V pair of cranial nerves, trigeminal nerve, n.

trigeminus and sensitive system of the face and head, symptoms of its damage Short anatomical data. Trigeminal nerve contains sensory fibers innervating the face, and motion fibers going to the masticatory muscles (Fig. 8). The first sensory neurons (pseodounipolar ganglionic cells) are located in the trigeminal, or the Gassepovov, site (ganglion trigeminale) - form, homologous spinal site. The peripheral processes of these neurons are in contact with the receptors that perceive temperature, pressure and touch. They form 3 branches: orbital nerve (n. opthalmicus), maxillary nerve (n. maxillaris) and mandibular nerve (n. mandibularis); these branches emerge from the cranial cavity, respectively, from upper orbital fissure; round and oval foramen on the way to the skin are, respectively, through supraorbital canal, infraorbital canal and mental foramen. The central processes of these neurons are part of tegmentum of pons and terminate in the sensory nuclei of trigeminal nerve: nucleus tractus n. trigemini (pain, temperatura), the zone which applies to cervical segments of the spinal cord, and nucleus sensorius superior (tactile sensitivity). Axons of these nuclei move to the opposite side and ends at ventral nuclei of the thalamus, where the axons of third neuronal impulses reach the lower segments of posterior central gyrus (area projection of the head). Area of innervations of the trigeminal nerve branches on the face, also at zone of segmental (nuclear) pain and temperature sensitivity on the face (zone Zeldera), is analogous to segmental innervations of the trunk and extremities (see Fig. 8, X, 3). The branches of the trigeminal nerve innervate fronto-parietal part of the head and face (sensitive innervations of skin of the back of the head is provided by upper cervical spinal nerve roots), mucosal membrane of the mouth, nose and sinuses, the front 2/3 of tongue, teeth and partially meninges. Motor nucleus of trigeminal n. (nucleus motorius n. trigemini) is localized in tegmentum of pons and receives impulses from the central anterior central gyrus on the cortico-nuclear pathways. The motor portion of the trigeminal n. exit with mandibular nerve and innervate m. masseter and some other muscles. Investigation of the function of the trigeminal nerve. Ascertain presence of subjective sensation of pain and sensory disorder (numbness) in the zone of innervations. In the presence of pain, refine its localization, duration, consistency, character, and its provoking factors. Pain and temperature sensitivity is checked from up to down (in the zones of the three branches of the nerve), and from the ear to the nose (in the zones of segmental innervations zone of Zeldera). Determines if the pain is at the points of exit of trigeminal nerve. To assess the function of masticatory muscles, try to find out whether a subject has difficulty in chewing and during examination-- atrophy of the masticatory muscles, presence of deviation of the lower jaw when you open your mouth or weakness by a muscle strain during chewing. Corneal reflex is explored by touching the cornea with a soft strip of paper or cotton wool, which normally causes closing of eyelid (facial nerve consists of its efferent part of the reflex). Mandibular reflex is studied

by e blow to the distal phalanx or by ownself, to mandibular near the chin of the subject with a little closure of mouth. Thus there is a reduction in masticatory muscles and the movement of the mandible. Mandibular reflex may be absent in healthy individuals, but it is reinforced by the bilateral lesion of the corticonuclear tract. Symptoms of t i min l n l sions topi l di nosis Damage to one of the sensory branches of the trigeminal nerve, causing pain and tactile hypoesthesia in the zone of innervation, and sometimes pain on palpation or percussion at the point of exit of the nerve, but the spontaneous pain usually do not happen. es The defect of the orbital nerve causes a weakening or loss of corneal reflex, mandibular nerve injury - a weakening or loss of mandibular reflex. With the defect of sensory root, hypesthesia arises in half of the face, mucous membranes of the mouth and nose, the fronto-parietal part of head, loss corneal and jaw reflexes. Any damage to nucleus tractus spinalis n. trigemini in the brain stem is disturbed by the sensitivity of the segmental type (in zones Zeldera), while the defect of the lower part of the core causes hypoesthesia of the lateral face and defect top of the kernel - hypoesthesia around the mouth and nose. Any damage to the thalamus, posterior third of hind femur of internal capsule and the postcentral gyrus causes hypoesthesia in the opposite half of the face and head, limbs and torso. a limited defect of lower third of the postcentral gyrus causes hypesthesia opposite side of the face. The defect of the motor nucleus or the motor portion of the trigeminal nerve causes flaccid paralysis of the masticatory muscles with their hypotrophy and loss of jaw reflex. Any damage to cortico-nuclear path, does not disrupt function of masticatory muscles, because the motor nucleus of the trigeminal nerve have bilateral cortical innervation. At stimulation of the motor nucleus or elevated excitability in most of the trigeminal nerve and massetory muscles, sometimes tonic spasm of masticatory s muscle develop-lockjaw (tetanus, meningitis, tetany, whooping, epileptic fit). Tri emi al e ral ia is manifested short-period (from several seconds to 1-2 minutes) attack of one-sided pain (sensation of punctures, burning or passing of an electric current) in the second or third, rarely the first branch of the nerve. During attack, patient often freezes, afraid to stir, and increase the pain. Pain attack can cause reflex contraction mimic and masticatory muscles on the side of pain (Tick pain). It is characterized by sudden start and finish attack, free from pain - "bright" intervals. Seizures occur spontaneously or provoked when talking, swallowing, chewing, tooth brushing, shaving. Many patients note the attacks when washing the face. Because of the fear of causing seizure, patients sometimes stop brushing teeth, rarely washes, shave. Pain never passes to the other side, but in rare cases (0.5-5%) It is bilateral. Neurological examination identify disorder, sometimes marked pain in exit output and mild hyper-or hypoesthesia in the area cutaneous innervation of the concerned branches, where "Triggers" zone is found, and stimulation provokes pain attack. Caus s and t atment of lesions of the t i eminal nerve. Lesions at branches of the trigeminal nerve are often caused by trauma, compression in the bone channels, tumor or herpes infection that attacks the Gasser's ganglion (Ganlionit-gasserov node). The defect of the nuclei of the trigeminal nerve is often caused by vascular, tumor or inflammation of the brain stem.The defect of the thalamus, posterior internal capsule and the femur postcentral gyrus is more often caused by cerebral stroke, tumor or trauma. Trigeminal neuralgia often caused by its compression in the output of large arteries of pons (usually superior cerebellar artery). The rare causes of neuroalgia include compression of the nerve tumor or aneurysm, multiple sclerosis. 
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The basis of treatment of trigeminal neuralgia is composing of medication. Carbamazepine, gabapentin are more effective drugs. With a heavy state of illnesses and lack of effect of medicine, we can use microsurgical reposition blood vessel compressing the trigeminal nerve. The main symptoms of tri eminal nerve lesions Symptoms of lesion Lo alization of defect Disorder of sensory in the area of innervations of one or all Branches of the trigeminal nerve or the whole branches of the trigeminal nerve, weakening or loss of corneal nerve and jaw reflexes Motor nucleus (the pons of the brain) or Violation of the function of masticator muscles, their atrophy mandibular nerve Segmental disorder of the sensitivity on the face Sensory nucleus (brain stem) (in areas Zeldera) Short bouts of severe unilateral pain in the second or third Trigeminal nerve neuralgia (usually due to branches of the nerve compression of the nerve root cerebellar artery)
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VII pair of cranial nerves, facial nerve, n. facialis Brief anatomical and physiological data. Facial nerve has motor, sensory and autonomic fibers. Its main part consists of motor fibers (actual facial nerve) innervating mimetic muscles of the face: the frontal (i.e. frontalis), the circular muscle of the eye (i.e. orbicularis oculi), buccal (i.e. buccalis), circular muscle of the mouth (i.e. orbicularis oris) and some other muscles of the head and neck. A small portion of the nerve (intermediate nerve, or n, intermedius) consists of sensory (taste) fibers that provide the perception of taste in the front 2/3 of tounge, and autonomic (parasympathetic) fibers in the lacrimal gland, the sublingual and submaxillary salivary glands. Anatomofunctional diagram of the facial nerve is in Fig. 9. Motor nucleus of facial nerve is located in the casing of the lower part of pons, its fibers go superiorly, together with the intermediate nerve connections at the border pons and the medulla oblongata in the of the cerebellopontine angle. Both are part of the facial nerve in the inner (down-channel, are in facial (fallopiev) canal. Next, it leaves the cranial cavity through the stylomastoid foramen on the base of the neck and scattered on the terminal branches. Also in area of facial nerve canal, exit stepes nerve (n. stapedius) to the stapes muscle (i.e. stapedius), regulating the voltage of the eardrum of the ear. Central motor neurons that provide voluntary movements of facial muscles are the inferior part of precentral gyrus. Part of the motor nucleus of the facial nerve, facial muscles innervated by the upper face (frontal, circular muscle of eyes), has cortical innervation of the two cerebral hemispheres. In contrast, the lower parts of nucleus, innervating the lower facial muscles receive innervations predominantly from contralateral cortical precentral gyrus (see Fig. 9). Therefore, disturbance of precentral gyrus on the opposite occurs with paresis of mimic muscles of only the lower part of face, but does not disrupt mimic m. with bilateral cortical innervations. Perception of taste front 2/3 language is carried sensory neurons, which are located in the geniculate site, located in the facial canal, and conducts the fibers, which are initially together with the lingual n. (a branch of mandibular nerve), then continue in the form of a drum in a string of the intermediate nerve These fibers reach the nucleus of solitary tract (n. tractus solitarius), from which the pulses are in the thalamus and then to the base of the postcentral gyrus. As part of the intermediate nerve, in addition to the sensory fibers, there are secretory fibers to the lacrimal glands of these neurons are localized in axons nucleus, located in pons next to the motor nucleus of facial nerve (n. salivatorius superior). To the lacrimal gland fibers are composed of a large petrosal nerve (and petrosus major), which departs from the facial nerve at the level of his knee early in the facial canal. Investigation of the function of the facial nerve. To assess the function of the facial nerve check for symmetry of the face, pronounced lines and wrinkles, if they have arisen. The subject being asked to mimic a

sample frown, eyes shut, to inflate his cheeks, a smile or show his teeth. The eyebrow reflex (afferent part is part of the orbital branch of trigeminal nerve) is caused by a blow hammer on the inner edge of the eyebrows, and manifested a slight decrease in contraction of eye muscles. Ascertain the presence of dry eyes, over lacrimation, hyperacousis (unpleasant increased of perception of sounds). To study the taste of sweet solution (or sour, bitter, salty), a substance applied to the symmetric plots tongue sticking out separately on both sides of its front 2 3. Symptoms of facial nerve injury and violation of innervation of facial muscles topical diagnosis. Any damage to the motor nucleus or the facial nerve itself, paresis or paralysis of facial muscles is presence on the side of damage - paralysis of facial muscles but peripheral type in whom alone there facial asymmetry in the form of smoothed Receivables forehead wrinkles, nasolabial folds, omissions and the mouth and distortion of the mouth in a healthy way. patient could not raise an eyebrow, completely close the eye (lagophthalmos hare eye), when he smile or grin, mouth skew to healthy side and lost superciliary and corneal reflexes on the damage side. When you try to blink, eyeball deviates upwards (physiological phenomena Bell) and you can see the protein shell of the eye (symptoms of Bell). Food is often gets stuck between the cheek and gingiva, the liquid pours out of the corner of his mouth. If the nerve damage is in the facial channel, there maybe dry eyes (defect and beginning of the facial canal to the branch of a major petrosal nerve) or watery (defeat in facial canal until branch of a large petrosal nerve), hyperacousis on the side of paralysis (failure in facial canal to stapedial branch of nerve) and taste perversion (ageusia) in front 2 3 of tongue (defect in facial canal to the branch of the tympanic strings). Lacrimation at defect the facial nerve caused by a breach of the normal outflow tears from his eyes in the lacrimal sac. The defect of the facial nerve in the pontocerebellum angle usually associated with damage to the trigeminal, abducens,vestibulocochlear nerve and the defect of function of the cerebellum, which allows you to do a topical diagnosis. The defect of the motor nucleus of the facial nerve is met significantly less than most of the nerve, and is often combined with lesions of the nucleus abducens, located side-by-side. The combination of flaccid paresis or paralysis in autonomic muscle paralysis of the external muscles of the eyes on one hand and the central hemiplegia on the opposite side is caused by lesions in one half of pons (on the side of paresis of facial muscles) and removing the nuclei of the facial nerve and the corticospinal tract (alternating Foville s syndrome). In some cases of paralysis, we observe external of the eye muscles, there is only a combination of paralysis of the facial muscles and the contralateral central hemiplegia (alternating Millard-Gubler syndrome). The defect of the lower division precentral gyrus or the cortico-nuclear path (corona radiata, internal capsule and brain stem) causes paresis of facial muscles on central type with opposite side. This paralysis of facial muscles is observed only the lower part of faces because facial muscles of the upper part of face is innervated by part of the nucleus of the facial nerve, receiving cortical innervation on both sides, and their function is not impaired when a unilateral lesion of the cortico-nuclear tract. Paresis of the facial muscles with central type is usually seen with central hemiparesis and paresis of hands on the same side (as a result of the defect of the cortico-spinnal tract, passing along with the cortico-nuclear tract). In patients with impaired consciousness, paresis of mimic muscles is manifested by the fact that a wing of the nose is not involved in the act of breathing heavily and his cheeks swell in exhalation and retract in inspiration (phenomenon of "sails" cheeks). The reasons of facial nerve and facial muscles defect treatment. Neuropathy of the facial nerve (paralysis of Bella) is most often associated with his ischemia, edema and compression in the narrow bone (facial) canal presumably infectious (viral) or infection-onno-allergic origin (Bell's palsy). Frequency of-disease is about 20 cases in 100 thousand people. Less likely, nerve disease develops due to injury temperal bone, cerebellopontine angle tumor, otitis, mastoidita, inflammation of the parotid gland or recurring herpes.
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Bell's palsy is often triggered by super-cooling. First, there is often pain in the mastoid process, in which developed acute hemiparesis or paralysis of facial muscles. Full recovery in Bell's palsy occurs in 70-80% of patients, usually within 1 month (Rarely 2-3).the remaining patients remained paresis of mimic muscles. Prognosis is worse in older patient, with concomitant diabetes mellitus and/or arterial hypertension. Faster recovery if take prednisone 60-80 mg / day in first 5-7 days, or methylprednisolone (250-500mg / 2 times a day for 3-5 days with subsequent application of prednisolone) and its phasing-out for 10-14 days. From the first days, it s recommended exercises facial muscles, stickers from adhesive plaster, to prevent hyperextension of affected muscles. If the defect of the facial nerve is not due to neuropathy, then the treatment is determined by the cause of the disease. Paralysis of facial muscles on the central type usually caused by cerebral stroke, other neurological diseases (head trauma, tumor, and other), that must be diagnosis and determine treatment. Main symptoms and syndromes of facial nerve lesions and the facial muscles lesion localization Symptoms and syndromes of lesion Localization of defect Flaccid paralysis of facial muscles + Facial canal a), dry eyes, hyperacousis, ageusia a) until the branch of a large petrosal nerve, (front 2/3 of tongue), b) over-lacrimation, hyperacousis, b) to stapedial branch of the nerve (after branch of major petrosal ageusia; nerve), c) over-lacrimation, ageusia c) to tympanic branches of string (after branch of stapedial nerve), d) over-lacrimation d) at the exit (foramen stylomastoideus) of the facial canal (after a discharge of all branches) Flaccid paralysis of all facial muscles Cerebellopontine angle together with trigeminal, abducens, vestibulocochlear nerve and cerebellar disorders The combination of flaccid paralysis Defect half of pons (on the side of paresis of facial muscles) and nuclei of of facial muscles, paralysis of the the facial, abducens nerve and the corticospinal tract. external muscles of the eyes ipsilateral and central contralateral (alternating Foville's syndrome). Same symptoms without paralysis, Defect in the half of pons (on the side of paresis of mimic muscles) nuclei external m. Of eyes (alternating of the facial nerve and the corticospinal tract. Millard-Gubler syndrome) Paresis of the facial muscles only the Lower part of anterior central gyrus and cortico-nuclear path (corona lower face - paresis of facial muscles radiata, internal capsule, half of the brain stem) contralaterally of central type (often in conjunction with central hemiparesis and paresis of the hand on the same side)

Vlll pair of cranial nerves vestibulo-cochlear nerve, n. ve tib locochleari
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Brief anatomical data. Vestibular system includes a location in the pyramid of the temporal bone labyrinth, vestibular nerve, the central vestibular nuclei and the path. Receptors vestibular system (the macula, or a fixed spot) located utricle and saccule, as well as ampula of three semicircular canals of the labyrinth. From these receptors receive signals bipolar cells, located in the vestibular site of internal auditory passage. The central processes of these cells form part of the vestibulocochlear nerve (n. vestibulocochlearis), connected to the cochlear nerve in the inner part of internal acoustic passage, go to the cerebellopontine angle, enter brainstem on the border between the pons and medulla oblongata and end in the four vestibular nuclei, situated near the bottom of the IV ventricle. Vestibular nuclei have connections with the cerebellum, oculomotor nerves, anterior horn of the spinal cord, somatosensory and optic systems. Maintaining a balance is achieved by cooperation of three sensory systems vestibular, optic, and somatosensory (main system - deep articular and muscular sensory). Great value is provided by medial longitudinal fasciculus, which provides connections between the vestibular nuclei, nuclei of oculomotor nerves cerebellum and , spinal cord. The auditory system includes the outer, middle and inner ear; consist of the cochlea, cochlear nerve, central acoustic nuclei and their pathways. Hair cell of Corti's organ of the cochlea are specialized acoustic receptors, which convert electrical impulses into mechanical vibrations wave in perilymph,which causes from movement of the auditory ossicles of the ear in response to the effects of sound waves from theouter ear. From these receptors, bipolar cells receive signals, located in a spiral channel of maleolus (scapus cochlear). The central processes of bipolar cells make up the cochlear part vestibulo-cochlear nerve, connect with vestiblar part of the internal auditory canal, cerebellopontine angle, enter the brain stem at the boundary between the pons and the medulla oblongata and the ventral and dorsal ends cochlear nucleus (n. cochlea ventralis et dorsalis). From these second neurons, impulses pass at the lower tubercles quadrigemina roof of the midbrain medial geniculate body and further into transverse temporal gyrus of Henchl representing the cortical hearing center. Investigation of function of vestibulo-cochlear nerve. Ascertain the presence of dizziness, decrease hearing and noise at ear (tinnitus). If there is dizziness, determine its nature and the factors contributing to intensification and weakening. The patient is asked to describe their sensation in detail and that in most cases allows you to answer in requests whether the vestibular vertigo (systems, or true) or has a different origin. Otorhinolaryngologist or otoneurologist examines a patient with abnormal hearing and perform necessary tests with a tuning fork, audiometry and other advanced investigation. Hearing acuity is approximately determined separately for each ear, and in whispered normal speech is distinguished at a distance of over 6 m, and conversational - at a distance of 15-20 m. Symptoms defeat vestibulo-cochlear nerve and topical diagnosis. The defect of the labyrinth, vestibular nerve and the vestibular nuclei or the ways in the brainstem causes vestibular (true), dizziness, which is characterized by a sense of movement (rotation, spinning, falling or rocking) of own body to the surroundings. The vestibular dizziness is often accompanied by nausea, vomiting, disturbance of balance (vestibular ataxia), nystagmus, which explain the connections of the vestibular system to autonomic center, reticular formation and oculomotor nerves. Vestibular vertigo often magnified (or appears) when the situation changes or fast movements of head. Nystagmus in vestibular damage usually has a distinct fast and slow phase. Any damage to the labyrinth is usually observed only vestibular dizziness, defect at vestibulo-cochlear nerve in addition to dizziness is often reduced hearing or there noise in the ear (the auditory part is damage), with
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the defect of the nucleus trunk usually reveal symptoms of destruction of other cranial nerves, motor or sensory disorders due to injury of pathways in the brain stem. Vestibular vertigo should be differentiated from other condition that patients often describe as dizziness. This can be presyncope condition, but when we look at detail inquiry. Dizziness is characterized by feeling faintness and "fog" in the head, vertigo (mush). Disequilibrium, instability, and shaky gait, which arise as a result of the defect of cerebellum, optic, extrapyramidal, or somatosensory systems are also often characterized by patients like dizziness, however, unlike in the vestibular dizziness, it appears when the patient stands or walks, and disappears when he sits or lies. Psychogenic dizziness often lasts for years, not accompanied by nystagmus and is always constant, not episodic, as dizziness of another genesis and sometimes it occurs in the form of attacks, combined with a sense of fear, anxiety, shortness of breath. Hearing loss and/or noise in the ear may be due to consequence of ear and neurological diseases. Obstruction of ear canal with plug of cerumen (earwax) is the most frequent causes of acute hearing loss. Different disease of the middle ear (otitis, otosclerosis, etc.) can cause the noise in the ear, hearing loss or even total deafness (conductive deafness). In cases where hearing loss cannot explain the pathology of the outer or middle ear, it s likely to be sensory-neural hearing loss caused by the defect of cochlear nerve or Corti's organ, located in cochlear. Any damage to the nerve in the cerebellopontine angle, hearing loss is usually associated with peripheral paresis of facial muscles (facial nerve lesion), sensory disturbance in the face (the defect of the trigeminal nerve) and/or cerebellar ataxia. A uni-/ipsilateral damage of auditory tract in the brainstem or the temporal lobe does not cause hearing loss, because there are bilateral relations between the auditory nuclei of the brain stem and the cortical hearing center. Very rarely reduced hearing occurs in a bilateral damage of the trunk or the temporal lobes of the cerebral hemispheres. Any damage to the temporal lobe may cause possible auditory hallucinations, epileptic seizures with auditory aura (the patient hears the sounds, melodies or voices before the seizure). Causes of vertigo and vestibular sensory neural hearing loss, and their treatment. Vestibular dizziness may be physiological during motion sickness, for example in a closed cabin of a ship or in a car, when monitoring moving objects (visual associated dizziness) or elevation (altitudinal dizziness). Increased sensitivity to the effects of these factors usually occurs in childhood and is called the peripheral vestibulopathy. The three most common causes of abnormal vestibular dizziness and vertigo are benign positional vertigo, vestibular neuronitis, and Meniere's disease. Benign positional vertigo arises only when motion or change of all body and/or head and usually lasts a few seconds. It often develops when a patient turns over from back on one side and suddenly feels that the room travel. Many people know at which movement or position causes vertigo or dizziness. Postural dizziness in most cases is idiopathic (the formation of the otoliths in the posterior semicircular channel), but sometimes it occurs after traumatic brain injury, viral infection, ear diseases, intoxication by alcohol or barbiturates. Otoneurological diagnosis is confirmed by the results of investigations. Vestibular neuronitis (vestibular neuritis/labyrinthitis) is manifested by sudden long (for several many hours or days), attack of dizziness, which often accompanied by nausea, vomiting, disorder of equilibrium. Any movement of the head or the body may increase dizziness, so patients move with great caution. There spontaneous and position (with a change in head position) nystagmus, vestibular ataxia, but hearing loss and other neurological symptoms does not appear, that differ vestibular neuronitis from stroke and other neurological diseases. Severe dizziness usually resolves within a few hours or days, but can continue as vestibular dysfunction in disequilibrium form while walking within a few days and even months. For Me nie`re disease is characterized by periodic attack of dizziness, combined with noise and obstruction in the ear and hearing loss. Dizziness often increases within minutes and remained intense from half hour to

a day and then gradually weakens. Hearing loss varies according to the degree of periods of attack and usually decreases after it after it endings. After recurrent attack, hearing gradually weakens. Disease usually begins with the defect of one ear. However, 50% of patients in the future damage the other ear. The cause of these disorders is hydrops (edema) of the labyrinth Central vestibular vertigo can be as manifestation of multiple sclerosis, cerebrovascular of disease or other diseases of the nervous system of with brain stem damage, which in most cases, become apparent and other symptoms of brainstem damage on the brain (paresis, disorders of sensation, disturbance of functions of cranial nerves). Treatment of vertigo should be directed to the main cause of dizziness (underlying disease), if possible, and to eliminate the subjective disorders. For positional vertigo, we can be used special method of manipulation of head, directed at the displacement of the otolith of the posterior semicircular canal to the inner ear. Effective vestibular exercise in patient is carried out independently under doctor's instructions. As pathogenetic therapy (improvement of blood flow in the inner ear), we use Betacerk to 24-48 mg/day, Stugeron of 75-150 mg/day and Pentoxyphylline of 1200 mg/day, and when necessary use anti-emetics and tranquilizers. Growing unilateral hearing loss (hypoacusia) may be caused by cerebellopontine angle neuroma, in which the lesion of the auditory nerve, often coupled with damage of the facial and trigeminal nerves, cerebellar ataxia for we conduct diagnostic MRI or CT of the head. Sensoryneural hearing loss may occur in many hereditary diseases, it may be a consequence of traumatic brain injury, raising supersonic influence barotrauma, such as explosions, toxic action of some drugs (streptomycin, quinine etc.), Meniere's disease, intracranial infection processes. Auditory hallucinations and auditory aura before epileptic seizure can be caused by tumor/swelling of temporal lobe. Treatment of hearing impairment is determined by its cause and is usually conducted by ENT specialists. Main symptoms of vestibulo-cochlear nerves and damage localization Symptoms of defect Localization of damage Vestibular vertigo (sensation of rotation, whirling, falling, or Labyrinth, rarely - vestibular nerve or rocking their bodies or the surrounding objects, often with the vestibular nuclei of brain stem nausea, vomiting, disequilibrium and nystagmus) The outer or middle ear, cochlear Hearing loss, noise in the ear (tinnitus) nerve, the cochlea Vestibular vertigo and hearing loss, noise in the ear Vestibular-cochlear nerve Hearing loss, noise in the ear in combination with peripheral paresis of facial muscles, sensory disturbance of the face, Cerebellopontine angle cerebellar ataxia Vestibular vertigo combined with symptoms of other cranial Brain stem (medulla oblongata and nerves, sensory disturbance in conduction type, central paresis pons) of extremities Auditory hallucinations, auditory aura (noise, melody, voice) Temporal lobe, Heschl gyrus before an epileptic seizure

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