Potential risk of Tinnitus

 

qEEG screening

Service code s9023

Please note that screening does NOT result in a medical diagnosis; it gives a probabilistic estimate of risk. In other words, the screening gives information on the presence of a pattern in the qEEG that is often – but not always – found in persons with a history of a particular condition.

Short description

Tinnitus can be objective (mostly caused by myoclonic contractions of the tensor tympani muscle or blood vessels, eustachian tube dysfunction and tumors of the middle ear) or subjective (auditory phantom phenomenon as a result of aberrant neural activity in the central auditory pathway).

All current models agree that tinnitus results from an imbalance between inhibition and excitation of thalamocortical circuits – thalamo-cortical dysrhythmia as a general theory for a host of neurophysiological symptoms. Recent research has demonstrated that qEEG parameters obtained from people with tinnitus generally deviate from qEEG patterns of people without tinnitus symptoms.

Additionally, psychometric data uncovered two distinct independent dimensions characterizing the individual tinnitus experience. These independent dimensions are (a) distress and (b) presence; the latter is described as the perceived intensity of sound experience that increases with tinnitus duration devoid of any considerable emotional burden. Apparently, presence, as well as long-term duration of the tinnitus percept does not necessarily result in emotional distress and annoyance.

However, if distress is present then symptoms of depression or anxiety are often present.

The effectiveness of tinnitus intervention requires a comprehensive understanding of its neurophysiological mechanisms. Here, qEEG screening can be helpful.

Results

By performing this qEEG screening you will get the information on:

  • whether neurophysiological alterations are present/accompanied subjective tinnitus experience (presence of qEEG pattern typical for subjective tinnitus),
  • whether thalamo-cortical dysrhythmia is present and whether proactive adaptation is happening,
  • whether you have tinnitus distress or just tinnitus presence,
  • which of the tinnitus characteristics (distress, tinnitus intensity, and tinnitus duration) are dominant.

Notes:

  • The results of qEEG analysis are put in context of published scientific studies, the individual’s health history, complaints, symptoms and psychometric and other evaluations (if available).
  • Present psychotropic medication use may affect the results.

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References

  1. Chen YC, Wang F, Wang J, Bo F, Xia W, Gu JP, et al. Resting-state brain abnormalities in chronic subjective tinnitus: a meta-analysis. Front Hum Neurosci 2017; 11: 22.
  2. De Ridder D, Vanneste S, Weisz N, et al. An integrative model of auditory phantom perception: tinnitus as a unified percept of interacting separable subnetworks. Neuroscience and Biobehavioral Reviews, 2014; 44: 16–32.
  3. Eggermont JJ, Roberts LE. The neuroscience of tinnitus. Trends Neurosci 2004; 27: 676–682..
  4. Jastreboff PJ. Phantom auditory perception (tinnitus): mechanisms of generation and perception. Neurosci Res 1990; 8: 221–254.
  5. Llinas RR, Ribary U, Jeanmonod D, Kronberg E, Mitra PP. Thalamocortical dysrhythmia: a neurological and neuropsychiatric syndrome characterized by magnetoencephalography Proc Natl Acad Sci USA 1999; 96: 15222-15227.
  6. Vanneste S, Plazier M, der Loo E, de Heyning PV, Congedo M, et al. The neural correlates of tinnitus-related distress. Neuroimage 2010; 52: 470–480.