Pathophysiology of tinnitus Ppt Powerpoint Presentation slides Aage R. Moller, Ph.D. (D. Med. Sci.) Medical Slideshow Treatment of tinnitus with acamprosate

Pathophysiology of tinnitus

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Slide 1 :

PATHOPHYSIOLOGY OF TINNITUS Aage R. Møller , Ph.D. (D.Med.Sci.) THE UNIVERSITY OF TEXAS AT DALLAS School of Behavioral and Brain Sciences

Slide 2 :

Slideshow illustratingPATHOPHYSIOLOGY OF TINNITUSbased on:Aage R. MøllerOtolaryngol Clin N Am vol 36 (2003) 249-266

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Cause of tinnitus Tinnitus can be caused by sounds generated in the body (objective tinnitus) or by abnormal neural activity in the nervous system (subjective tinnitus)

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Objective tinnitus Turbulent flow in blood vessels where constricted; pathologies such as arterio-venous malformations, glomus tumors and aneurysms (often pulsatile tinnitus). Temporomandibular joint disorders, spontaneous contarctions of middle ear muscles or palatal myoclonous (clicking sounds). Breathing sound (patulous Eustachian tube)

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Objective tinnitus The sound is conducted to the cochlear through bone conduction and processed in the ear and nervous system as any other sound from the outside Can often be heard by an observer (auscultation)

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Subjective tinnitus Perception of sound in the absence of any physical sound The sound that the patient hears has not been processed in the ear as sounds from the environment. The abnormal neural activity that cause tinnitus may be generated in the ear but more often somewhere in the nervous system. Can only be heard by the patient

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There are many forms of subjective tinnitus Mild tinnitus: Does not interfere noticeably with everyday life Moderate tinnitus: May cause some annoyance and may be perceived as unpleasant Severe (disabling) tinnitus: Affects a person’s entire life in major ways

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Some individual’s tinnitus may be illustrated by Edvard Munch’s: The Scream

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How prevalent is tinnitus? The prevalence of tinnitus is poorly known. Tinnitus is disturbing for some, and a few individuals suffer from tinnitus (Møller, 2006). Some statistics show prevalence of 4.4% - 15.1% (Hoffmann and Reed 2004) Tinnitus is more prevalent over the age of 60 years Prevalence of severe above 50 years: 7.6 - 20.1%

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Tinnitus depends on the circumstances Most people over the age of 70 years will perceive tinnitus if placed in a sound insulated room such as an audiometric test booth. Some people’s tinnitus gets stronger when exposed to sounds, while other people find relief by sound.

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Little is known about the cause of subjective tinnitus Tinnitus is often associated with: Noise exposure Age Hearing loss Deprivation of sound Administrations of ototoxic antibiotics Vestibular Schwannoma Ménière's disease Vascular contact with the auditory nerve TMJ and neck muscle spasm

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Where is tinnitus generated? Patients often refer their tinnitus to one or both ears, and less often to the center of their head Tinnitus has therefore often been regarded as a disorder of the ear, but it has become evident that the location of the abnormalities is more often the nervous system

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The fact that tinnitus is normally referred to the ear placed the focus on the ear for finding pathologies It was a step forward when the nervous system became the target in studies of tinnitus

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The fact that tinnitus can occur after the auditory nerve is severed brought evidence that the nervous system must be the site of the physiological abnormalities that cause the sensation of tinnitus

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Many forms of tinnitus are phantom sensations similar to the phantom limb syndrome giving tingling and pain

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Severe tinnitus is often accompanied by altered perception of sound Sounds are distorted Decreased tolerance for sounds (hyperacusis) Sounds are painful and arouse fear (phonophobia)

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Subjective tinnitus has similarities with central pain

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Expression of neural plasticity is involved in many forms of tinnitus and central neuropathic pain Causes:1. Hyper-excitability 2. Re-routing of information

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Expression of neural plasticity may cause re-routing of information to the non-classical auditory system in patients with severe tinnitus

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The perception of tinnitus in some patients is affected by stimulation of the somatosensory system (electrical stimulation of the median nerve at the wrist) Indicating that the non-classical auditory pathways are involved

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The non-classical pathways(extralemniscal or non-specific pathways) Receive input from more than one sense Use dorsal and medial thalamic nuclei that project to secondary cortices bypass the primary cortices provide subcortical projections to other parts of the CNS

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From: Møller: Sensory Systems, 2003 Classical auditory pathways Non-classical auditory pathways

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From: Møller: Sensory Systems, 2003

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Signs of involvement of the non-classical auditory pathways:Perception of loudness of nonsense sounds is affected by electrical stimulation of the median nerve at the wrist

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Who have signs of involvement of the non-classical auditory pathways? Some patients with tinnitus Young individuals (below age 16) Some autistic individuals

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Other signs of involvement of the somatosensory system in tinnitus Gaze related tinnitus Neck muscles and tinnitus TMJ and tinnitus Sensation of sound from touching the skin

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Re-routing of information through expression of neural plasticity can be caused by: Change in synaptic efficacy Creation or elimination of synapses Sprouting or elimination of axons and dendrites

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Bifurcation: Both route A and B receive input because both synapses are effective

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Bifurcation Only route B receives input because the synapse (A) is ineffective

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Severe tinnitus is often associated with affective (mood) disorders Depression Phonophobia

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Activation of the non-classical auditory pathways may open a subcortical route to the limbic system The amygdala may thereby receive input from the auditory system through a subcortical pathway The amygdala is involved in fear and other mood disorders

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Connections from the auditory system to the amygdala Cortical-cortical connections (the “high route”) Subcortical connections (the “low route”)

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From: Møller: Sensory Systems, 2003 Connections between the classical and the non-classical auditory systems and the amygdala showing both the “high route” and the “low route”

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From: Møller: Sensory Systems, 2003 Connections from the amygdala

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Subcortical connections to the amygdala may explain why some individuals with severe tinnitus have depression and some experience fear of sound (phonophobia) The subcortical connection from the medial part of the thalamus may provide an abnormal input to the limbic system may cause inescapable fear

Slide 36 :

What can cause expression of neural plasticity? Deprivation of input Novel input (overstimulation) Trauma Unknown factors

Slide 37 :

Neural plasticity plays greater role in generating symptoms and signs than previously assumed Many forms of tinnitus are plasticity disorders

Slide 38 :

The sympathetic nervous system is involved in some forms of pain and in some forms of severe tinnitus Reflex sympathetic dystrophy (RSD) (Complex regional pain syndrome; CRPS type I) Some forms of tinnitus can be cured by sympathectomy

Slide 39 :

Management of central neuropathic pain and tinnitus Two different approaches: Treat the condition Treat the cause (reverse the plastic changes)

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Successful treatment depends on: Diagnosis of the different forms of tinnitus Selection of adequate treatment

Slide 41 :

Questions to be asked for diagnosis of tinnitus

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1. What is the anatomical location of the physiological abnormality? The ear The auditory nerve The central auditory nervous system

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2. What is the abnormality that causes tinnitus? Hyperactivity? Reduced inhibitory input from the ear Is the auditory system in itself hyperactive? Rerouting of information? Is the non-classical nervous system involved? Is the auditory cortex re-organized?

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Who should diagnose and treat patients with severe tinnitus? Audiologists Otolaryngologists Neurologists Psychiatrists Neurosurgeons

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Therapy There is no treatment for tinnitus that is comparable to common pharmacological treatment of pain.

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Medical treatment Pain Analgesics: Opioids, etc. Tinnitus Benzodiazepines Enhance GABAergic inhibition

Slide 47 :

Reversal of neural plasticity Pain “TENS” (Transderm electric nerve stimulation) Dorsal column stimulation Stimulation of the (motor) cortex Stimulation of the thalamus

Slide 48 :

Reversal of neural plasticity Tinnitus Sound stimulation (TRT) Electrical stimulation of the ear (cochlear implants) Microvascular decompression Stimulation of the auditory cortex Stimulation of the thalamus?

Slide 49 :

Stimulation of somatosensory system can relieve tinnitus Electrical stimulation of the ear or the skin behind the ears has been used to treat tinnitus Few systematic studies of efficacy have been published

Slide 50 :

Stimulation of the auditory cortex Magnetic or electrical stimulation of the auditory cortex May function because it activates the thalamus through the cortico- thalamic efferents

Slide 51 :

From: Møller: Sensory Systems, 2003 Ascending pathways from the central nucleus of the inferior colliculus (ICC) to the ventral portion of the MGB and their connections to auditory cortical radiations. Most of the connections have reciprocal descending connections; only one of which are shown (between AI and the MGB). M: Medial (or magnocellular) division of MGB, D: Dorsal division, V: ventral division. OV: ovoid part of the MGB.

Slide 52 :

Approval of treatments The use of currently established test criteria (double blind) for new treatments may impede development of effective treatments for many forms of tinnitus Placebo effect is considerable (often about 40%), but placebo effect is short lasting - treatment is expected to be long lasting Therefore, even a treatment that is not better than placebo in tests may be an effective treatment in praxis because its efficacy does not decrease over time as the effect of a placebo treatment does

Slide 53 :

Future Prediction is very difficult, especially about the future Niels Bohr

Slide 54 :

From where may progress in treatment of tinnitus come in the future? Multidisciplinary approach Better understanding of the function of the nervous system Better understanding of pathologies of the nervous system Better understanding of neural plasticity Learning from other disorders such as pain

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FutureProgress in so many other areas of care of the sick has depended on Studies of epidemiology Basic research (pathophysiology) Clinical research (experience of different kinds of treatment)

Slide 56 :

Important to have words for disorders We cannot think about matters that do not have names The same words are used to describe very different forms of tinnitus and pain Using the same names for fundamentally different disorders hamper treatment

Slide 57 :

CONCLUSIONS Tinnitus is far more complex than earlier assumed Expression of neural plasticity is involved in many forms of tinnitus Better methods for diagnosis of tinnitus are needed Understanding the pathophysiology of tinnitus is important for development of new treatments

Slide 58 :

REFERENCE LITERATURE 1. Langguth, B., Hajak, G., Kleinjung, T., Cacace, Møller, A. 2007. Tinnitus, Pathophysiology and Treatment. Progress in Brain Research 166, 1-542. 2. Møller, A.R. 2006. Hearing: Anatomy, Physiology, and Disorders of the Auditory System, 2nd Ed. Academic Press, Amsterdam. 3. Møller, A.R. 2007. Tinnitus and Pain. In: Langguth, B., Hajak, G., Kleinjung, T., Cacace, A., 4. Møller, A.R., (Eds.), Tinnitus: Pathophyiology and Treatment, Vol. 166. Elsevier, Amsterdam. pp. 47-53.

	armoller@gmail.com 1 Years ago. Category: Otolaryngology

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