The Brain Bases of Phantom Auditory Phenomena: From Tinnitus to Hearing Voices

Cynthia Gayle Wible, Ph.D.*

Harvard Medical School

VA Boston Healthcare System

940 Belmont Street

Psychiatry 116A

Brockton, MA 02301

*Corresponding Author:

Dr. Cynthia G. Wible

Laboratory for Neuroscience

Harvard Medical School

Psychiatry Department 116A

VA Boston Healthcare System

940 Belmont Street

Brockton, MA 02301

Fax 508-586-0894

cindy@bwh.harvard.edu

Abstract

The phenomenology and neural bases of phantom auditory perceptions are reviewed. A variety

of phantom auditory phenomena are discussed, from tinnitus to hearing voices. It is claimed that

the phenomenology or qualia of the hallucinatory experience may correspond to how the

auditory system is organized into functional regions (neural architecture) and how auditory

percepts are represented at the single neuron level within this system. There may be a one-to-

one correspondence between the type of experience (e.g., hearing a tone versus hearing a voice)

and the representational qualities or aspects of sound representation in different parts of the

auditory and speech processing stream or system. The literature does not support the supposition

that certain features of auditory hallucinations correspond to either neurological or psychiatric

disease. Clinical aspects of auditory hallucinations are also discussed that may be of interest to

clinical practitioners with patients who have auditory hallucinations.

Keywords: auditory hallucinations, tinnitus, music hallucinations, voices, schizophrenia

1

The phenomenology of phantom auditory phenomena.

Phantom auditory phenomena or auditory hallucinations (AH) consist of auditory perception in

the absence of external stimulation. AH range from hearing short simple sounds to hearing

voices (speech). Voice hallucinations also range from simple short lived phenomena (hearing

one’s name called) to hearing full sentences or dialogues and the feeling of a presence of a being

or entity. This apparent continuum of complexity may be related to the characteristics of the

brain regions that are involved in the hallucination; this will be discussed in the next section.

AH can arise for a number of reasons, but are thought to arise from central brain dysfunction or

abnormal activity in the brain. Even tinnitus, a simple form of auditory hallucination, which is

characterized by hearing a buzzing, ringing or tone sound, is thought to result from abnormal

brain activity and is not usually alleviated by peripheral treatments1. So, although tinnitus is

often precipitated by hearing loss or peripheral damage, the experience of hearing tinnitus

sound(s) comes from abnormal activity in the brain. Tinnitus is common and has been

estimated to occur in up to 20% of the population 2. Like tinnitus, musical hallucinations are

most often associated with either hearing loss or neurological damage, but this is not the case

with voice hallucinations3. If voices are heard in neurologically-impaired patients, they are often

localized on one side and hence don’t have the same experiential quality as hearing a “real”

voice4. Auditory hallucinations of voices or auditory verbal hallucinations (AVH) are the most

frequent symptom of schizophrenia. Bleuler 5 observed that “Almost every schizophrenic who is

hospitalized hears voices, occasionally or continually.” Silbersweig & Stern6 estimated that up

to 74% of schizophrenic patients hear voices, which can be experienced as conversing with each

other or commenting on ongoing behavior and are often sentences or dialogs, not just single

words. Schizophrenic AVH are usually very different from the common auditory hallucination

2

of hearing one’s name that occurs in neurologically healthy individuals7. Schizophrenic AVH or

voices are experienced as coming from a person or a presence and seem “real” as if someone is

actually speaking. There is often an elaborate system of beliefs and attributions concerning the

voice and its origins. There may be more than one voice and the voices can have conversations

with each other. Some patients hear voices that comment on their ongoing behavior. Some have

the feeling that the voice constitutes another person inside of their body. The voices may also

have a frightening or punitive tone. A first person account of what it is like to hear voices was in

a special issue of the journal Cognitive Neuropsychiatry that was dedicated to the topic of

auditory hallucinations; the following is a quote from an article by Cockshutt8:

“For me, and I can only speak for myself, the voices are externalized …. and real. There

is no point in pretending otherwise. I could say that I understand that they are a false

manifestation of my internal thoughts. The truth is that for me that is the unreal aspect of

it all because by pretending to believe that the voices are unreal I am, in essence, creating

a false reality.”

In summary, auditory hallucinations form a continuum of complexity. On one end are simple

tones and noises, followed by music which is more complex and organized. Voice hallucinations

may be next in the continuum, and can also be categorized within the speech system as simple

(hearing brief single words or unintelligible speech-like sounds) or more complex (hearing a

voice or voices speaking full sentences or dialogs accompanied by a feeling that the voice has an

external source or is real or corporeal). The next section of this article will describe

representational aspects of the auditory speech system in the brain that may correspond to the

phenomenological aspects of auditory hallucinations.

3

The brain bases of phantom auditory phenomena: Tones and Speech.

In the previous section, a continuum of complexity in AH was described that can range from

hearing simple tones to hearing a voice with a feeling of a source or a feeling that it comes from

a real person. The later type of hallucination is most often associated with schizophrenia

(hearing a voice narrative with a feeling of a source or presence). However, brain lesions can

produce schizophrenia-like voice hallucinations9. Therefore, the type of hallucination

experienced may depend on the brain areas involved, not the type of disease. The cortex is made

up of small functional regions of neurons that respond similarly; the size and juxtaposition of

these cortical maps is what I refer to as “architecture.” The adjacency or cortical location of a

map can convey an abundance of information about what type of inputs it receives, the output of

the computation, and the function of the region. For example, neurons within a region might all

respond to faces more than other visual attributes or they might respond to visual objects and

also exhibit size and shape constancy. These attributes constitute information about the neuronal

representation. The size and shape of these regions varies considerably, especially beyond

primary cortical regions where a columnar organization may be present. I will review evidence

that the continuum of complexity in AH matches the representational structure and cortical

architecture of progressively higher order auditory cortical regions. This type of correspondence

between hallucinations and cortical architecture and representation has been found in the visual

system. Unlike language, the visual system in non-human primates is comparable to humans and

has been mapped in great detail. Visual cortex is divided into different regions whose neurons

respond primarily to color, to objects, to faces and other visual categories. A one-to-one

correspondence was found between the type of visual hallucination experienced in human

subjects and activity in visual regions such that color hallucinations were associated with activity

4

in visual regions representing color, face hallucinations were associated with activity in those

cortical regions representing faces and so on10,11.

Within this framework, hearing simple tones or ringing sounds would correspond to a

dysfunction of more primary, tonotopically-organized regions of cortex. It is well known from

single unit or single neuron recording in animals that the primary auditory cortex is tonotopically

organized into maps where neurons within a small region respond optimally to tones within a

specific frequency and nearby regions respond to surrounding frequencies. Mirror symmetric

tonotopic maps resembling those previously found in macaque monkeys have now been found in

the human primary auditory cortex12. These investigators used very high resolution functional

magnetic resonance imaging (FMRI) and found mirror symmetric tonotopic maps in Heschl’s

gyrus or primary auditory cortex that shared a low frequency border. Primary auditory cortex

has been implicated as a generator of tinnitus in animals and human subjects. For example, the

modulation of (both excitatory and inhibitory) activity in primary auditory cortex was found to

be the basis of tinnitus in a recent report using an animal model whose results replicated previous

work13. If primary auditory cortex is responsible for the experience of tinnitus, then interventions

that change brain activity in this region should affect tinnitus in human subjects. Human

neuroimaging and magnetoencephalography (MEG) studies show that the primary auditory

cortex is reorganized in subjects with tinnitus. There is an expansion of the frequency

representation in the auditory cortex that corresponds to the perceived tinnitus frequencies; the

degree of the shift is related to the severity of the tinnitus 14,15. These findings have been used to

successfully treat tinnitus in a patient with auditory nerve damage who was deaf in the left ear.

FMRI was used to map out the auditory response in primary auditory cortex and to visualize the

abnormally-activated regions. This FMRI activity was used as a guide to place electrodes for

5

focal extradural electrical stimulation of the primary auditory cortex. This procedure was

reported to suppress tinnitus completely15. Recently, researchers have begun to investigate

hypotheses about the interactions between other regions and auditory cortex in inhibiting

tinnitus, but current evidence suggests that the perception is clearly generated within primary

auditory cortex16. Hence, abnormal activity or over-activation in the primary auditory cortex that

is tonotopically organized corresponds to the experience of hearing tones or simple sounds when

none are present in the environment. The next section will explore the possibility that more

complex auditory hallucinations such as speech are also a result of neural overactivation and that

the phenomenological aspects of the hallucinations can be linked to the neuronal representational

properties and architecture of higher order cortical regions that are further up in the stream of

auditory processing.

Neural bases of speech perception and production

This describes progressively higher order auditory processing stages that form the neural basis of

speech perception. Although these regions are subsequent to primary auditory cortex, the

processing of information is thought to be highly recursive and interactive and does not proceed

in a strictly linear fashion. For speech perception, a spectral-temporal analysis of the auditory

signal is performed in primary auditory cortex, and an auditory phonological representation is

activated in the middle portion of the superior temporal sulcus (STS) (see Figure 1). A more

posterior region of the STS houses amodal (or multimodal) phonological representations and can

be activated by written or spoken words. To initiate speech production, these representations are

then translated into prearticulatory motor codes for the vocal tract in

6

the Sylvian parietal-temporal area (Spt), a region near the temporal-parietal boundary (this

summary is based on a model and synthesis from Hickok and Poeppel17,18). Spt interacts with

middle and inferior frontal regions to produce the articulatory codes for speech production. The

posterior STS and Spt are active during speech perception, production and during subvocal

rehearsal for working memory. Phonemic representations in the STS also make contact with

widespread semantic representations in the temporal lobe and other regions. Over-activation that

extends beyond primary auditory cortex would be predicted to cause the perception of phonemes

(perhaps in the form of incomprehensible words) or whole single word auditory representations.

Hug et al.4 described an epileptic patient who exhibited a progressive auditory hallucination such

that tonal tinnitus transformed into the perception of noise and then finally to incomprehensible

voices, as would be predicted from the structure of the auditory speech system.

7

Figure 1. Regions involved in speech perception and production. Several posterior language regions that are involved in the perception and production of speech17,18. The primary auditory cortex (green), a middle portion of the superior temporal sulcus [STS] (yellow) that houses auditory phonological representations. An amodal phonological region (dark blue) in the posterior STS that is involved in amodal phonological representation. The Sylvian-parietal-temporal (Spt) in light blue usually in the left hemisphere provides the interface between the phonological networks in the bilateral superior temporal gyrus and STS and the articulatory networks in the anterior or prefrontal language system.

Voices are usually experienced within a social context and within conversation with another

person. Under naturalistic conditions, auditory voice and visual face and body gestures are

experienced simultaneously. The audiovisual nature of the speech signal is reflected in an area

that is in the posterior region of the STS, or PSTS. A large portion of this region is dedicated to

audiovisual speech processing in human subjects. This area (especially the right PSTS) functions

in the recognition of voices, as opposed to recognizing verbal or semantic content19. The PSTS

is part of a system that extends upward into the inferior parietal region where intentions are

formed and sent to motor regions of the brain. The PSTS and inferior parietal regions are often

referred to as the temporal-parietal occipital junction (TPJ). This system, or collection of tightly

functionally coupled regions, has interesting representational and architectural properties that

may correspond to characteristics present in schizophrenia-like voice hallucinations.

The audiovisual signal that conveys speech also contains information about person identity

(agency), as well as information about intentions and emotional state (in the form of prosody and

emotional gestures). TPJ functionality reflects the fact that the voice is experienced

simultaneously with social representations of persons and emotion. A dominant role of this

region is in the representation of dynamic multimodal gestures (primarily sight, sound and

touch), including audio-visual speech20. Audiovisual speech representation is adjacent to or

partially overlapping in the TPJ with the neural territory responsible for prosody perception

(prosody is the melodic quality of the voice that can convey both emotion and meaning), the

perception of emotional expressions, the perception of eye gaze, and the perception of social

attention21-27. .

8

The coding of agency (or intention or purpose) is automatically activated or perceived along with

gestures or movements and is an inherent part of the representation. Jellema et al.28 recorded

neuronal activity within monkey STS that combined information about reaching or grasping with

activity related to attention or gaze direction. This combination of information results in a

cellular representation of the intentionality of movements28. FMRI studies in human subjects

show that the PSTS is the only brain region in humans that responded differentially to intentional

versus unintentional movement, leading to the conclusion that this region is a core substrate for

conveying the perception of agency29. The consequence of this coupling of gesture with a code

for agency is that if the speech representations in TPJ were erroneously activated, then there

would be an accompanying feeling of agency or a feeling of someone acting. Hence, over-

activation of audio-visual speech gestures could cause the perception of a voice and the feeling

of a presence with intentions. This could be the basis of a feeling of a source or presence that

accompanies the auditory hallucination of a voice in schizophrenia-like voice hallucinations.

This could also be an underlying reason for the often elaborate system of beliefs about the

purpose and origin of the voice. There is direct evidence for these suppositions: Cortical

stimulation of the TPJ in a non-psychotic human subject produced a feeling of a shadowy

presence, and the subject imbued this presence with certain intentions30. In other words, the

voice hallucinations feel real because they activate the part of cortex that corresponds to the

perception of speaking to another person; at this cortical level of processing, the intention of the

person and the audio-visual speech signal are encoded and perceived automatically and

simultaneously.

9

When audio-visual representations are activated in the PSTS, neurons provide rapid feedback

input to unimodal sensory regions, and especially to the auditory cortex in both animals and

humans 26,27,31. This feedback is automatic and occurs without conscious attention. Hence, the

over-activation or erroneous activation of audio-visual speech representations excites earlier

auditory regions and could perpetuate abnormal neural activity.

Another aspect of schizophrenia-like voice hallucinations is that the voices often speak in dialogs

or narratives. The TPJ (bilaterally) is preferentially involved in narrative comprehension,

ascompared to word or even sentence comprehension28. Therefore, this region may be used to

both perceive and construct narratives. This observation might account for the fact that

schizophrenic subjects are deficient in generating or building linguistic context and in

understanding narrative32.

The TPJ is also selectively involved in the theory of mind or the ability to attribute and represent

other’s mental states (also an important part of social communication and understanding speech

and actions) as well as in self representation21,22,25. Figure 2 shows the overlapping functionality

in this region and depicts the approximate cortical regions for many of the functions discussed in

this section 33-38. In fact, the TPJ may be the core region in the brain that underlies the

perception of social interaction24,33. Simply put, over-activation of this region may cause the

perception of social interaction such as being in a conversation with another person or hearing a

conversation. As discussed above, the overlap between voice and dynamic person and emotion

representation may be the basis for the experience of a voice and of a presence that constitutes

schizophrenia-like auditory hallucinations.

10

There are several lines of evidence that the TPJ is involved in schizophrenia-like auditory

hallucinations26,27. First, a lesion in the TPJ, or epilepsy, can cause schizophrenia-like psychoses,

including AVH9,27. One of the most accurate but difficult ways to study auditory voice

hallucinations is the symptom capture method. In this method, the brain is imaged during the

hallucination and also during periods when the hallucination is absent. One of the best symptom

capture studies of schizophrenic voice hallucinations was performed using a patient whose

hallucinations had a periodicity (the hallucination would last for approximately 26 seconds with

a period of silence for 26 seconds) that matched well with the requirements of FMRI imaging 39.

This study showed that activity in the PSTS and middle temporal region was evident

immediately before the hallucination. Also, the neural activity persisted throughout the

11

Figure 2. Summary figure of the overlap of functional regions in the TPJ (inferior parietal and PSTS) involved in eye gaze (red); audiovisual speech (light blue); self representation (yellow); theory of mind/agency (green); emotional perception of faces and prosody (dark blue). Re-representation of data respectively from references34-38.

hallucination and spread to inferior parietal and then to frontal cortex. This case study is

consistent with the supposition that schizophrenia-like auditory hallucinations of voices arise

from activity in the TPJ40. Additional supporting evidence for this theory comes from reports

that transcranial magnetic stimulation (TMS) applied to the TPJ has also been found to alleviate

schizophrenic auditory hallucinations (as well as other symptoms)41. TMS uses a coil to apply

electromagnetic energy to the patient’s scalp/skull and has the ability to suppress or alter patterns

of neural activity in brain regions beneath the coil.

Music Hallucinations

Where in the auditory processing stream does the perception of music occur? There is relatively

little research on the perception of musical hallucinations and on music perception in general,

apart from other types of auditory perception. Apparently, the neural territory for music

perception overlaps with speech perception in the superior temporal cortex 42,43. However, music

was found to activate more dorsomedial regions, including insular and inferior parietal regions42.

A review of musical hallucinations concluded that they can result from underlying pathology in

the ear or the brain44. The findings that music activates more dorsomedial regions are consistent

with a report of a patient who developed musical hallucinations after resection of a right insular

glioma45. However, additional studies are needed to determine the underlying neural basis of

music hallucinations because the findings are somewhat divergent in this area of research46,47.

Clinical aspects and implications of auditory hallucinations.

Auditory hallucinations -- especially music and voice hallucinations -- are thought to be under-

reported. Brain regions involved in producing auditory hallucinations are also involved in

normal hearing, auditory attention, and working memory tasks. Therefore, all of these functions

12

may be impaired in patients with auditory hallucinations. These factors should be considered

when evaluating patients who may be experiencing hallucinations. Oliver Sacks describes

several case studies of persons with musical hallucinations in his book Musicophilia 48,

whichprovides insight into these unusual experiences, including the emotional reactions and

coping strategies of patients with music hallucinations. This book is recommended reading for

patients with music hallucinations, their family members and health care providers.

Auditory hallucinations can be associated with various etiologies, including brain damage,

epilepsy, psychiatric disorders or hearing loss. One report of patients referred for hearing

impairment showed a high prevalence of auditory hallucinations (33%) that consisted of

“humming or buzzing (35.9%), shushing (12.8%), beating or tapping (10.6%), ringing (7.7%),

other individual sounds (15.4%), multiple sounds (12.6%), voices (2.5%) or music (2.5%)”49.

Patients who experience music or voice hallucinations would probably benefit from a

neurologic or psychiatric consultation. This is especially true if the hallucinations are present

for extended periods (months or longer), and are distressful or interfering with daily function.

One study indicated that patients who hear auditory hallucinations, and especially voices, felt

that they would benefit if they could describe the experience in more detail with health

practitioners50. Clinicians asking questions about the content and sensory aspects of the

hallucination may comfort patients and may also provide valuable information about treatment

strategies and referrals.

Voice hallucinations in particular can be a prominent and sometimes defining feature of

schizophrenia. Schizophrenia is often accompanied by other symptoms such as hallucinations of

people and delusions (e.g., people are spying on me, watching me, etc.) as well as affective

13

inexpressiveness and attention deficits. However, voice hallucinations that comment on the

patient’s actions or that consist of hearing two or more voices conversing may alone indicate

schizophrenia if they are experienced for more than two months (see the Diagnostic and

Statistical Manual of Mental Disorders for diagnostic criteria and more specific information).

Because voices can sometimes command patients to harm themselves or others, clinicians should

be vigilant for this type of hallucination. Strategies exist that can be used to assess the negative

characteristics of unpleasant voices and to assess the potential risk resulting from hearing voices

51. Behavior management protocols (such as listening to music and other coping skills) can be

taught to patients with persistent auditory hallucinations51.

Summary

This article reviewed evidence for understanding auditory hallucinations within a framework that

is based on the functional architecture and single neuron representational properties of the

auditory processing stream. Hallucinations of short-lived sounds may correspond to the aberrant

activation of more primary auditory regions. Hallucinations of voices and a feeling of a presence

or that someone is speaking may correspond to the activation of audiovisual speech

representations in the TPJ. In the normal brain, this region is activated when someone is actually

speaking. These gesture representations automatically convey agency and intention, and

synchronize speech regions. The TPJ is also used to perceive and construct narratives, a feature

that may account for the elaborate conversational nature of schizophrenia-like auditory voice

hallucinations. Auditory hallucinations are frequently reported by patients in audiology clinics.

The brain regions that were described to be involved in auditory hallucinations are also used for

speech perception, speech production and working memory. Some of these neural regions are

14

also used for affect perception and production (in the form of gestures and prosody) and social

attention. Therefore, clinicians should be sensitive to the fact that hallucinations may interfere

with these functions. Patients who experience hallucinations report a need to discuss the

phenomenological aspects of the hallucinations and their meaning with caretakers. An

assumption underlying the framework described in this article is that the experiences seem very

real and are not under the control of the patient. The type of auditory hallucination (simple or

schizophrenia-like) does not show a one-to-one correspondence to the cause (e.g. psychosis,

epilepsy, hearing loss). This observation should be kept in mind for patients who are referred to

other specialties (neurology, psychiatry) because the intensity, type of hallucination or distress

caused by the hallucination need to be considered in order to identify and implement an effective

treatment program.

15

Acknowledgements

This work was supported by an NIMH grant: 1 R01 MH067080-01A2 and by the Harvard

Neuro-Discovery Center (formally HCNR). Funded also by the Biomedical Informatics Research

Network (U24RR021992); National Institute of Mental Health.

Conflict of Interest Statement: The author declares that the research was conducted in the

absence of any commercial or financial relationships that could be construed as a potential

conflict of interest.

Figure Legends.

Figure 1. Several posterior language regions that are involved in the perception and production

of speech (ref). The primary auditory cortex (green), a middle portion of the STS (yellow) that

houses auditory phonological representations. An amodal phonological region (dark blue) in the

posterior STS that is involved in amodal phonological representation. The Sylvian-parietal-

temporal (Spt) in light blue only in the left hemisphere provides the interface between the

phonological networks in the bilateral superior temporal gyrus and STS and the articulatory

networks in the anterior or prefrontal language system.

Figure 2. Summary figure of the overlap of functional regions in the TPJ (inferior parietal and

PSTS) involved in eyegaze (red); audiovisual speech (light blue); self representation (yellow);

theory of mind/agency (green); emotional perception of faces and prosody (dark blue). Re-

representation of data respectively from references (Nummenmaa et al., 2010; Wright et al.,

2003; Blanke and Arzy, 2005; Young, Dodell-Feder, & Saxe, (2010); Adolfs et al., 2002).

16

References

1. Folmer RL, Griest SE, Martin WH. Chronic tinnitus as phantom auditory pain.

Otolaryngol Head Neck Surg. 2001 Apr;124(4):394-400. PubMed PMID: 11283496.

2. Demeester K, van Wieringen A, Hendrickx JJ, Topsakal V, Fransen E, Van Laer L, De

Ridder D, Van Camp G, Van de Heyning P. Prevalence of tinnitus and audiometric

shape. B-ENT. 2007;3 Suppl 7:37-49. PubMed PMID: 18225607

3. David, A. S. (2004). The cognitive neuropsychiatry of auditory verbal hallucinations: an

overview. Cognitive Neuropsychiatry, 9(1–2), 107–123.

doi:10.1080/13546800344000183.

4. Hug A. Bartsch A. Gutschalk A. (2011) Voices behind the left shoulder: Two patients

with right-sided temporal lobe epilepsy. Journal of the Neurological Sciences 305 (2011)

143–146.

5. Bleuler, E. (1950). Dementia praecox; or, the group of schizophrenias (1911) (J. Zinkin,

Trans.). New York: International UniversitiesBleuler, E. (1950).

6. Silbersweig, D., & Stern, E. (1996). Functional neuroimaging ofhallucinations in

schizophrenia: toward an integration of bottomup and top-down approaches. Molecular

Psychiatry, 1(5), 367–375.

7. Ohayon MM, Priest RG, Caulet M, Guilleminault C. Hypnagogic and hypnopompic

hallucinations: pathological phenomena? Br J Psychiatry. 1996 Oct;169(4):459-67.

PubMed PMID: 8894197.

8. Cockshutt G. Choices for voices: a voice hearer's perspective on hearingvoices. Cogn

Neuropsychiatry. 2004 Feb-May;9(1-2):9-11. PubMed PMID: 1657157.

17

9. Peroutka, S.J. et al. (1982). Hallucinations and delusions following a right

temporoparietooccipital infarction. Johns Hopkins Med J 151, 181-185.

10. Ffytche, D. H., Howard, R. J., Brammer, M. J., David, A., Woodruff, P., & Williams, S.

(1998). The anatomy of conscious vision: an fmri study of visual hallucinations. Nature

Neuroscience, 1(8), 738– 742. doi:10.1038/3738.

11. Santhouse, A. M., Howard, R. J., & ffytche, D. H. (2000). Visual hallucinatory

syndromes and the anatomy of the visual brain. Brain, 123(Pt 10), 2055–2064.

doi:10.1093/brain/123.10.2055. PMID: 18225607

12. Formisano et al. 2003. Mirror-symmetric tonotopic maps in human primary auditory

cortex. Neuron. Nov 13;40(4):859-69

13. Yang S, et al., 2011 Homeostatic plasticity drives tinnitus perception in an animal model.

Proc Natl Acad Sci U S A. 2011 Sep 6;108(36).

14. Mühlnickel W, Elbert T, Taub E, et al: Reorganization of auditorycortex in tinnitus. Proc

Natl Acad Sci USA 95:10340–10343, 1998

15. De Ridder D, De Mulder G, Walsh V, Muggleton N, Sunaert S, Møller A. Magnetic and

electrical stimulation of the auditory cortex for intractable tinnitus. Case report. J

Neurosurg. 2004 Mar;100(3):560-4.

16. Rauschecker JP, Leaver AM, Mühlau M. Tuning out the noise: limbic-auditory

interactions in tinnitus. Neuron. 2010 Jun 24;66(6):819-26. PubMed PMID: 20620868;

PubMed Central PMCID: PMC2904345.

17. Hickok, G., & Poeppel, D. (2004). Dorsal and ventral streams: a framework for

understanding aspects of the functional anatomy of language. Cognition, 92(1–2), 67–99.

doi:10.1016/j.cognition. 2003.10.011.

18

18. Hickok, G., & Poeppel, D. (2007). The cortical organization of speech processing. Nature

Reviews. Neuroscience, 8(5), 393–402. doi:10.1038/nrn2113.

19. Kriegstein KV, Giraud AL. Distinct functional substrates along the right superior

temporal sulcus for the processing of voices. Neuroimage. 2004 Jun;22(2):948-55.

PubMed PMID: 15193626.

20. Pelphrey, K.A., Morris, J.P., Michelich, C.R., Allison, T., and Mccarthy, G. (2005).

Functional anatomy of biological motion perception in posterior temporal cortex: an

FMRI study of eye, mouth and hand movements. Cereb Cortex 15, 1866-1876.

21. Baron-Cohen, S., Wheelwright, S., and Jolliffe, T. (1997). Is There a "Language of the

Eyes"? Evidence from Normal Adults, and Adults with Autism or Asperger Syndrome.

Visual Cognition 4, 311-331.

22. Decety, J., and Lamm, C. (2007). The role of the right temporoparietal junction in social

interaction: how low-level computational processes contribute to meta-cognition.

Neuroscientist 13, 580-593.

23. Puce, A., and Perrett, D. (2003). Electrophysiology and brain imaging of biological

motion. Philos Trans R Soc Lond B Biol Sci 358, 435-445.

24. Redcay, E. (2008). The superior temporal sulcus performs a common function for social

and speech perception: implications for the emergence of autism. Neurosci Biobehav Rev

32, 123-142.

25. Saxe, R., and Wexler, A. (2005). Making sense of another mind: the role of the right

temporo-parietal junction. Neuropsychologia 43, 1391-1399.

19

26. Wible, C.G., Preus, A.P., and Hashimoto, R. (2009). A Cognitive Neuroscience View of

Schizophrenic Symptoms: Abnormal Activation of a System for Social Perception and

Communication. Brain Imaging Behav 3, 85-110.

27. Wible, C.G. Hippocampal Temporal-Parietal Junction Interaction in the Production of

Psychotic Symptoms: A Framework for Understanding the Schizophrenic Syndrome, in

submission.

28. Jellema, T., Baker, C.I., Wicker, B., and Perrett, D.I. (2000). Neural representation for

the perception of the intentionality of actions. Brain Cogn 44, 280-302.

29. Morris, J. P., Pelphrey, K. A., & McCarthy, G. (2008). Perceived causality influences

brain activity evoked by biological motion. Soc Neurosci, 3(1), 16-25.

30. Blanke, O., Ortigue, S., Landis, T., & Seeck, M. (2002). Stimulating illusory own-body

perceptions. Nature, 419(6904), 269–270. doi:10.1038/419269a.

31. Ghazanfar, A.A., Chandrasekaran, C., and Logothetis, N.K. (2008). Interactions between

the superior temporal sulcus and auditory cortex mediate dynamic face/voice integration

in rhesus monkeys. J Neurosci 28, 4457-4469.

32. Ditman, T., and Kuperberg, G.R. (2010). Building coherence: A framework for exploring

the breakdown of links across clause boundaries in schizophrenia. J Neurolinguistics 23,

254-269.

33. Redcay, E., Dodell-Feder, D., Pearrow, M.J., Mavros, P.L., Kleiner, M., Gabrieli, J.D.,

and Saxe, R. (2010). Live face-to-face interaction during fMRI: a new tool for social

cognitive neuroscience. NeuroImage 50, 1639-1647.

20

34. Nummenmaa, L., Passamonti, L., Rowe, J., Engell, A.D., and Calder, A.J. (2010).

Connectivity analysis reveals a cortical network for eye gaze perception. Cereb Cortex

20, 1780-1787.

35. Wright, T.M., Pelphrey, K.A., Allison, T., Mckeown, M.J., and Mccarthy, G. (2003).

Polysensory interactions along lateral temporal regions evoked by audiovisual speech.

Cereb Cortex 13, 1034-1043.

36. Blanke, O., and Arzy, S. (2005). The out-of-body experience: disturbed self-processing at

the temporo-parietal junction. Neuroscientist 11, 16-24.

37. Young, L., Dodell-Feder, D., and Saxe, R. (2010). What gets the attention of the

temporo-parietal junction? An fMRI investigation of attention and theory of mind.

Neuropsychologia 48, 2658-2664.

38. Adolphs, R., Damasio, H., and Tranel, D. (2002). Neural systems for recognition of

emotional prosody: a 3-D lesion study. Emotion 2, 23-51.

39. Lennox, B. R., Park, S. B., Jones, P. B., & Morris, P. G. (1999). Spatial and temporal

mapping of neural activity associated with auditory hallucinations. Lancet, 353(9153),

644. doi:10.1016/S0140-6736(98)05923-6.

40. Allen P, Larøi F, McGuire PK, Aleman A. The hallucinating brain: a review of structural

and functional neuroimaging studies of hallucinations. Neurosci Biobehav Rev.

2008;32(1):175-91. Epub 2007 Aug 15. Review. PubMed PMID: 17884165.

41. Hoffman RE, Gueorguieva R, Hawkins KA, Varanko M, Boutros NN, Wu YT, Carroll K,

Krystal JH. Temporoparietal transcranial magnetic stimulation for auditory

hallucinations: safety, efficacy and moderators in a fifty patient sample. Biol Psychiatry.

2005 Jul 15;58(2):97-104. PubMed PMID: 15936729.

21

42. Rogalsky C, Rong F, Saberi K, Hickok G. Functional anatomy of language and music

perception: temporal and structural factors investigated using functional magnetic

resonance imaging. J Neurosci. 2011 Mar 9;31(10):3843-52. PubMed PMID: 21389239;

PubMed Central PMCID: PMC3066175.

43. Peretz I, Gosselin N, Belin P, Zatorre RJ, Plailly J, Tillmann B. Music lexical networks:

the cortical organization of music recognition. Ann N Y Acad Sci. 2009 Jul;1169:256-65.

PubMed PMID: 19673789.

44. Cope TE, Baguley DM. Is musical hallucination an otological phenomenon? A review of

the literature. Clin Otolaryngol. 2009 Oct;34(5):423-30. Review. PubMed PMID:

19793274.

45. Isolan GR, Bianchin MM, Bragatti JA, Torres C, Schwartsmann G. Musical

hallucinations following insular glioma resection. Neurosurg Focus. 2010Feb;28(2):E9.

PubMed PMID: 20121444.

46. Mori T, Ikeda M, Fukuhara R, Sugawara Y, Nakata S, Matsumoto N, Nestor PJ, Tanabe

H. Regional cerebral blood flow change in a case of Alzheimer's disease with musical

hallucinations. Eur Arch Psychiatry Clin Neurosci. 2006 Jun;256(4):236-9. Epub 2005

Nov 29. PubMed PMID: 16311897.

47. Griffiths TD. Musical hallucinosis in acquired deafness. Phenomenology and brain

substrate. Brain. 2000 Oct;123 ( Pt 10):2065-76. PubMed PMID: 11004124.

48. Sacks, O. Musicophilia: Tales of Music and the Brain (2007) Alfred A. Knopf, Canada.

ISBN 1400040817

22

49. Cole MG, Dowson L, Dendukuri N, Belzile E. The prevalence and phenomenology of

auditory hallucinations among elderly subjects attending an audiology clinic. Int J Geriatr

Psychiatry. 2002 May;17(5):444-52. PubMed PMID: 11994933.

50. Coffey M, Hewitt J. 'You don't talk about the voices': voice hearers and community

mental health nurses talk about responding to voice hearing experiences. J Clin Nurs.

2008 Jun;17(12):1591-600. PubMed PMID: 18482121.

51. Buccheri RK, Trygstad LN, Buffum MD, Lyttle K, Dowling G. Comprehensive

evidence-based program teaching self-management of auditory hallucinations on

inpatient psychiatric units. Issues Ment Health Nurs. 2010 Mar;31(3):223-31. PubMed

PMID: 20144034.

23