Neurobiology of Auditory Hallucination in Schizophrenia

Auditory hallucination, or the erroneous sense of sound, is a symptom of schizophrenia. Despite the fact that auditory hallucinations are one of the most common symptoms of schizophrenia, little is known about how they occur. Based on many research materials and prior investigations, this review paper seeks to identify and summarize the current available information on the pathophysiology of auditory hallucinations. This research investigates the history and context of hallucinations in schizophrenia, as well as their development and the incidence of pathogenesis. It investigates the effects of auditory hallucinations on the human brain and brain activity.  Lastly, this paper looks at the treatment modes available for auditory hallucinations in schizophrenia including medical and therapeutic practices.

The Neurobiology of Auditory Hallucination in Schizophrenia

Introduction

Schizophrenia is a serious and chronic psychiatric disorder that upsets every aspect of a patient’s life. It is characterized by delusions, hallucinations, social withdrawal, and cognitive impairment (Mueser, 2004). The most predominant type of hallucination in schizophrenia is the auditory form of hallucination, followed by visual hallucination (Karia, Shah, De Sousa, & Sonavane, 2013). Auditory hallucinations are perceptions of external voices or external speech accompanied by a strong convincing sense of reality in the absence of a stimulus. They are the most common symptoms of schizophrenia. Schizophrenic individuals tend to experience false perceptions of sound, like hearing voices, music playing animal sounds, and other sounds such as footsteps and knocks. Research has shown that nearly 74% of patients identified with schizophrenia report cases of auditory hallucinations in the course of their disorder. Although auditory hallucinations constitute one of the leading symptoms of schizophrenia, there is little knowledge of how they develop.

Previous research and literature on auditory hallucinations have provided a brief history and background of and a phenomenal account of its pathogenesis that is clinically grounded (Handest, Klimpke, Raballo, A. et al. Rev. Phil. Psych 2016). Along with past research contributions, several other studies are being conducted by biological psychologists. The studies employ various neuroimaging techniques to determine the growth and development of the auditory hallucinations inside the human brain. Magneto-encephalographic studies have indicated that various forms of auditory hallucination in schizophrenia are caused by different neural activities in different regions of the brain (Reulbach Bleich, Maihofner, Kornhuber, & Sperling, 2007). Waters, Badcock, Michie, and Maybery (2006) developed a cognitive model that combines deficits in contextual memory and intentional inhibition. They found out that this combination is crucial in the development of auditory hallucinations. Failure in intentional inhibition creates unnecessary and uncontainable mental actions that are not acknowledged by the human brain because they do not have related cues that would ordinarily enable recognition.

Structural correlational meta-analysis studies have found a significant negative correlation between structural changes in the human brain and the severity of auditory hallucinations. Recent researchers have found out that magnetic stimulation, use of drugs ((Karia, Shah, De Sousa, & Sonavane, 2013), and cognitive-behavioral therapy have proven to be the best ways of treating persistent auditory hallucinations.

This paper review aims at identifying and providing a summary of the currently available information on the pathogenesis of the auditory hallucinations, basing on several research and previous studies. It explores the history and background of the hallucinations in schizophrenia, its development and the occurrence of the pathogenesis. It looks at the impact of the auditory hallucinations on the human brain and brain activities. It also looks at the treatment modes available for auditory hallucinations in schizophrenia including medical and therapeutic practices. This study aims at providing a deeper understanding of the development, pathogenesis, and progress of auditory hallucination in schizophrenia based on the views of early research and current neurological studies. Finally, it discusses the present medication and therapies available for treating obstinate auditory hallucinations.

History and Background

Green et al (1994) conducted a research on patients suffering auditory hallucinations and non-hallucinating patients using control groups. Hallucinations are said to cause sensory modality activation in specific areas of the brain that are involved in normal sensation. They affect the primary and association cortical and subcortical areas, Para limbic and limbic areas, Wernicke's and Broca’s areas, the ventral striatum, and the thalamus areas of the human brain.

Auditory hallucinations in schizophrenia can be examined using three characteristic dimensions:

The Perceptual dimension

This bases its argument on the idea of “hearing a voice”. The voices not only speak to the person but also pass some kind of electricity through the person’s body, beating and paralyzing the person. For the schizophrenia patients, auditory hallucinations are not imaginations but real perceptions. If auditory hallucinations are felt as sounds of someone speaking, it can be said that the person experiencing the hallucinations has a neuronal origin in the brain areas that encode the perception of normal speech. Normal perception of speech and sounds is encoded in a human's left posterior temporal lobe. Therefore, auditory hallucinations in schizophrenia can be defined as a speech perceptual phenomenon that is misattributed and misinterpreted to an external agent and is caused by hyper-excitation of neuronal activity in the posterior temporal lobe region of the human brain.

The Cognitive dimension

The cognitive dimension argues from the “cannot control the voice” point of view. After the person feels paralyzed by the voices, the electric feeling from the voices seems to take the person’s thoughts away. Cognitive theories that elucidate auditory hallucinations hold that inner speech is interpreted erroneously as emanating from an external source. Arguing from a cognitive point of view, people are said to perceive their thoughts as having sound. Patients with auditory hallucinations are said to hear sounds of sentences communicated to them by a real person. Cognitive theorists base their hypotheses on the possibility of confusions about the source of information or sounds they hear. It, therefore, argues that hallucinations are confusions.

The Emotional Dimension

This dimension views the voice heard as “evil”. The patient hears sounds that seem like curses and threats from the main and the most common content of the voices heard.

Auditory hallucinations, therefore, can be understood as coming from an internal speech which has not been clearly identified as emanating from outside an individual. This happens due to defective self-monitoring (Frith, 1992). Other scholars have recommended that the hallucinations can be observed as misattributions of speech, misinterpretations of internal experiences, misattributed cognition, and the competition between psychological resources and auditory stimuli. Developmental neuronal pathology is also considered as an internal generator of hallucinatory perceptions.

Speech Perception and Hemisphere Symmetry

There have been empirical tests to determine whether auditory hallucinations in schizophrenia are speech perception distortions and whether they are placed to the left hemisphere of the human brain. Experimental paradigms such as the dichotic listening (DL) paradigm are used to assess perception and localize the processing to either the right or left hemisphere. Patients are instructed to focus their attention and responses to only one of the ear stimulus, either left or right, so as to develop a stimulus-driven top-down or bottom-up processing conflict. In such a way, it is easier to assess attention contribution as well as the perception of the stimulus. Research has shown that there is an inverse relationship between right ear performance and auditory hallucinations. This supports the impression that auditory hallucinations in patients with schizophrenia inhibit speech perception sounds that emanate from the outside, which is localized to the left hemisphere, or the left temporal lobe (Hugdahl K., 2008).

Pathogenesis of Auditory Verbal Hallucinations

Although auditory hallucination in one of the most studied symptoms of psychiatry, its pathogenesis remains unknown to date. The most commonly reported symptoms of schizophrenia are the auditory verbal hallucinations. Recent empirical studies on phenomenological psychiatry have indicated that verbal hallucinations are caused by specific alterations in a patient’s self-awareness that involve both morbid objectification of inner speech and pathological changes in space experience (Frith, 1979). However, the major limitations to studying the pathogenesis of AHs include; generalizations that result from the reduction of this mental phenomenal group into specific experience structures; and the occurrence of the verbal hallucinations are quite sudden and sometimes accurate, which limits studies on the understanding of their formation. These limitations occur as a result of the unpredictable nature of the schizophrenia disease (Henriksen M.G, 2015).

Corollary Discharge Dysfunction

The malfunctioning of the efference copy or corollary discharge mechanisms can be a major source of schizophrenia, mainly auditory hallucinations. This malfunctioning compromises the patients' ability to make sensorimotor adaptations. However, researchers and various studies have not been able to demonstrate a vivid relationship between neurobiological indicators of malfunctioning of the corollary discharge mechanism and auditory hallucinations. This is because of the effects of medication for treatment of the symptoms and not the mechanism. It can also be as a result of the undetermined contribution of experienced hallucinations to the test measures taken (Ford J.M, 2005).

Functional Neuroimaging

Neuroimaging research has indicated a differential distribution of blood flow to the right and left superior temporal gyri (STG) during CV-syllables dichotic exhibitions. Various neuroimaging techniques have shown that language cortices and auditory association are active in schizophrenic patients affected by auditory hallucinations. Neuroimaging techniques have been used for the past two decades to examine the common symptoms of schizophrenia, mainly auditory hallucinations. It has greatly assisted researchers and scientists to clearly recognize the human brain regions and the networks entailed in assessing the symptom. Previous studies have indicated that variations in the anatomy as well as the function of cortical areas of the brain responsible for auditory perception and speech output are accountable for auditory hallucinations (Allen, Larøi, McGuire, & Aleman, 2008).

Neuroimaging Techniques

Structural Imaging Studies

These are studies used to analyze auditory hallucinations basing on voxel-based morphometry (VBM) and the region of interest (ROI). These studies have indicated that auditory hallucinations linked with a reduction in and gray matter volume situated in the bilateral superior temporal gyrus as well as the non-temporal lobe regions. The left superior temporal regions are involved in the perception of semantic and phonological characteristics of speech. The findings of these studies suggest that alterations in the neural systems that are involved at different levels of language processing are dangerous to auditory hallucinations in patients suffering from schizophrenia.

Functional Imaging

Functional imaging concentrates on studying patients with auditory hallucinations have reported functional and metabolic abnormalities in speech and language. An example of such studies is the positron emission tomography (PET) fluorodeoxyglucose (FDG-PET). Magnetic resonance perfusion imaging has indicated an increased cerebral blood flow in the left STG in patients diagnosed with auditory hallucinations. Patients suffering from AH also experience increased the likelihood of activation in the bilateral frontotemporal network. Dysfunction of these regions can trigger insufficient activation of language areas. A few functional imaging inquiries have commenced the process of examining neural associates of the emotional and phenomenological features of auditory hallucinations. Functional Magnetic Resonance Imaging is an example of functional neuroimaging and has proved to be an influential approach of assessing neural actions during auditory hallucinations (Woodruff et al 1995).

Gyrification studies

Gyrification refers to the abnormalities in the morphology of the cortical surface. Gyrification studies include post-mortem brain photography to check the relation between cortical folding in the patients’ temporal lobe and auditory hallucination. It has to do with the folding of the cerebral cortex. The most recent gyrification studies have shown that auditory hallucinations correlate with insular surface area. AH, pathophysiology has been said to cause functional abnormalities in a patient's language system.

Neurochemistry

This is a study to examine the relationship between dopaminergic function and auditory hallucinations. Distorted dopamine synthesis capacity is less likely to be associated with subclinical auditory hallucinations. Thus, it can be more difficult to investigate this relationship because of the antipsychotic medications involved (Shergill et al., 2007). Neuroimaging findings and results have provided important information that will help to decide on the brain regions that can be targeted clinical trials such a transcranial magnetic stimulation.

In conclusion, there is inadequate neuroimaging evidence that can help in understanding the neurological substrate of auditory hallucinations. Different neuronal activities may induce different auditory hallucinations in patients suffering from schizophrenia, which is signified by different cortical regions of the brain.

Treatment for Auditory Hallucination

Even with developed antipsychotics, schizophrenia patients continue to suffer from persistent auditory hallucinations. Apart from pharmacological immunizations such as Tiapride, several therapies have been developed to treat hallucinations in schizophrenia (Frith, 1979). They include; transcranial magnetic stimulation, hallucination-focused integrative treatments, and cognitive behavior therapy.

Tiapride

This is a substituted benzamide drug that is anti-psychotic in nature. It consists of a selective D3 and D2 dopamine receptor opponent activity in the limbic areas of the human brain. The drug has proved to be useful in treating auditory hallucinations. However, it has its side effects which may include drowsiness, dizziness, orthostatic hypotension, and extrapyramidal symptoms (Peters & Faulds, 1994).

Transcranial Direct Current Stimulation (tDCs)

This for of treatment is usually applied to patients who are resistant to medication. It is a painless, non-invasive stimulation of the brain that involves the use of direct electrical currents to cause stimulation to specific areas of the brain. Constant, low-intensive currents are passed through two electrodes that are placed over a patient’s head to modulate neuronal activity. There are two kinds of tDCs which are the cathodal and the anodal stimulation. Anodal activity excites neuronal activity whereas cathodal activity inhibits the neuronal activity. It is also known as Electro Convulsive Therapy (ECT) and is done under anesthesia.

Cognitive Behavioral Therapy (CBT)

One of the treatments that have been found to be most effective for psychotic symptoms including auditory hallucinations is the cognitive behavioral therapy. CBT includes the establishment of a formulation basing on voice assessment, assessment of other symptoms, responses to the hearing of voices, and voice appraisals (“National Institute for Clinical Excellence”, 2009). The formulation is applied to facilitate treatment through the creation of an adaptive common understanding of the hallucinations, enhancing coping skills, creating adaptive reactions to voice, and modification of assessments that relate to distress. This is done through behavioral experiments and Socratic questioning (Thomas, 2011). The cognitive behavioral therapy involves the use of measures such as the psychotic symptom rating scales (PSYRATS), the schedule for assessment of insight (SAI), and the positive and negative syndrome scale (PANSS).

The PSYRATS assesses various extents of voice experiences including distress, frequency, and impact. The PANSS clinical rating scale is an interview-based measure that assesses the negative, positive, and general psychotic symptoms and other associated symptoms. Finally, the SAI is a clinical scale for rating the awareness of illness, relabeling psychotic experiences, and compliance with treatment. The cognitive behavioral therapy enhances post-treatment improvements in auditory hallucinations. It has been established to reduce the behavioral and emotional impact of psychotic phenomena such as delusions and auditory hallucinations in schizophrenia, which are known to be resistant to medication (National Institute for Clinical Excellence, 2009). However, 50% of the patients have been said not to respond to this therapy.

Hallucinations-focused integrative Therapy (HIT)

This is a form of treatment applied in a community treatment setting. It involves several therapies such as family treatment, cognitive behavioral therapy, rehabilitative interventions, antipsychotic medications, motivational and attitudinal techniques, psychoeducation and coping training. It is very cost-effective as compared to other therapies. The implementation of HIT needs competency and therapists should be properly trained. Its difference from other therapies is its cost factor and the fact that it is offered to both patients and their relatives alike. It has been proved to have a major impact on schizophrenia patients with auditory hallucinations. According to the World Health Organization Quality of Life Schedule, patients who receive HIT show significant improvements in the quality of life lived (Wiersma Jenner, Nienhuis, & Willige, 2004).

Conclusion

Patients with schizophrenia often live in great isolation. Thus, interventions that help improve social behavior have been proven to be beneficial to these patients since they will no longer live in isolation and their levels of socialization will increase. New studies should be conducted to test the validity of the models proposed and used by previous researchers to explain the neurobiology of auditory hallucinations in schizophrenia disease. Difficulties relating to assessing of measuring subjective mental experiences should be considered in order to clearly study and understand the neural correlates of auditory hallucinations. Interventions such as functional neuroimaging cognitive studies, behavioral and molecular studies are greatly hoped to enhance knowledge about schizophrenia and auditory hallucinations.

References

Allen, P., Larøi, F., McGuire, P. K., & Aleman, A. (2008). The hallucinating brain: a review of structural and functional neuroimaging studies of hallucinations. Neuroscience & Biobehavioral Reviews, 32(1), 175-191.

Ford, J. M., & Mathalon, D. H. (2005). Corollary discharge dysfunction in schizophrenia: can it explain auditory hallucinations?. International Journal of Psychophysiology, 58(2), 179-189.

Frith, C. D. (1979). Consciousness, information processing, and schizophrenia. The British Journal of Psychiatry, 134(3), 225-235.

Henriksen M.G, A. R. (2015, September). The Pathogenesis of Auditory Verbal Hallucinations in Schizophrenia: A Clinical–Phenomenological Account. Philosophy, Psychiatry, & Psychology,, 22, 165-181.

Hugdahl K., E.-M. L. (2008, March 28th). Auditory hallucinations in schizophrenia: the role of cognitive, brain structural and genetic disturbances in the left temporal lobe. Frontiers in Human Neuroscience, 1(6), 1-10.

Karia, S., Shah, N., De Sousa, A., & Sonavane, S. (2013). Tiapride for the treatment of auditory hallucinations in schizophrenia. Indian Journal of Psychological Medicine, 35(4), 397.

Mueser, K.T, Mc Gurk, S.R (2004) “Schizophrenia,” The Lancet, vol. 363, no. 9426, pp. 2063–2072.

National Institute for Clinical Excellence (2009). Schizophrenia: core interventions in the treatment and management of schizophrenia in primary and secondary care (update). London: Department of Health.

Peters, D. H., & Faulds, D. (1994). Tiapride. Drugs, 47(6), 1010-1032.

Reulbach, U., Bleich, S., Maihofner, C., Kornhuber, J., & Sperling, W. (2007). Specific and unspecific auditory hallucinations in patients with schizophrenia: a magnetoencephalographic study. Neuropsychobiology, 55(2), 89-95.

Shergill, S. S., Kanaan, R. A., Chitnis, X. A., O’Daly, O., Jones, D. K., Frangou, S., ... & McGuire, P. (2007). A diffusion tensor imaging study of fasciculi in schizophrenia. American Journal of Psychiatry, 164(3), 467-473.

Thomas, N. R. (2011, november 10th). Cognitive Behavioural Therapy for Auditory Hallucinations:Effectiveness and Predictors of Outcome in a Specialist Clinic. Behavioural and Cognitive Psychotherapy,, 39, 129-138.

Thomas, N., Rossell, S., Farhall, J., Shawyer, F. and Castle, D. (2011) Cognitive Behavioural Therapy for Auditory Hallucinations: Effectiveness and Predictors of Outcome in a Specialist Clinic, Behavioural and Cognitive Psychotherapy, 39(2), 129–138.

Waters, F., Badcock, J., Michie, P., & Maybery, M. (2006). Auditory hallucinations in schizophrenia: Intrusive thoughts and forgotten memories. Cognitive Neuropsychiatry, 11(1), 65–83.

Wiersma, D., Jenner, J. A., Nienhuis, F. J., & Willige, G. (2004). Hallucination focused integrative treatment improves quality of life in schizophrenia patients. Acta Psychiatrica Scandinavica, 109(3), 194-201.

Woodruff, P., Brammer, M., Mellers, J., Wright, I., Bullmore, E., Williams, S., ... & Abukmeil, S. (1995). Auditory hallucinations and perception of external speech. The Lancet, 346(8981), 1035-1036.