About Heru H, M.D., DSTHT,M.S., CCC-SLP Expertise I can almost answer any question related to my profession as an otolaryngologist (ear nose and throat, head and neck surgeon) and speech language pathologist. I`m a faculty member and a surgeon from Indonesia and I`d love to help if I can.
Question Kindly explain a crackling, static like sound in my right ear.
Years ago I lost most of my hearing in that ear due to meniere's, but recently have been experiencing this annoying sound. It it seems to start from time to time and then stops for a short while.
I will appreciate your comments. Thank you.
Answer Hi there
You had a symptom known as Tinnitus.
Tinnitus is the perception of noise in the absence of an acoustic stimulus. It can occur as a pure tone or multiple tones and can be high pitched, low pitched, ringing, buzzing, roaring, clicking, hissing, rough, pulsatile, or steady. Because it is a symptom and not a disease, its
treatment varies and is often unsuccessful.
If a person has objective tinnitus, which is audible to the physician or another person or has a pulsating character, certain conditions are suspected. The differential diagnosis includes vascular abnormalities, eustachian tube abnormalities, and tympanic muscle problems.
Subjective tinnitus is more common than objective tinnitus. Almost all persons experience tinnitus at some time.
Patients perceive noise that is not generated in their surroundings.
Subjective tinnitus is complicated by an inability to obtain an objective measure of its severity, and its cause is unknown. The symptom of tinnitus can be likened to headache with multiple causes. It may be caused by abnormal conditions in the cochlea, the cochlear nerve, the ascending auditory pathway, or the auditory cortex. It has been postulated that the cochlear hair cells injured by noise or head trauma may discharge repetitively, stimulating nerve fibers to discharge synchronously in a way that the central auditory system cannot discriminate from actual sound. In the central nervous system or in the auditory pathways, spontaneous activity within individual auditory nerve fibers may also be synchronized because of injury or metabolic abnormality, resulting in tinnitus. It is
also possible that hyperactivity in the nuclei of the ascending auditory pathways may stimulate the auditory cortex in a similar manner. An alternate theory proposes that injury to cochlear integrity from any cause reduces the suppressive influence of the central nervous system, allowing increased neuronal activity higher in the auditory system.
In obtaining complete histories of tinnitus patients, several etiologic factors are prominent. These are classified as otologic, cardiovascular, metabolic, neurologic, pharmacologic, dental, and psychologic factors
The largest number of patients with tinnitus appear to have a history of noise exposure or are experiencing presbycusis. In both instances, there is a high-frequency neurosensory hearing loss. Seventy-five percent of
patients have a 30+ dB hearing loss from 3 to 8 kHz. This hearing loss is the single most consistent factor in patients with tinnitus. Generally, the pitch of the tinnitus occupies the region of the greatest hearing
deficit or the most abrupt loss.
A variety of other otologic disorders appear to accentuate or cause tinnitus, especially Meniere's disease, in which almost all patients complain of the symptom. However, only 4% of these patients have severe and intractable symptoms that are unresolved by any form of management.
Three percent of patients had severe tinnitus secondary to prolonged otitis, and 2% had recurrent labyrinthitis. Although most patients with otosclerosis have tinnitus, only 4% said it was significant. Dizziness is commonly associated with tinnitus. Thirty-five percent of patients were dizzy at least part of the time, and a smaller percentage were dizzy all of the time. This rate of dizziness is higher than in the standard population for the respective age groups, and the symptom should be considered in the workup.
Cardiovascular problems are frequently associated with tinnitus. Thirty percent of patients with severe symptoms had one or more cardiovascular complaints. The high incidence of cardiovascular disease is consistent with the age group (>60 years), but it is still likely that hypertension is a major factor in the onset or severity of the patient's disease.
Twenty-two percent of the patients who had tinnitus in our study had significant hypertension, and more than 1% related specific cardiovascular incidents to the onset of their complaints.
Secondary vascular disorders must be excluded in evaluating these patients. These conditions include anemia (ie, tinnitus secondary to increased cardiovascular output) and extensive arteriosclerosis, in which tinnitus tends to be objective and pulsatile.
Thyroid dysfunction can be associated with tinnitus. Hyperthyroidism, by increasing cardiac output, can cause a pulsatile or rushing noise.
Hypothyroidism has also caused this complaint. It is severe in about 4% of this population.
Hyperlipidemia (too high blood fat contain) is increasingly reported as a factor in tinnitus, particularly in association with fluctuating neurosensory hearing loss and associated dizziness. Vitamin A and/or B deficiency has been described as causing tinnitus.
Five percent of patients report that tinnitus was the result of major trauma. Trauma generally included a skull fracture or closed head injury.
Whiplash injuries have initiated tinnitus, suggesting that abnormal proprioceptive input from nerve fibers in the neck and shoulder or possibly brain stem injuries are factors. Tinnitus after whiplash injury usually occurs 7 to 10 days after the accident, and the appearance of tinnitus immediately after head trauma without clearly defined ear
abnormalities or vestibular disease is uncommon. Therefore, the physician must be careful in assigning a causal relationship to this injury.
Past meningitis (brain infection)may be the cause of tinnitus. Multiple sclerosis can also have severe tinnitus in its constellation of symptoms.
Ten percent of patients relate the onset of significant tinnitus to initiation of or changes in pharmacologic therapy. All classes of medication are considered possible causes of tinnitus. These include anti-inflammatories, antibiotics, and antidepressants.
Aspirin and aspirin-containing compounds were identified as the most common inciting medications. As little as 600 to 1000 mm/day of aspirin can create symptoms. Aspirin-containing medications, such as Percodan, Darvon, Bufferin, or Ecotrin, are often overlooked as possible causes of tinnitus.
Nonsteroidal anti-inflammatories, including Naprosyn and ibuprofen, are frequently implicated but not often considered. The effect of these drugs is similar to aspirin, although not as severe.
Antibiotics, chiefly the aminoglycosides, cause tinnitus. It occurs in most cases of antibiotics used concurrently with diuretics.
Quinine-containing compounds and the synthetic analogues can elevate the severity of tinnitus.
Mercury, arsenic, lead, and other heavy metals in high doses can cause symptoms. A thorough history and alteration of medications are essential components in treating patients with this complaint.
Temporomandibular joint disorders and dental abnormalities must be considered in taking the general history, in the physical examination, and in devising a treatment course for tinnitus. Forty-five percent of patients with severe tinnitus describe active temporomandibular joint problems at some time. Thirty-eight percent of patients who have severe tinnitus describe it as concurrent with an increase in the severity of their temporomandibular joint complaints. The tinnitus is generally low pitched, rough, and associated with a feeling of fullness in the ear.
Psychologic factors play a major role. Stress often increases the perception of tinnitus severity, and depression frequently accentuates the complaint. In some cases, the tinnitus itself may be the cause of the psychologic disorder. Sixteen percent of the population with tinnitus admitted to depression. Many more probably were unwilling to admit to it or did not recognize the symptoms. Some studies concluded that 20% to 50%
of patients were clinically depressed, and about half the depressed patients had a long history of depression before the onset of tinnitus.
There is undoubtedly a significant population in which depression plays a major role and for which treatment must be appropriately directed, but it is not effective to apportion patients with tinnitus into groups who are
psychologically disturbed and those who are not, because treatment may ultimately prove beneficial to both.
If symptoms your are mild, several guidelines should be observed. My best suggestion is to contact an ENT specialist (Ear Nose and Throat) in which the physician should discuss with you all the etiologic factors and status of the complaint. You should be reassured that a tumor is an unlikely cause.
You should be relize that 25% of patients will improve significantly, 50% will improve to some degree, and the remaining 25% will remain unchanged.
A small proportion have progressive symptoms.
If you had tinnitus you should avoid chocolate, coffee, tea, cola, or other caffeine-containing beverages or medications. Fifty-four percent of patients with severe tinnitus took excessive amounts of caffeinated beverages daily. You should also stop smoking.
Medications should be reevaluated, with specific avoidance of aspirin-containing compounds, nonsteroidal anti-inflammatory drugs, or other implicated medications.
You should avoid disturbing noise, use noise protection, and employ home masking techniques, which include music at night or the radio tuned between the FM stations at a level of “white noise” that masks out the tinnitus. A bedside masker can also be recommended.
If you had a history of depression or anxiety, psychologic testing and evaluation are advisable. This allows the physician to have your emotional status reviewed before additional treatment and to tailor medications to the results.
So do contact an ENT or at least an Audiologist to have your hearing assesst.
