum. With more common tumors, neurosurgery with radiation therapy is performed. Intratumoral injections are also possible in the external auditory canal of a 10% solution of quinine hydrochloride 0.5 ml up to 20 injections. When the tumor spreads to the canal of the carotid artery, freezing is carried out using a Cooper cryosurgical probe. Glomus tumors must be diagnosed and removed at an early stage.

Neuroma of the VIII nerve refers to benign neurogenic tumors of the cerebellopontine angle with an unfavorable clinical course. It originates from the cells of the Schwann membrane of the vestibular portion of the VIII nerve from the bottom of the internal auditory canal to the entrance to the medulla oblongata. It is more common in people 30-60 years of age. It accounts for 6% of all intracranial tumors and 35% of tumors of the posterior cranial fossa.
In 2-3% of cases, neurinoma is bilateral. Growing slowly.

There are three stages of the disease.

The first stage of development is otiatric (a tumor up to 1.5 cm) is characterized by cochleo-vestibular symptoms: constant noise in the ear, sensorineural hearing loss, tone-speech dissociation (speech intelligibility is impaired with relative preservation of tonal hearing), occasionally pain in the ear or headache, slight disturbances of static balance, some uncertainty of gait, dizziness.

The tuning fork experiments of Rinne and Federichi are positive. The tonal audiogram has a horizontal and then a descending character, mainly in the high-frequency region, with no bone-air interval. There is an increase in the level of auditory discomfort, the absence of lateralization of the sounds of the audible range in Weber's experience in the presence of lateralization of ultrasounds in a healthy ear. FUNG is not detected, the time of reverse adaptation increases to 15 minutes, its threshold is shifted to 30-40 dB (normally 0-15 dB). With impedanometry, the decay of the acoustic reflection of the stapes is noted. Normally, for 10 s the amplitude of the reflex remains constant, or decreases to 50%. The half-life of the reflex within 1.5 s is considered pathognomonic for neuroma of the VIII nerve. Stirrup reflex (ipsi and contralateral) may not be caused by stimulation of the affected side. Otoacoustic emission (UAE) is not recorded on the affected side. With audiometry for auditory evoked potentials, the peak-to-peak interval I and V of VSWR is extended. With large tumors, CSWP is not caused.

Patients do not parse words during a telephone conversation, severe fatigue of hearing is noted. 75% of patients have chronic imbalance with instability when walking, horizontal spontaneous nystagmus in the healthy direction. With caloric and rotational tests, pronounced asymmetry of nystagmus is often observed.

On radiographs of the temporal bones according to Stenvers, an expansion of the internal auditory canal can be noted. On computer and magnetic resonance imaging, a tumor of the YIII nerve is determined. Magnetic resonance imaging has a higher resolution in the diagnosis of neurinoma, especially in combination with the introduction of contrast agents that increase the information content of the image (Fig. 1.13.1).

Fig. 1.13.1

The second stage is otoneurological (a tumor from 1.5 to 4 cm) is characterized by headache, increased hearing loss, statokinetic disorders, unilateral cerebellar symptoms, lack of caloric nystagmus on the affected side, trigeminal dysfunction (paresthesia, decreased or absent corneal reflex), paresis abduction nerve (convergent strabismus and diplopia). An increase in the thresholds of the acoustic reflex and its accelerated decay are noted. Coarse spontaneous nystagmus appears in the direction of the affected ear (cerebellar). With damage to the facial nerve in the internal auditory canal, peripheral paresis of the facial muscles, inhibition of lacrimation and salivation are observed. Due to the compression of n.intermedius (XIII pair), which goes along with the facial nerve, the taste sensitivity to sweet and salty in the front two thirds of the tongue is disturbed. There is a headache in the back of the head (the initial phenomena of intracranial hypertension). At this stage, there is a destruction of the internal auditory canal and protein-cell dissociation in the cerebrospinal fluid.

The third stage is neurosurgical (a tumor of 4 to 6 cm or more) is manifested by sharp hearing loss, up to deafness, loss of vestibular function. The symptoms of damage to the cerebellum, pyramidal system and severe intracranial hypertension (congestive optic nerves, severe headache, nausea, vomiting, etc.) are added. Along with damage to the facial, intermediate, and abducent nerves, dysfunction of the trigeminal and abducent nerves in the bridge-cerebellar corner is more often observed. In the future, bulbar disorders, damage to many cranial nerves, including visual impairment up to blindness, paralysis of the eye, disorder of swallowing, phonation, and a decrease in smell develop. Pronounced hydrocephalus develops. Statokinetic function is disturbed by the central type with dissociation and disharmonization of reactions.

The first two stages of neurinoma are of particular interest to otologists, when, with timely diagnosis and surgical treatment, the further spread of the tumor can be prevented. In the initial diagnosis of unilateral sensorineural hearing loss, it is necessary to exclude neuroma using the most modern diagnostic methods.

Differentiate neuroma with Meniere's disease, arachnoiditis of the cerebellar triangle and hearing loss of various origins with a whole eardrum.

Surgical treatment. The most favorable outcomes in stages I and II of the tumor. Neurosurgical approaches to neuroma are carried out through the posterior and middle cranial fossae, and the otiatric access is trans-pyramidal through the mastoid, temporal bone to the internal auditory canal. The otiatric method is more gentle (Gorokhov A.A., 1989).

Patients with benign and malignant tumors of the ear are immediately sent to the hospital. After treatment, they are under the dynamic supervision of a part physician. A checkup by their otolaryngologist is carried out at least once every 6 months. Upon testimony, military personnel shall be examined in accordance with Articles 8,9,10 of the Order of the Ministry of Defense of the Russian Federation No. 315 of 1995.
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Benign Neurogenic Tumors of the Ear

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