Tinnitus is described as ringing, roaring, hissing, or pulsatile. It is classified as subjective and objective. Objective tinnitus is very rare and consists of a sound heard by both the patient and the physician such as arterial bruits, venous hums, and palatal and stapedial myoclonus. Subjective tinnitus is the most common and is only appreciated by the patient. It affects 50 million people in the US. About 0.5% to 2% of people request urgent medical assistance either for acute unbearable tinnitus or for chronic tinnitus that worsened suddenly. The number one culprit of tinnitus is hearing loss.
Causes and differential diagnosis of tinnitus
There is no standard diagnostic criterion for tinnitus. Self-report is the base for determining tinnitus presence. In a subset of psychiatric patients (eg, with schizophrenia) tinnitus may be confused with auditory hallucinations.
The causes of tinnitus could be peripheral or central. Peripheral causes usually involve cochlear pathologies associated with hearing loss (eg, noise-induced hearing loss or Meniere disease), acoustic neuroma or vestibular nerve damage due to infection, an autoimmune disorder, or diabetes. Central causes of tinnitus include stroke, demyelinating lesions, traumatic brain injury, and arteriovenous malformations. Other causes of tinnitus include the use of ototoxic drugs and neck trauma.
Pathophysiologically, tinnitus is understood as the result of an adaptive mechanism to a diminished input: when the neural output stemming from the cochlea is weakened, the auditory system automatically compensates the loss by augmenting its gain. In such situations, tinnitus is compared to that of phantom limb pain. Indeed, a strong positive correlation between the amount of cortical reorganization and the subjective strength of tinnitus was found in a study by Muhlnickel and colleagues.1 Other theories have also been described that are non-adaptive in nature and connect tinnitus to the somatosensory system or the hypothalamic-pituitary axis, specifically cortisol.
Interestingly in tinnitus, many brain areas are affected beyond the auditory system and pathway. In fact, electrophysiological data show that various electroencephalogram (EEG) abnormalities involving different brain areas are associated with tinnitus. Particularly, quantitative EEG showed unilateral localized focus of high frequency activity over the temporal lobe auditory cortex in tinnitus patients. Other areas involved in tinnitus include the anterior cingulate cortex, dorsal lateral prefrontal cortex, insula, supplementary motor area, orbitofrontal cortex, parahippocampus, posterior cingulate cortex, and the precuneus.
Imaging studies also showed involvement of certain regions including auditory structures (auditory brain stem, medial geniculate nucleus, primary and secondary auditory cortex and temporo-parietal association areas) as well as cortical and subcortical areas found on positron emission tomography (PET) scan and functional MRI (amygdala, hippocampus, anterior cingulate, and orbitofrontal cortex).2
Dr Chemali is Director, Neuropsychiatry Clinics; Director, Behavioral Neurology-Neuropsychiatry Fellowship; Director, Global Implementation Program in Neuropsychiatry, Behavioral and Social Sciences; Associate Professor, Harvard Medical School, Massachusetts General Hospital, Boston, MA. Dr Nehme is Psychiatry Fellow, Consult-Liaison Psychiatry, Cambridge Health Alliance, Cambridge, MA. The authors report no conflicts of interest concerning the subject matter of this article.
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