Pulsatile tinnitus mri protocol,ears tinnitus problems 6th,ears ring neck muscles,tinnitus dizziness nausea headache heartburn - Downloads 2016

Author: admin, 06.05.2016. Category: Buzzing In Ears

Objective: Tinnitus is a common otologic symptom secondary to numerous etiologies such as noise exposure, otitis, Meniere’s disease, otosclerosis, trauma, medications, and presbycusis.
Conclusion: Treating physicians need to have a very compassionate attitude towards these patients and statements such as “there is nothing that can be done” are very inappropriate and should be strongly condemned.
Pulsatile tinnitus (PT) originates from sounds produced by vascular structures within the cranial cavity, head and neck region and thoracic cavity, which are transmitted to the cochlea by bony and vascular structures. Atherosclerotic carotid artery disease (ACAD) is a common cause of PT in older than 50 years of age patients, especially when associated risk factors for atherosclerosis such as hypertension, angina, hyperlipidemia, diabetes mellitus, and smoking are present.
Pseudotumor cerebri syndrome is a common cause of venous PT, especially in young and obese females. Pulsatile tinnitus in pseudotumor cerebri syndrome is believed to result from the systolic pulsations of the CSF originating mainly from the arteries of the Circle of Willis. Idiopathic PT, essential PT and venous hum are terms used interchangeably to describe patients with PT of unclear etiology. Myoclonic contractions of the tensor veli palatini, levator veli palatini, salpingopharyngeus and superior constrictor muscles can result in objective PT.
Myoclonus of the stapedial muscle has also been reported as a cause of pulsatile tinnitus (42). Associated symptoms of hearing loss, aural fullness, dizziness, headaches and visual disturbances, such as visual loss, transient visual obscurations, retrobulbar pain and diplopia are suggestive of associated Pseudotumor cerebri syndrome (35,37). Older patients with history of cerebrovascular accident, transient ischemic attacks, hyperlipidemia, hypertension, diabetes mellitus and smoking should be suspected of having ACAD (36). Otoscopy is essential for the detection of middle ear pathology such as a high or exposed jugular bulb, aberrant carotid artery, and glomus tumor.
Auscultation of the ear canal, peri-auricular region, orbits, cervical region and chest is essential for detection of objective PT, bruits and heart murmurs. Pure tone (air and bone conduction) and speech audiometry should be performed in all patients. Complete blood count and thyroid function tests should be obtained in patients with increased cardiac output syndrome to exclude anemia and hyperthyroidism. Duplex carotid ultrasound (including the subclavian arteries) and echocardiogram should be obtained in patients suspected of ACAD and valvular disease respectively (35).
Radiologic evaluation needs to be individualized according to the clinical presentation, physical and audiometric findings. Pseudotumor cerebri syndrome patients should be treated for any associated disorders such as morbid obesity.
Symptomatic high-dehisced jugular bulb can be repaired with pieces of cortical bone or cartilage (37). Ligation of the ipsilateral to the tinnitus IJV has been recommended in the literature for patients with idiopathic PT. Recent advances in tinnitus research have led to a better understanding and management of this common otologic symptom.
National Center for Health Statistics: Basic data on hearing levels of adults 25-74 years, United States 1971-1975. Sismanis A, Callari RH, Slomka WS, Butts FM: Auditory evoked responses in benign intracranial hypertension syndrome.
MIXED HEARING LOSS Whenever the hearing loss of a patient includes a mixture of both conductive and sensorineural characteristics, is said to have a mixed hearing loss. Superior ventral cochlear nucleus (SVCN) Erythroblastosis typically causes hearing loss that centers around 3000–4000 Hz.
Central Auditory Processing Disorders (CAPD) CAPD characterized by decreased understanding of speech in the presence of background noise. FUNCTIONAL HEARING LOSS Functional or psychogenic hearing loss is the customary diagnosis when there is no organic basis for the patients apparent deafness. Functional Overlay It is entirely possible for hearing loss of functional origin to be superimposed on true organic hearing impairment. History: A 34-year-old woman with otosclerosis and hearing loss for over 10 years Refuse to use hearing aids She often says, What?
Audiometric Patterns in Functional Hearing Loss There is no characteristic audiometric pattern in functional hearing loss, but the consistent inconsistencies serve to alert the physician. Malingering Malingering is the deliberate fabrication of symptoms that the patient knows do not exist.
Based upon sound characteristics, tinnitus can be classified as non-pulsatile (or continuous) which is the most common type and pulsatile.
Pulsatile tinnitus arises from either increased flow volume or stenosis of a vascular lumen. This syndrome is characterized by increased intracranial pressure without focal signs for neurological dysfunction except for occasional fifth, sixth, and seventh cranial nerve palsies.
These pulsations, which are increased in magnitude in the presence of intracranial hypertension, are transmitted to the exposed medial aspect of the dural venous sinuses (transverse and sigmoid) compressing their walls synchronously with the arterial pulsations. A possible cause of idiopathic PT is believed to be turbulent blood flow produced in the IJV as it curves around the lateral process of the atlas (40).


These contractions can range between 10 and 240 per minute and may be confused with the arterial pulse. Rhythmic movements of the tympanic membrane can be present in patients with tensor tympani myoclonus. This should be performed in a quiet room, preferably with a modified electronic stethoscope.
Serum lipid profile and fasting blood sugar should be requested in patients suspicious for ACAD.
Patients with a retrotympanic mass should have a high-resolution temporal bone computed tomography (CT) at their initial evaluation (47).
These patients responds well to weight reduction and medical management with Acetazolamide (Diamox). A thorough evaluation should be performed in all patients in order to accomplish accurate diagnosis and effective management. Tinnitus Retraining Therapy (TRT) as a method for treatment of tinnitus and hyperacusis patients. Treatment of tinnitus by intratympanic instillation of lignocaine (lidocaine) 2 per cent through ventilation tubes. Lidocaine test in patients with tinnitus: rationale of accomplishment and relation to the treatment with carbamazepine. Effect of intratympanically administered gentamycin on hearing and tinnitus in Meniere’s disease.
The usefulness of nimodipine, an L-calcium channel antagonist, in the treatment of tinnitus.
Otologic manifestations of benign intracranial hypertension syndrome: diagnosis and management.
Benign intracranial hypertension without papilledema: Role of 24-hour cerebrospinal fluid pressure.
Hearing deficiency may have started originally as a conductive failure (otosclerosis) and later developed a superimposed sensorineural component. In clinical practice, most cases with an original sensorineural etiology remain in that classification without an added conductive element. In chronic otitis media some toxic inflammatory metabolite produces a cochleitis or labyrinthitis. This example a warning to physicians to avoid assuring any patient that his hearing loss can be corrected merely by removing cerumen, because mixed hearing loss may be found subsequently. In every case of mixed hearing loss one should determine how much of the deficit is conductive and how much is sensorineural.
If the patient does not understand any better with a hearing aid or when the voice is raised, hearing is not improved even if the conductive portion of the mixed hearing loss is corrected.
17 The auditory pathway consists of a series of transducers that repeatedly change the speech stimulus so that it can be handled effectively by the cortex. Characteristic Features of central hearing loss : Hearing tests do not indicate peripheral hearing impairment. This may be caused by injury to SVCN spheroid cells, the second-order neurons of the ascending auditory pathway, even in the presence of normal hair cells in the organ of Corti. Common complaints include inability to study or read in the presence of noise, slowing of reading speed caused by noise(vacuum cleaners or air conditioners ) and suspicion by family members that the patient has a hearing loss.
The inability to hear results entirely or mainly from psychological or emotional factors, and the peripheral hearing mechanism may be essentially normal. Psychogenically induced hearing loss usually is a uniform flat- tone loss in all frequencies, suggestive of a well-marked conductive impairment. Usually, the hearing impairment is bilateral, and the bone conduction level is the same as the air conduction level. Since these two types of tinnitus have very diverse etiologies, pathophysiology as well as treatment, they will be described as separate entities. Diagnosis of this condition should be made only after appropriate evaluation and elimination of other disorders, such as pseudotumor cerebri syndrome.
Myoclonic contractions of the soft palate can be present in patients with palatal myoclonus.
Auscultation with an electronic stethoscope has been found more sensitive than traditional auscultation (45). If a glomus tympanicum, aberrant internal carotid artery, or jugular bulb abnormality is diagnosed, no other imaging studies are needed.
It is strongly recommended that this procedure be considered only after careful elimination of any other causes of PT, especially pseudotumor cerebri syndrome. The difficulty may have been sensorineural in the beginning ( presbycusis ), and a conductive defect (middle-ear infection ) may have developed subsequently. In contrast, most cases that start as conductive hearing impairment later develop some sensorineural involvement. The sensorineural deficit may be caused by penetration of the oval window with exposure of the perilymph.


Prognosis: In mixed hearing loss the prognosis depends on the relative proportion of conductive and sensorineural pathology. There is no characteristic audiometric pattern, except that the disparity between the hearing level and the speech interpretation is quite marked.
Central pathology must be included in the differential diagnosis of the hearing loss producing a 4000-cycle dip on the audiogram. If people talk to a person with CAPD while he or she is involved in auditory concentration such as listening to a television program, the person will often not hear.
The basis for functional hearing loss in most patients is psychogenic, the product of emotional conflict, ( neurotic anxiety ). Hysterical blindness and paralysis are other examples of the same type of somatization or conversion reaction. In a patient with unilateral functional deafness there may be complete absence of bone conduction on the side of the bad ear, though the good ear has normal acuity. If the patient claims he has one good and one bad ear, and the examiner obstructs his good ear with a finger, then shouts into it loudly enough to be heard easily by bone conduction alone, the malingerer claims he hears nothing.
Venous PT type can originate not only from primary venous pathologies, but also from conditions causing increased intracranial pressure by transmission of arterial pulsations to the dural venous sinuses (35).
Wide opening of the oral cavity during examination may result in elimination of the soft palate contractions.
When objective PT is detected, its rate should be compared to the patient’s arterial pulse. For patients with glomus jugulare tumors, CT examination of the neck also should be obtained to detect any possible synchronous chemodectomas along the carotid arteries. Tensor tympani and stapedial myoclonus may respond to section of the respective muscles via tympanotomy (42). In some cases the conductive and the sensorineural elements may have started simultaneously ( severe head injury affecting both the inner ear and the middle ear ). Despite meticulous surgical care, the inner ear also can be traumatized readily and made more susceptible to infection.
The best way to approximate the conductive and the sensorineural components of a hearing loss is to perform all possible tests for estimating the patients sensorineural potential or cochlear reserve. If the sensorineural component is slight, the surgical prognosis is good, and under favorable circumstances the hearing may approximate the level of the bone conduction. In certain cases, central hearing loss may mimic peripheral causes of deafness, including occupational deafness.
However, if one gets the persons attention by calling his or her name before speaking, the first sentence will not be missed, and hearing is normal. Tinnitus is a characteristic feature of hysterical deafness, and patients often claim that the noise is unbearable. Too spectacular an improvement with a hearing aid, especially when the patient has set the controls at minimal amplification, or a sudden disproportionate improvement in hearing after a simple procedure such as drum massage or insufflating the eustachian tube. Such a patient even may deny hearing shouts directed at the bad ear in spite of the good hearing in the opposite ear. Pulsatile tinnitus secondary to the antihypertensive medications enalapril maleate or verapanil hydrochloride subsides soon after discontinuation of these agents (37). In surgical trauma to the inner ear, high-frequency hearing loss often falls below the preoperative level, and the patient may complain of reduced discrimination though his pure-tone threshold is improved.
However, the discrimination is not improved much, even after correction of the conductive defect. The chief function of the auditory cortex is to interpret and to integrate these impulses and to provide the listener with the exact meaningful information intended by the speaker, or to permit the listener to react appropriately to the actual implication of the sound. The spheroid cells of the superior ventral cochlear nucleus (SVCN) show an anatomical frequency gradient, low ventral to high dorsal. Treatment : altering the listening environment to obtain the best possible signal-to-noise ratio. Hearing acuity usually varies, depending on the patients emotional state at the time of testing. In complete deafness the presence of cochlear nerve reflexes with loud noises indicates either malingering or hysteria. If the patient hears and discriminates well when speech is made louder, then the conductive element probably is a major cause of the hearing difficulty, and there is a good chance that surgery will improve the hearing. A similar adverse effect is noted in the ear opposite the tumor when certain words are interrupted periodically or accelerated. Labyrinthitis Otosclerosis was at one time thought to retain its purely conductive character for years; today it is recognized that this condition develops sensorineural impairment in same cases.



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