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A Heuristic Pathophysiological Model of Tinnitus

  • Dirk De RidderEmail author
Chapter

Keypoints

  1. 1.

    Tinnitus pathophysiology should explain both tinnitus distress and tinnitus intensity.

     
  2. 2.

    Distress in tinnitus is most likely generated by an aspecific distress network consisting of the amygdala–anterior cingulate and anterior insula.

     
  3. 3.

    Tinnitus intensity might be encoded by gamma band activity in the contralateral auditory cortex.

     
  4. 4.

    This gamma band activity might result from thalamocortical dysrhythmia.

     
  5. 5.

    Tinnitus distress can be seen as phase-synchronized co-activation of the auditory cortex activity and the aspecific distress network.

     
  6. 6.

    For tinnitus to be perceived consciously, it requires the auditory cortex activity be embedded in a larger network.

     
  7. 7.

    This larger network could be the global workspace, the self-perception network.

     
  8. 8.

    The tinnitus network changes in time, hypothetically via an allostatic mechanism.

     
  9. 9.

    In chronic tinnitus, the parahippocampus, insula, and dorsolateral prefrontal cortex networks are critical.

     
  10. 10.

    The parahippocampus is involved via its auditory sensory gating mechanism, suppressing redundant auditory information.

     

Keywords

Tinnitus Gamma Theta Thalamocortical dysrhythmia Distress Deafferentation Plasticity Reorganization Networks 

Abbreviations

AC

Auditory cortex

ACC

Anterior cingulate cortex

BA

Brodman area

BOLD

Blood oxygen level dependent

BPS

Band pass small

BPW

Band pass wide

BRAI²N

Brain research center antwerp for innovative & interdisciplinary neuromodulation

CAS

Complex adaptive systems

DACC

Dorsal part of ACC

DLPFC

Dorsolateral prefrontal cortex

EEG

Electroencephalography

ERP

Event related potential

FMRI

Functional magnetic resonance imaging

Hz

Hertz

IC

Inferior colliculus

ICA

Independent component analysis

IPS

Intraparietal sulcus

IEEG

Intracranial EEG

LORETA

Low resolution electro tomography

LTP

Long term potentiation

MCS

Minimally conscious state

MD

Mediodorsal

MEG

Magnetoencephalography

MGB

Medial geniculate body

NB

Nucleus basalis

OF

Other frequency

PET

Positron emission tomography

PCC

Posterior cingulate cortex

PVS

Persistent vegetative state

RTMS

Repetitive transcranial magnetic stimulation

SMA

Supplementary motor area

SPL

Superior parietal lobule

STG

Superior temporal gyrus

STS

Superior temporal sulcus

TF

Tinnitus frequency

TQ

Tinnitus questionnaire

TPJ

Temporoparietal junction

TRI

Tinnitus research initiative

VMPFC

Ventromedial prefrontal cortex

VTA

Ventral tegmental area

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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.TRI Tinnitus Clinic Antwerp, BRAI2N & Department of NeurosurgeryUniversity Hospital AntwerpEdegemBelgium

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