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08.05.2015

Pulsatile tinnitus venous causes, treatment tinnitus melbourne - Plans Download

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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.
Tinnitus is a very common symptom and is classified as the perception of a sound in the absence of an external auditory stimulus. People often describe the sensation of subjective tinnitus as a sound of ringing, hissing, machinery or cicadas, among many others, coming from one or both ears. As tinnitus is a subjective symptom, quantification of its severity is based on a patient’s description of its effect on their daily functioning and quality of life. The natural history of most cases of tinnitus is that the patient gets used to the sound or habituates to it. Often all that patients are seeking is an explanation of the symptoms and the underlying cause and exacerbating factors, with the exclusion of significant pathology. Sudden onset of tinnitus and hearing loss or a blocked ear can occasionally represent what is termed the sudden sensorineural hearing loss syndrome.
When a patient presents with asymmetric hearing loss or singlesided tinnitus, imaging of the brain and cerebellopontine angle is indicated to exclude the unlikely presence of central pathology, the most common of which is a vestibular schwannoma (acoustic neuroma). Meniere’s disease is a disorder affecting inner ear homeostasis, classically manifested by episodic vertigo lasting hours, fluctuating hearing loss, tinnitus and aural fullness. When a patient describes the sound of tinnitus resembling pulsation, clicking or related to breathing or swallowing, a mechanical or structural lesion is more likely and must be ruled out.
The most common underlying cause of pulsatile tinnitus is the most benign and relates to a degree of Eustachian tube dysfunction.
True pulsatile tinnitus originates from vascular structures within the head, skull base, neck and thoracic cavity, and is transmitted to the cochlea by bony or vascular structures.
Usually both a CT scan of the skull base and magnetic resonance imaging, angiography and venogram are required. Conductive hyperacusis of the superior semicircular canal dehiscence syndrome is a rare condition that causes pulsatile tinnitus. Myoclonic contractions of the tensor veli palatini, levator veli palatini, salpingopharyngeus, superior pharyngeal constrictor and the stapedius muscles are another uncommon cause of tinnitus. Monfared obtains a lumbar puncture or spinal tap in most patients with venous phase pulsatile tinnitus unless the diagnosis is made through an ophthalmologic examination or other causes are identified. About 15% of the adult population report some degree of tinnitus with less than 2% of people describing it as a distressing symptom. There are a number of wellvalidated questionnaires that can be used in this regard such as the Tinnitus Handicap Inventory (figure 1). This is commonly used in people who only notice their tinnitus when there is no or minimal background sound. The aim is to use a specific sound program to assist in habituation of the tinnitus and sensibly focuses on the aberrant central connections that have been established. Because of the presumed pathophysiological connection with alternate neural tinnitus pathways and the limbic system, any physiological or emotional stress has the capacity to exacerbate tinnitus.
Often patients notice the tinnitus and a full or blocked feeling but do not appreciate that their hearing is also impaired.


This often occurs after a head cold and is related to pulsations being transmitted down a partially blocked Eustachian tube to the middle ear. It is due either to increased blood flow or stenosis, and can be classified as arterial or venous. The tinnitus is usually a clicking sound ranging between 10 and 240 clicks per minute, which can occasionally be confused with a pulsatile sensation.
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. Occasionally severe noise exposure, especially of an impulsive nature can leave one with permanent tinnitus. It is in those with more severe tinnitus and associated symptoms that a range of management options should be considered. Occasionally there may be a medically or surgically correctable cause of hearing loss such as a perforated tympanic membrane (figure 2). Another diagnosis to consider in bilateral pulsatile tinnitus is benign intracranial hypertension, although this can also cause unilateral symptoms (figure 5).
Benign raised intracranial pressure, abnormalities of the jugular bulb, stenosis of the transverse or sigmoid sinuses, abnormalities of other draining veins of the skull base, and other causes of raised intracranial pressure are possibilities. An enlarged jugular bulb on the involved side is common in persons with venous type pulsatile tinnitus. Age, genetic susceptibility, accumulated noise exposure, infections, trauma, Meniere’s disease, otosclerosis (especially with cochlear involvement), and more serious pathology such as a vestibular schwannoma can all be causes of auditory damage and thus tinnitus. During the initial assessment it is important to spell out that the initial aim is to rule out any serious underlying causes (which are very rare) and then to minimise the intrusiveness of tinnitus. While some of these could be classified as alternative, anything that can minimise the feedback loop to the accessory tinnitus pathways is helpful. Stenosis of the transverse sinuses can be caused by post-infectious thrombosis with partial recanalisation or by prominent arachnoid granulations. A number of studies have shown that many people will experience tinnitus when placed in an anechoic environment or after using occlusive earplugs. The initial injury leads to generation of the tinnitus, which is then modified by central connections to the limbic system and trigeminal nucleus.
Therefore any abnormalities in these areas can act as non-ear exacerbating factors to the tinnitus. It is very important to say that there are many things that can be done, but it is also important to state that the quest to completely get rid of the tinnitus is counterproductive.
The usual management of tinnitus begins with an explanation of the underlying pathophysiology of tinnitus as previously described.
Essentially one should have the volume of the masking noise just below that of the tinnitus and over a period of time reduce the volume of the masking noise. In significantly intrusive tinnitus with any more than mild hearing loss, consideration of hearing aids need be made, even if patients do not identify that their hearing is a problem. One of the most common causes of physiological stress is lack of sleep and of course any other systemic disease process.
This process is thought to facilitate the brain’s ability to habituate to the underlying tinnitus as opposed to removing it entirely.


This situation often leads to a vicious feedback loop where, as the tinnitus becomes more intrusive and distressing, further activation of the limbic system leads to further exacerbation of the same system and so on and so forth.
If the severe hearing loss is accompanied by significant tinnitus, cochlear implantation has recently been shown to be a very efficacious management option. When symptoms are severe, consideration of direct venography is made, allowing more accurate diagnosis and measurement of trans-stenotic pressure gradients.
Subjective tinnitus is a sound that cannot be detected externally, and is by far the most common form, while objective tinnitus is a sound that an examiner can hear. Almost all medications have at some stage been associated with tinnitus but usually this is coincidental. Often patients will feel that it is their tinnitus causing a degree of hearing loss but it is the other way around. Most of what we think of as objective tinnitus is related to transmission of sound to an otherwise normal ear; however, this externally derived sound is not always audible to the examiner. The modern approach to tinnitus often parallels the management of chronic pain and as a way of explanation can be likened to phantom limb pain following amputation. It is interesting that even when the hearing aids are removed the degree of tinnitus is still improved. Clues as to the cause of the tinnitus can be gained by otoscopy and auscultation of the chest, neck and skull. It is, presumably, almost impossible to experience tinnitus without some degree of damage to the hearing mechanism. A large component of this is cognitive behavioural therapy and aims to minimise the link between the tinnitus and the central activation of the limbic system. If occlusion of the internal jugular vein minimises the sound then a venous cause is more likely. This article will focus on subjective tinnitus, with objective tinnitus being dealt with more briefly at the end. The combination of severe tinnitus and severe hearing loss is difficult to manage, as a standard hearing aid is unable to amplify sound adequately to impart a benefit. While there are few centres dedicated to specific tinnitus retraining therapy, most psychologists with an interest in cognitive behavioural therapy can make a big difference. This allows direct stimulation of the cochlear nerve itself, vastly improving hearing and in almost all cases significantly improving tinnitus.
The most common cause is an arachnoid granulation but can also occur as a result of chronic ear disease with or without holesteatoma (figure 8).
Not infrequently, all of the investigations are unremarkable and the diagnosis of idiopathic or essential tinnitus is then made. Similar to subjective tinnitus discussed above, often all that patients are looking for is reassurance that there is no serious pathology.



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