Positron emission tomography of cortical centers of tinnitus

Mirz, Frank; Pedersen, C.; Ishizu, Koji; Johannsen, Peter; Ovesen, Therese; Stødkilde‐Jørgensen, Hans; Gjedde, Albert

doi:10.1016/s0378-5955(99)00075-1

Cited by 199 publications

(139 citation statements)

References 73 publications

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“…The role of thalamus in tinnitus pathophysiology has been previously discussed by several authors. Thalamic abnormalities in tinnitus sufferers have been widely reported in both structural (Mühlau et al, 2006) and functional (Mirz et al, 1999) studies, and it has been suggested, from EEC or MEG studies, that tinnitus would result from thalamo-cortical dysrhythmia (Llinás et al, 1999;Moazami-Goudarzi et al, 2010).…”

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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“…Fortunately many patients are able to voluntarily modify their TI, for example by eye gaze or facial movement (Levine, 1999b). In others, the TI level can be modulated in other ways, for example by a noise masker (Mirz et al, 1999;Melcher et al, 2000), by the administration of pharmacological treatments such as lidocaine (Staffen et al, 1999;Andersson et al, 2000) or by the application of neural stimulation using a TMS coil (de Ridder et al, 2004;. TI-related activity can be identified by taking advantage of these manipulations to create experimental paradigms that lend themselves to statistical subtraction.…”

Section: Human Neuroimaging Studiesmentioning

confidence: 99%

“…A majority of functional neuroimaging studies fail to reach such numbers and to illustrate this point, we highlight sample size throughout our review. **** Figure 2 here**** Suppression of TI using noise maskers and residual inhibition The effect of masking noise on suppressing TI-related activity has been investigated within the inferior colliculus using fMRI (Melcher et al, 2000) and within auditory cortex using PET (Mirz et al, 1999). Mirz's study was based on the prediction that TI-related spontaneous activity could be reduced through masking.…”

Section: Human Neuroimaging Studiesmentioning

confidence: 99%

“…Two group studies are worth mentioning here. In the same PET study of noise masking that was previously described, Mirz et al (1999) also contrasted periods of lidocaine-based TI suppression with baseline rest periods. For the ten patients who responded to the drug, it was found to reduce activity in right prefrontal and parietal regions regardless of TI laterality, but it did not significantly modulate activity in auditory cortex.…”

Section: Human Neuroimaging Studiesmentioning

confidence: 99%

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The mechanisms of tinnitus: Perspectives from human functional neuroimaging

2009

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In this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power. AbstractIn this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power.

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“…The technical aspects of these were discussed in detail elsewhere . These methods have been applied with success in human tinnitus patients to identify various brain areas active during phantom perceptions, and to examine the effects of some treatments (see for example Giraud et al, 1999;Mirz et al, 1999;Reyes et al, 2002). There is now good evidence from PET and magnetic encephalography that a reorganization of the frequency axis in the human auditory cortex occurs much as described above (Lockwood et al, 1998;Mühlnickel et al, 1998).…”

Section: Cortical Reorganization and Tinnitusmentioning

confidence: 99%

The role of central nervous system plasticity in tinnitus

Saunders

2007

Journal of Communication Disorders

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Tinnitus is a vexing disorder of hearing characterized by sound sensations originating in the head without any external stimulation. The specific etiology of these sensations is uncertain but frequently associated with hearing loss. The "neurophysiogical" model of tinnitus has enhanced appreciation of central nervous system (CNS) contributions. The model assumes that plastic changes in the primary and non-primary auditory pathways contribute to tinnitus with the former perhaps sustaining them, and the latter contributing to perceived severity and emotionality. These plastic changes are triggered by peripheral injury, which results in new patterns of brain activity due to anatomic alterations in the connectivity of CNS neurons. These alterations may change the balance between excitatory and inhibitory brain processes, perhaps producing cascades of new neural activity flowing between brainstem and cortex in a self-sustaining manner that produces persistent perceptions of tinnitus. The bases of this model are explored with an attempt to distinguish phenomenological from mechanistic explanations.Learning outcomes-(1) Readers will learn that the variables associated with the behavioral experience of tinnitus are as complex as the biological variables. (2) Readers will understand what the concept of neuroplastic brain change means, and how it is associated with tinnitus. (3) Readers will learn that there may be no one brain location associated with tinnitus, and it may result from interactions between multiple brain areas. (4) Readers will learn how disinhibition, spontaneous activity, neural synchronization, and tonotopic reorganization may contribute to tinnitus.

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Positron emission tomography of cortical centers of tinnitus

Cited by 199 publications

References 73 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

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

The role of central nervous system plasticity in tinnitus

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