Causes of pulsatile tinnitus radiology, tinnitus causes tmj - .

Inner ear disorders that increase hearing sensitivity (such as SCD) can cause pulsatile tinnitus.
Arteriovenous fistulae cause loud noises, synchronous with the pulse, that can often be heard by others with a stethescope, or sometimes by simply putting one's ear next to the person's head. Background: Pulsatile tinnitus, unlike idiopathic tinnitus, usually has a specific, identifiable cause. Tinnitus is the conscious, usually unwanted perception of sound that arises or seems to arise involuntarily in the ear of the affected individual. Pulsatile tinnitus is usually unilateral, unless the underlying vascular pathology is bilateral. The most common classification of tinnitus cases in the literature is subjective (heard by the patient only) versus objective (perceptible to the examiner also). Vascular stenoses: Arteriosclerotic plaques and stenoses in the vessels of the head and neck are the most common cause of pulsatile tinnitus in the elderly (1). Fibromuscular dysplasia, a segmental, nonatheromatous vascular disease that often leads to stenosis, can cause pulsatile tinnitus, particularly in younger persons. Elongations and loops in the arteries that supply the brain are occasionally described as a cause of pulsatile tinnitus (3). Aneurysms: Aneurysms of the internal carotid artery or the vertebral artery often lead to turbulent bloodflow, but it is surprisingly rare for them to become clinically manifest as pulsatile tinnitus. Arteriovenous fistulas can cause unbearably loud pulsatile roaring sounds that can often be heard by the clinician too. With the exception of headaches, pulsatile tinnitus is the most common clinical symptom in dural arteriovenous fistulas and acquired arteriovenous short-circuits to the cerebral veins or sinuses (3). If there are no other venous abnormalities, venous tinnitus is perceived as right-sided more frequently than left-sided, because the right jugular vein is dominant in 70% to 80% of cases (23). Intracranial hypertension: Pulsatile tinnitus can be caused by an increase in intracranial pressure (24).
It should never be forgotten that intracranial hypertension can also be caused by cerebral sinus thrombosis. Other factors that should be mentioned as causes of increased intracranial pressure are cerebral neoplasias and other intracranial space-occupying lesions, craniocervical transition disorders, cranial stenoses, and hydrocephalic CSF flow disorders.
Anatomical variants and abnormalities of the veins and sinuses: Atypical formations of the jugular bulb favor the development of venous tinnitus.
Rare causes of pulsatile tinnitus include meningocele of the temporal bone (34), cholesterol granulomas (35), and perilymph fistulas (21). Clinical warning signs are focal neurological symptoms, signs of intracranial pressure, and objective pulsatile tinnitus.
As a symptom, pulsatile tinnitus has many, highly varied causes and involves several clinical disciplines. Schrock A, Strach K, Kuhnemund M, Bootz F, Eichhorn KW: Seltene Ursache eines pulssynchronen Tinnitus. Dietz RR, Davis WL, Harnsberger HR, Jacobs JM, Blatter DD: MR imaging and MR angiography in the evaluation of pulsatile tinnitus. Park IH, Kang HJ, Suh SI, Chae SW: Dural arteriovenous fistula presenting as subjective pulsatile tinnitus.
Swartz JD: An approach to the evaluation of the patient with pulsatile tinnitus with emphasis on the anatomy and pathology of the jugular foramen. Russell EJ, De Michaelis BJ, Wiet R, Meyer J: Objective pulse-synchronous essential tinnitus due to narrowing of the transverse dural venous sinus.
Remley KB, Coit WE, Harnsberger HR, Smoker WRK, Jacobs JM, McIff EB: Pulsatile tinnitus and the vascular tympanic membrane. Vattoth S, Shah R, Cure JK: A compartment-based approach for the imaging evaluation of tinnitus. Most cases of tinnitus are subjective, but occasionally the tinnitus can be heard by an examiner. It is perfectly possible for the cause of tinnitus to lead to contralateral symptoms: Closure of a vessel on one side of the body may lead to a compensatory acceleration in flow in the open vessel, which then becomes symptomatic as tinnitus.
However, because such findings are also common in asymptomatic patients, particularly the elderly, they must be evaluated cautiously and should not be grounds for not searching carefully for another cause.

The frequency of vascular loops in the inner ear is higher in individuals with pulsatile tinnitus than chance alone would predict (11).
The classic cause is a carotid-cavernous fistula in cases of fracture of the base of the skull. In otosclerosis, arteriovenous microfistulas over the oval window lead to pulsatile tinnitus (1).
In very general terms, it seems that venous tinnitus is often favored by anatomical predisposition and triggered by physiological conditions. One of the causes, particularly in young, overweight women, is pseudotumor cerebri, more accurately described as idiopathic intracranial hypertension. If there is a unilateral transverse sinus thrombosis, venous blood has to flow out through the open opposing side, where the increase in blood flow can lead to tinnitus. Naturally, it must be determined whether the tinnitus is actually synchronous with the pulse.
Accordingly, other possibilities for vascular tinnitus include dehiscence (missing bone) of the jugular bulb -- an area in the skull which contains the jugular vein, and an aberrantly located carotid artery. Otologic problems, especially hearing loss, are the most common causes of subjective tinnitus.
The transfer of flow sounds to the inner ear by bone conduction may be a cause of pulsatile tinnitus (12). Paraganglioma occurs bilaterally in 10% of cases; it can cause bilateral symptoms in these patients (20). They are heard only when they are so loud that they can no longer be suppressed by the hearing organs and auditory pathway, usually as venous tinnitus. Stenoses, strictures, and segmentation of the sinus (particularly the transverse sinus) are also associated with pulsatile tinnitus (31). If venous hum caused by anemia has been ruled out, an arteriovenous fistula must also always be considered. An enlarged jugular bulb on the involved side is common in persons with venous type pulsatile tinnitus. Common causes of conductive hearing loss include external ear infection, cerumen impaction, and middle ear effusion.
Pulsatile tinnitus requires both a functional organ of hearing and a genuine, physical source of sound, which can, under certain conditions, even be objectified by an examiner.
This determines whether neurological complications (focal symptoms, elevated intracranial pressure, intracranial hemorrhage) may arise in addition to tinnitus (14). Compression of the occipital artery against the mastoid process therefore often reduces tinnitus. Dural arteriovenous fistulas are the classic cause of objective pulsatile tinnitus, but not all arteriovenous fistulas cause tinnitus that can be heard by the clinician (17, 18). Tympanic paragangliomas are otoscopically visible as a reddish pulsating space-occupying lesion behind the tympanic membrane.
Venous hum, often overlooked, can be heard through a stethoscope and is thought to be caused by altered bloodflow behaviors, usually in anemia. Ligature of the jugular vein, the first-line therapy, should therefore be reserved for persistent cases that cause a high degree of suffering.
This is also true of emissary veins (condylar or mastoid), which might be associated with tinnitus but are also found frequently.
Provocation and rotation maneuvers (Table 2) can be used to distinguish whether the tinnitus sounds are arterial or venous in origin. If no other causes can be identified for confirmed pulsatile tinnitus that is synchronous with the pulse, DSA is indicated.
Sensorineural hearing loss may be caused by exposure to excessive loud noise, presbycusis, ototoxic medications, or Meniere's disease.
Pulsatile tinnitus can be classified by its site of generation as arterial, arteriovenous, or venous. Pulsatile tinnitus requires hearing, as there is usually a genuine physical source of sound (3). Angiography reveals tears of the intima, with membranes and intimal cusps, or segmental narrowings of the lumen over longer distances, caused by the intramural hematoma.


Common causes at the arteriovenous junction include arteriovenous fistulae and highly vascularized skull base tumors. Blood vessels can become narrowed from outside as a result of intracranial hypertension, but the reverse is also true: A primary sinus stenosis can also be the cause of intracranial hypertension.
Objective tinnitus usually is caused by vascular abnormalities of the carotid artery or jugular venous systems.
Common venous causes are intracranial hypertension and, as predisposing factors, anomalies and normal variants of the basal veins and sinuses.
Initial evaluation of tinnitus should include a thorough history, head and neck examination, and audiometric testing to identify an underlying etiology. In our own series of patients, pulsatile tinnitus was most often due to highly vascularized tumors of the temporal bone (16%), followed by venous normal variants and anomalies (14%) and vascular stenoses (9%). Unilateral or pulsatile tinnitus may be caused by more serious pathology and typically merits specialized audiometric testing and radiologic studies.
In patients who are discomforted by tinnitus and have no remediable cause, auditory masking may provide some relief.
Thorough history-taking and clinical examination are the basis for the efficient use of imaging studies to reveal the cause of pulsatile tinnitus. Epidemiologic data reveal that approximately one fourth of persons with tinnitus are discomforted by it, whereas the remaining three fourths experience the condition without significant symptoms.3Tinnitus takes different forms and has different classification proposals. One classification system stresses distinctions between vibratory and nonvibratory types, while another system groups the different forms of tinnitus into subjective or objective classes.Vibratory tinnitus is caused by transmission to the cochlea of vibrations from adjacent tissues or organs. Nonvibratory tinnitus is produced by biochemical changes in the nerve mechanism of hearing.Subjective tinnitus, which is more common, is heard only by the patient.
Objective tinnitus can be heard through a stethoscope placed over head and neck structures near the patient's ear.The mechanism that produces tinnitus remains poorly understood. Tinnitus may originate at any location along the auditory pathway from the cochlear nucleus to the auditory cortex. Some leading theories include injured cochlear hair cells that discharge repetitively and stimulate auditory nerve fibers in a continuous cycle, spontaneous activity in individual auditory nerve fibers, hyperactivity of the auditory nuclei in the brain stem, or a reduction in the usual suppressive activity of the central auditory cortex on peripheral auditory nerve activity.4This article discusses the causes of subjective and objective tinnitus, and techniques used for evaluating tinnitus. Conductive hearing loss is caused by the inhibition of sound transmission to the inner ear. It is continuous and less disturbing than the tinnitus of Meniere's disease.14Ototoxic medications or substances are another common cause of bilateral tinnitus.
Temporomandibular joint disorder has been associated with vertigo and tinnitus, although the exact mechanism is unclear.Various metabolic abnormalities may be associated with tinnitus.
These abnormalities include hypothyroidism, hyperthyroidism, hyperlipidemia, anemia, and vitamin B12 or zinc deficiency.Many patients with tinnitus exhibit signs of psychologic disorders.
Although tinnitus may be a contributing factor to the development of depression, the common association of tinnitus and depression may be the result when depressed patients, particularly those with sleep disturbances, focus and dwell on their tinnitus more than patients who are without an underlying psychologic disorder.OBJECTIVE TINNITUSObjective tinnitus is rare.
Patients with objective tinnitus typically have a vascular abnormality, neurologic disease, or eustachian tube dysfunction.4Patients with vascular abnormalities complain of pulsatile tinnitus. This type of tinnitus is a soft, low-pitched venous hum, which can be altered by head position, activity, or pressure over the jugular vein.4Congenital arteriovenous shunts are usually asymptomatic, while the acquired type often are associated with pulsatile tinnitus. The symptoms may disappear with Valsalva's maneuver or when the patient lies down with the head in a dependent position.Evaluation of TinnitusHISTORYThe evaluation of a patient with tinnitus begins by taking a thorough history.
Precipitous onset can be linked to excessive or loud noise exposure or head trauma.LocationUnilateral tinnitus can be caused by cerumen impaction, otitis externa, and otitis media.
Tinnitus associated with unilateral sensorineural hearing loss is the hallmark of acoustic neuroma.PatternContinuous tinnitus accompanies hearing loss.
Tinnitus of venous origin can be suppressed by compression of the ipsilateral jugular vein.Specific testing for sensorineural or conductive hearing loss is the next part of the examination. Patients with unilateral or pulsatile tinnitus are more likely to have serious underlying disease and typically merit referral to an otolaryngologist.2,5 A full clinical evaluation should precede radiologic studies. Because pulsatile tinnitus suggests a vascular abnormality, the preferred imaging study is contrast-enhanced computed tomography (CT) or magnetic resonance imaging (MRI) of the brain21 (Figure 2).

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