The analogy between tinnitus and pain: A suggestion for a physiological basis of chronic tinnitus

Tonndorf, Juergen

doi:10.1016/0378-5955(87)90054-2

Cited by 206 publications

(130 citation statements)

References 10 publications

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“…Tinnitus would reflect an integrated interneuronal neurotransmission pathway including the frontal, temporal, and parietal lobes, thalamus, and cerebellum (Shulman, 2005). A major hypothesis on the pathophysiological mechanisms is that tinnitus would involve a lesion leading to deafferentation of excitatory inputs on thalamic relay cells (Tonndorf, 1987;Moller, 1997;Lockwood et al, 1998). This would lead to a thalamic deactivation (Llinás et al, 2005), disrupting in turn thalamo-cortical interactions (Jeanmonod et al, 1996;Llinás et al, 1999), and leading to the appearance of tinnitus.…”

Section: Discussionmentioning

confidence: 99%

Involvement of cortico-subcortical circuits in normoacousic chronic tinnitus: A source localization EEG study

Houdayer

Teggi

Velikova

et al. 2015

Clinical Neurophysiology

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HIGHLIGHTS• We used sLORETA to study the cerebral activity in normoacousic tinnitus sufferers.• EEG sources were decreased in left temporal and inferior parietal gyri in patients.• Cortico-thalamo-cortical circuits can be involved without thalamic deafferentation. ABSTRACTObjective: To better characterize brain circuits dysfunctions in normoacousic tinnitus sufferers. Methods: 17 normoacousic chronic, unilateral high-pitched tinnitus sufferers (6 females, 43.6 ± 9.8 y.o, disease duration 22 ±35 months) underwent a 29-channel resting-state electroencephalography (EEG -5 min opened-eyes, 5 min closed-eyes) and auditory oddball paradigm for event-related potentials analyses (ERPs -NI, P2 and P300). Cortical 3D distribution of current source density was computed with sLORETA. Results were compared with 17 controls (9 females, 45.7 ± 15.1 y.o). Results: Eyes opened, tinnitus sufferers had lower alpha and beta sources in the left inferior parietal lobule. Eyes closed, tinnitus sufferers had decreased alpha sources in the left inferior temporal and post-central gyri, and low gamma sources in the left middle temporal gyrus. EEG data did not correlate with tinnitus sufferers' clinical features. Subjects with tinnitus had shorter Nl and P2 latencies. P300 did not differ between groups. sLORETA solutions showed decreased sources of these ERPs in the left inferior temporal gyrus in the tinnitus group. Conclusions: We showed cortico-thalamo-cortical involvements in normoacousic tinnitus with hyperexcitability of the left auditory cortex and inferior temporal gyrus. Significance: This might reflect processes of maladaptive cortical plasticity and memory consolidation. Further validation is needed to establish the value of this tool in customizing therapeutic approach.

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Section: Discussionmentioning

confidence: 99%

Involvement of cortico-subcortical circuits in normoacousic chronic tinnitus: A source localization EEG study

Houdayer

Teggi

Velikova

et al. 2015

Clinical Neurophysiology

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“…Thus, a clear clinical analogy exists between phantom pain and disabling tinnitus (10,11): (i) Both symptoms are wholly subjective perceptions and may change in character and quality and (ii) both symptoms occur in the deafferented area. The frequency spectrum of the tinnitus reflects the individual's hearing loss (12), neuropathic pain is felt as coming from the area that was initially innervated by the injured neural structure (2), and phantom pain is perceived in the missing body part (2,13).…”

mentioning

confidence: 99%

Phantom percepts: Tinnitus and pain as persisting aversive memory networks

Ridder¹,

Elgoyhen

Romo

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

543

482

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Phantom perception refers to the conscious awareness of a percept in the absence of an external stimulus. On the basis of basic neuroscience on perception and clinical research in phantom pain and phantom sound, we propose a working model for their origin. Sensory deafferentation results in high-frequency, gamma band, synchronized neuronal activity in the sensory cortex. This activity becomes a conscious percept only if it is connected to larger coactivated "(self-)awareness" and "salience" brain networks. Through the involvement of learning mechanisms, the phantom percept becomes associated to distress, which in turn is reflected by a simultaneously coactivated nonspecific distress network consisting of the anterior cingulate cortex, anterior insula, and amygdala. Memory mechanisms play a role in the persistence of the awareness of the phantom percept, as well as in the reinforcement of the associated distress. Thus, different dynamic overlapping brain networks should be considered as targets for the treatment of this disorder.A fundamental concept in psychology and philosophy of the mind is the notion of perception: The act of interpreting and organizing a sensory stimulus to produce a meaningful experience of the world and of oneself. A stimulus produces an effect on the different sensory receptors, inducing sensation. Further processing of this sensory stimulation generates an internal representation of the outer and inner world called a percept. Since the first days of psychology, two challenging questions have existed: How is sensory information encoded and, in particular, how is this represented information transformed into the individual awareness of a conscious percept (1)? Our understanding of sensory encoding, perception, and consciousness is challenged with a further degree of complexity in the case of phantom perception, the conscious awareness of a percept in the absence of an external stimulus. Deciphering the underlying neural correlates of phantom perception is a scientific endeavor that will aid in understanding the active processes of selecting, organizing, and interpreting information, which ultimately lead to the formation of a conscious percept within the brain.Although some cases of phantom percepts have been described for the visual, olfactory, and gustatory systems, the vast majority of sensory phantoms are those present in the somatosensory (phantom limb perception/phantom limb pain and neuropathic pain) (2) and auditory (tinnitus) (3) modalities. Upfront we are challenged with the following questions: In the absence of an external sensory stimulus, where and how in the brain is the conscious percept generated? In addition, are the neural substrates underlying the generation of a conscious phantom percept similar for the auditory and somatosensory modalities? If so, can we advance in our understanding and treatment of tinnitus on the basis of what is known for phantom limb and phantom pain perception and vice versa? Here, we address these questions and propose a working model of how pha...

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“…This auditory deafferentation can cause an increase in spontaneous activity of auditory nerve fibers. This extra activity is the supposed source of the ongoing tinnitus 16 . Making an analogy with a neural theory regarding chronic intractable pain, Tonndorf then suggests that, acoustic masking with its relatively short RI might mechanically re-activate the large diameter, inner-hair-cell fibers in largely the same manner as the large-diameter pain fibers are temporarily re-activated by scratching or by vibratory stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…According to gate control theory, the activity of the large diameter, inner-hair-cell fibers act to shut-off (for a time) the aberrant signaling from the small diameter, outer-hair-cell fibers. Thus perception of the tinnitus is stopped for a period of time 16 . Similarly, but more briefly, Vernon & Meikle 15 in 1981 speculated that the mechanism of residual inhibition may be related to mechanisms that suppress pain for a period of time after electrical stimulation.…”

Section: Discussionmentioning

confidence: 99%

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Alterations in early auditory evoked potentials and brainstem transmission time associated with tinnitus residual inhibition induced by auditory electrical stimulation

Mahmoudian¹,

Lenarz²,

Esser³

et al. 2013

The International Tinnitus Journal

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The analogy between tinnitus and pain: A suggestion for a physiological basis of chronic tinnitus

Cited by 206 publications

References 10 publications

Involvement of cortico-subcortical circuits in normoacousic chronic tinnitus: A source localization EEG study

Involvement of cortico-subcortical circuits in normoacousic chronic tinnitus: A source localization EEG study

Phantom percepts: Tinnitus and pain as persisting aversive memory networks

Alterations in early auditory evoked potentials and brainstem transmission time associated with tinnitus residual inhibition induced by auditory electrical stimulation

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