Microvascular compression may sometimes cause tinnitus. According to Levine (2006) the quality is similar to a "typewriter", and it is fully suppressed by carbamazepine. It seems to us that response to carbamazepine is not a reliable indicator of microvascular compression as this drug stabilizes nerves and lowers serum sodium. Nevertheless, this quality of tinnitus probably justifies a trial of oxcarbamazine (a less toxic version of carbamazepine).
Being exposed to loud noise on a regular basis from heavy equipment, chain saws or firearms are common causes of hearing loss and tinnitus. Noise-induced hearing loss and tinnitus can also be caused by listening to loud music through headphones or attending loud concerts frequently. It is possible to experience short-term tinnitus after seeing a concert, but long-term exposure will cause permanent damage.
It is possible that the most common cause of pulsatile tinnitus is sigmoid sinus diverticulum and dehiscence, which can be collectively referred to as sinus wall abnormalities or SSWA. The sigmoid sinus is a blood carrying channel on the side of the brain that receives blood from veins within the brain. The blood eventually exits through the internal jugular vein. Sigmoid sinus diverticulum refers to the formation of small sac-like pouches (diverticula) that protrude through the wall of the sigmoid sinus into the mastoid bone behind the ear. Dehiscence refers to absence of part of the bone that surrounds the sigmoid sinus in the mastoid. It is unknown whether these conditions represent different parts of one disease process or spectrum, or whether they are two distinct conditions. These abnormalities cause pressure, blood flow, and noise changes within the sigmoid sinus, which ultimately results in pulsatile tinnitus. Narrowing of the blood vessel that leads into the sigmoid sinus, known as the transverse sinus, has also been associated with pulsatile tinnitus.
In the advance online edition of Nature on January 12, 2011, the researchers reported that the number of neurons tuned to the high frequency had jumped by 79% compared to control rats. The scientist then tested 2 different tones in a second group of rats but stimulated the vagus nerve only for the higher one. The neurons tuned to the higher tone increased by 70%, while those tuned to the lower one decreased in number. This showed that the tone alone wasn’t enough to initiate the change; it had to be accompanied by VNS.
The accepted definition of chronic tinnitus, as compared to normal ear noise experience, is five minutes of ear noise occurring at least twice a week.[50] However, people with chronic tinnitus often experience the noise more frequently than this and can experience it continuously or regularly, such as during the night when there is less environmental noise to mask the sound.
If the source of the problem remains unclear, you may be sent to an otologist or an otolaryngologist (both ear specialists) or an audiologist (a hearing specialist) for hearing and nerve tests. As part of your examination, you may be given a hearing test called an audiogram. An imaging technique, such as an MRI or a CT scan, may also be recommended to reveal any structural problem.
Tinnitus can arise anywhere along the auditory pathway, from the outer ear through the middle and inner ear to the brain's auditory cortex, where it's thought to be encoded (in a sense, imprinted). One of the most common causes of tinnitus is damage to the hair cells in the cochlea (see "Auditory pathways and tinnitus"). These cells help transform sound waves into nerve signals. If the auditory pathways or circuits in the brain don't receive the signals they're expecting from the cochlea, the brain in effect "turns up the gain" on those pathways in an effort to detect the signal — in much the same way that you turn up the volume on a car radio when you're trying to find a station's signal. The resulting electrical noise takes the form of tinnitus — a sound that is high-pitched if hearing loss is in the high-frequency range and low-pitched if it's in the low-frequency range. This kind of tinnitus resembles phantom limb pain in an amputee — the brain is producing abnormal nerve signals to compensate for missing input.
Pulsatile tinnitus is generally caused by abnormalities or disorders affecting the blood vessels (vascular disorders), especially the blood vessels near or around the ears. Such abnormalities or disorders can cause a change in the blood flow through the affected blood vessels. The blood vessels could be weakened from damage caused by hardening of the arteries (atherosclerosis). For example, abnormalities affecting the carotid artery, the main artery serving the brain, can be associated with pulsatile tinnitus. A rare cause of pulsatile tinnitus is a disorder known as fibromuscular dysplasia (FMD), a condition characterized by abnormal development of the arterial wall. When the carotid artery is affected by FMD, pulsatile tinnitus can develop.
Changing Prescriptions, OTC Medications and Food Additives. Sometimes the cause of tinnitus is a prescription (such as an antibiotic), an over the counter medication or a food additive. As an example, two very common prescriptions that have been shown to cause tinnitus are quinine and chloroquine, which are both used to prevent malaria. Certain diuretics and cancer medications can also cause tinnitus. Even something as simple as OTC aspirin can generate tinnitus in some people. The food additives NutraSweet, Splenda and Aspartame have all been linked to tinnitus, and a whole host of other side effects, in clinical studies. These man-made food additives should be eliminated from your diet completely. If any of your medications are causing your tinnitus, your doctor may recommend stopping, reducing or switching them out for other medicines to see if that helps cure your tinnitus.
The researchers paired electrical stimulation of the vagus nerve — a large nerve that runs from the head to the abdomen — with the playing of a tone. Vagus nerve stimulation (VNS) is known to release chemicals that encourage changes in the brain. This technique, the scientists reasoned, might induce brain cells (neurons) to tune to frequencies other than the tinnitus one. For 20 days, 300 times a day, they played a high-pitched tone to 8 rats during VNS.
An assessment of hyperacusis, a frequent accompaniment of tinnitus,[56] may also be made.[57] The measured parameter is Loudness Discomfort Level (LDL) in dB, the subjective level of acute discomfort at specified frequencies over the frequency range of hearing. This defines a dynamic range between the hearing threshold at that frequency and the loudnes discomfort level. A compressed dynamic range over a particular frequency range is associated with subjectve hyperacusis. Normal hearing threshold is generally defined as 0–20 decibels (dB). Normal loudness discomfort levels are 85–90+ dB, with some authorities citing 100 dB. A dynamic range of 55 dB or less is indicative of hyperacusis.[58][59]
Ask your doctor about experimental therapies. No cure for tinnitus has been found but research is ongoing, so you should be open to experimental therapies. Electronic and magnetic stimulation of the brain and nerves might correct the overactive nerve signals that cause tinnitus. These techniques are still in development, so ask your doctor or hearing specialist if trying one might be right for you.[6]
Tinnitus can occur as a sleep disorder - -this is called the "exploding head syndrome". This most often occurs while falling asleep or waking up. It is a tremendously loud noise. Some theorize that this syndrome is due to a brief seizure in auditory cortex. It is not dangerous.(Green 2001; Palikh and Vaughn 2010). Logically, anticonvulsants might be useful for treatment.
Often people bring in very long lists of medications that have been reported, once or twice, to be associated with tinnitus. This unfortunate behavior makes it very hard to care for these patients -- as it puts one into an impossible situation where the patient is in great distress but is also unwilling to attempt any treatment. Specialists who care for patients with ear disease, usually know very well which drugs are problems (such as those noted above), and which ones are nearly always safe.
When TRT was developed in the 1980s by neuroscientist Dr. Pawel Jastreboff (now at Emory University in Atlanta), it was designed to be administered according to a strict protocol. Today, the term TRT is being used to describe modified versions of this therapy, and the variations make accurate assessment of its effectiveness difficult. Individual studies have reported improvements in as many as 80% of patients with high-pitched tinnitus. In a Cochrane review of the one randomized trial that followed Jastreboff's protocol and met the organization's standards, TRT was much more effective in reducing tinnitus severity and disability than a technique called masking (see below).
If the source of the problem remains unclear, you may be sent to an otologist or an otolaryngologist (both ear specialists) or an audiologist (a hearing specialist) for hearing and nerve tests. As part of your examination, you may be given a hearing test called an audiogram. An imaging technique, such as an MRI or a CT scan, may also be recommended to reveal any structural problem.
