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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Visual Hallucinations in the Psychosis Spectrum and Comparative Information From Neurodegenerative Disorders and Eye Disease</title><author><name sortKey="Waters, Flavie" sort="Waters, Flavie" uniqKey="Waters F" first="Flavie" last="Waters">Flavie Waters</name><affiliation><nlm:aff id="AF0001"><institution>Clinical Research Centre, Graylands Hospital, North Metropolitan Health Service Mental Health</institution>,<addr-line>Perth, Western Australia</addr-line>,<country>Australia</country>;</nlm:aff></affiliation><affiliation><nlm:aff id="AF0002"><institution>Centre for Clinical Research in Neuropsychiatry, School of Psychiatry and Clinical Neurosciences, the University of Western Australia</institution>,<addr-line>Perth, Western Australia</addr-line>,<country>Australia</country>;</nlm:aff></affiliation></author><author><name sortKey="Collerton, Daniel" sort="Collerton, Daniel" uniqKey="Collerton D" first="Daniel" last="Collerton">Daniel Collerton</name><affiliation><nlm:aff id="AF0003"><institution>Northumberland, Tyne and Wear NHS Foundation Trust, Bensham Hospital, Gateshead and Newcastle University</institution>,<addr-line>Newcastle Upon Tyne</addr-line>,<country>UK</country>;</nlm:aff></affiliation></author><author><name sortKey="Ffytche, Dominic H" sort="Ffytche, Dominic H" uniqKey="Ffytche D" first="Dominic H." last="Ffytche">Dominic H. Ffytche</name><affiliation><nlm:aff id="AF0004"><institution>Institute of Psychiatry, King’s College London</institution>,<addr-line>London</addr-line>,<institution></institution><country>UK</country>;</nlm:aff></affiliation></author><author><name sortKey="Jardri, Renaud" sort="Jardri, Renaud" uniqKey="Jardri R" first="Renaud" last="Jardri">Renaud Jardri</name><affiliation><nlm:aff id="AF0005"><institution>Laboratoire de Neurosciences Fonctionnelles & Pathologies, Université Droit & Santé (UDSL), Univ Lille Nord de France and Centre Hospitalier Universitaire (CHU Lille), Hôpital Fontan</institution>,<addr-line>Lille</addr-line>,<country>France</country>;</nlm:aff></affiliation></author><author><name sortKey="Pins, Delphine" sort="Pins, Delphine" uniqKey="Pins D" first="Delphine" last="Pins">Delphine Pins</name><affiliation><nlm:aff id="AF0005"><institution>Laboratoire de Neurosciences Fonctionnelles & Pathologies, Université Droit & Santé (UDSL), Univ Lille Nord de France and Centre Hospitalier Universitaire (CHU Lille), Hôpital Fontan</institution>,<addr-line>Lille</addr-line>,<country>France</country>;</nlm:aff></affiliation></author><author><name sortKey="Dudley, Robert" sort="Dudley, Robert" uniqKey="Dudley R" first="Robert" last="Dudley">Robert Dudley</name><affiliation><nlm:aff id="AF0006"><institution>School of Psychology, Newcastle University</institution>,<addr-line>Newcastle Upon Tyne</addr-line>,<country>UK</country>;</nlm:aff></affiliation><affiliation><nlm:aff id="AF0007"><institution>South of Tyne Early Intervention in Psychosis Service, Northumberland, Tyne and Wear NHS Foundation Trust</institution>,<addr-line>Newcastle Upon Tyne</addr-line>,<country>UK</country>;</nlm:aff></affiliation></author><author><name sortKey="Blom, Jan Dirk" sort="Blom, Jan Dirk" uniqKey="Blom J" first="Jan Dirk" last="Blom">Jan Dirk Blom</name><affiliation><nlm:aff id="AF0008"><institution>Parnassia Psychiatric Institute</institution>,<addr-line>The Hague</addr-line>,<country>The Netherlands</country>;</nlm:aff></affiliation><affiliation><nlm:aff id="AF0009"><institution>Department of Psychiatry, University of Groningen</institution>,<addr-line>Groningen</addr-line>,<country>The Netherlands</country>;</nlm:aff></affiliation></author><author><name sortKey="Mosimann, Urs Peter" sort="Mosimann, Urs Peter" uniqKey="Mosimann U" first="Urs Peter" last="Mosimann">Urs Peter Mosimann</name><affiliation><nlm:aff id="AF0010"><institution>University Hospital of Old Age Psychiatry</institution>,<addr-line>University of Bern, Bern</addr-line>,<country>Switzerland</country>;</nlm:aff></affiliation></author><author><name sortKey="Eperjesi, Frank" sort="Eperjesi, Frank" uniqKey="Eperjesi F" first="Frank" last="Eperjesi">Frank Eperjesi</name><affiliation><nlm:aff id="AF0011"><institution>Ophthalmic Research Group, School of Life and Health Sciences, Aston University</institution>,<addr-line>Birmingham</addr-line>,<country>UK</country>;</nlm:aff></affiliation></author><author><name sortKey="Ford, Stephen" sort="Ford, Stephen" uniqKey="Ford S" first="Stephen" last="Ford">Stephen Ford</name><affiliation><nlm:aff id="AF0012"><institution>Department of Psychiatry, Sir Charles Gairdner Hospital, North Metropolitan Health Service Mental Health – Older Adult Program</institution>,<addr-line>Perth, Western Australia</addr-line>,<country>Australia</country>;</nlm:aff></affiliation></author><author><name sortKey="Lar I, Frank" sort="Lar I, Frank" uniqKey="Lar I F" first="Frank" last="Lar I">Frank Lar I</name><affiliation><nlm:aff id="AF0013"><institution>Department of Psychology: Cognition and Behaviour, University of Liège</institution>,<addr-line>Liège</addr-line>,<country>Belgium</country></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24936084</idno><idno type="pmc">4141306</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4141306</idno><idno type="RBID">PMC:4141306</idno><idno type="doi">10.1093/schbul/sbu036</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">002D11</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002D11</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Visual Hallucinations in the Psychosis Spectrum and Comparative Information From Neurodegenerative Disorders and Eye Disease</title><author><name sortKey="Waters, Flavie" sort="Waters, Flavie" uniqKey="Waters F" first="Flavie" last="Waters">Flavie Waters</name><affiliation><nlm:aff id="AF0001"><institution>Clinical Research Centre, Graylands Hospital, North Metropolitan Health Service Mental Health</institution>,<addr-line>Perth, Western Australia</addr-line>,<country>Australia</country>;</nlm:aff></affiliation><affiliation><nlm:aff id="AF0002"><institution>Centre for Clinical Research in Neuropsychiatry, School of Psychiatry and Clinical Neurosciences, the University of Western Australia</institution>,<addr-line>Perth, Western Australia</addr-line>,<country>Australia</country>;</nlm:aff></affiliation></author><author><name sortKey="Collerton, Daniel" sort="Collerton, Daniel" uniqKey="Collerton D" first="Daniel" last="Collerton">Daniel Collerton</name><affiliation><nlm:aff id="AF0003"><institution>Northumberland, Tyne and Wear NHS Foundation Trust, Bensham Hospital, Gateshead and Newcastle University</institution>,<addr-line>Newcastle Upon Tyne</addr-line>,<country>UK</country>;</nlm:aff></affiliation></author><author><name sortKey="Ffytche, Dominic H" sort="Ffytche, Dominic H" uniqKey="Ffytche D" first="Dominic H." last="Ffytche">Dominic H. Ffytche</name><affiliation><nlm:aff id="AF0004"><institution>Institute of Psychiatry, King’s College London</institution>,<addr-line>London</addr-line>,<institution></institution><country>UK</country>;</nlm:aff></affiliation></author><author><name sortKey="Jardri, Renaud" sort="Jardri, Renaud" uniqKey="Jardri R" first="Renaud" last="Jardri">Renaud Jardri</name><affiliation><nlm:aff id="AF0005"><institution>Laboratoire de Neurosciences Fonctionnelles & Pathologies, Université Droit & Santé (UDSL), Univ Lille Nord de France and Centre Hospitalier Universitaire (CHU Lille), Hôpital Fontan</institution>,<addr-line>Lille</addr-line>,<country>France</country>;</nlm:aff></affiliation></author><author><name sortKey="Pins, Delphine" sort="Pins, Delphine" uniqKey="Pins D" first="Delphine" last="Pins">Delphine Pins</name><affiliation><nlm:aff id="AF0005"><institution>Laboratoire de Neurosciences Fonctionnelles & Pathologies, Université Droit & Santé (UDSL), Univ Lille Nord de France and Centre Hospitalier Universitaire (CHU Lille), Hôpital Fontan</institution>,<addr-line>Lille</addr-line>,<country>France</country>;</nlm:aff></affiliation></author><author><name sortKey="Dudley, Robert" sort="Dudley, Robert" uniqKey="Dudley R" first="Robert" last="Dudley">Robert Dudley</name><affiliation><nlm:aff id="AF0006"><institution>School of Psychology, Newcastle University</institution>,<addr-line>Newcastle Upon Tyne</addr-line>,<country>UK</country>;</nlm:aff></affiliation><affiliation><nlm:aff id="AF0007"><institution>South of Tyne Early Intervention in Psychosis Service, Northumberland, Tyne and Wear NHS Foundation Trust</institution>,<addr-line>Newcastle Upon Tyne</addr-line>,<country>UK</country>;</nlm:aff></affiliation></author><author><name sortKey="Blom, Jan Dirk" sort="Blom, Jan Dirk" uniqKey="Blom J" first="Jan Dirk" last="Blom">Jan Dirk Blom</name><affiliation><nlm:aff id="AF0008"><institution>Parnassia Psychiatric Institute</institution>,<addr-line>The Hague</addr-line>,<country>The Netherlands</country>;</nlm:aff></affiliation><affiliation><nlm:aff id="AF0009"><institution>Department of Psychiatry, University of Groningen</institution>,<addr-line>Groningen</addr-line>,<country>The Netherlands</country>;</nlm:aff></affiliation></author><author><name sortKey="Mosimann, Urs Peter" sort="Mosimann, Urs Peter" uniqKey="Mosimann U" first="Urs Peter" last="Mosimann">Urs Peter Mosimann</name><affiliation><nlm:aff id="AF0010"><institution>University Hospital of Old Age Psychiatry</institution>,<addr-line>University of Bern, Bern</addr-line>,<country>Switzerland</country>;</nlm:aff></affiliation></author><author><name sortKey="Eperjesi, Frank" sort="Eperjesi, Frank" uniqKey="Eperjesi F" first="Frank" last="Eperjesi">Frank Eperjesi</name><affiliation><nlm:aff id="AF0011"><institution>Ophthalmic Research Group, School of Life and Health Sciences, Aston University</institution>,<addr-line>Birmingham</addr-line>,<country>UK</country>;</nlm:aff></affiliation></author><author><name sortKey="Ford, Stephen" sort="Ford, Stephen" uniqKey="Ford S" first="Stephen" last="Ford">Stephen Ford</name><affiliation><nlm:aff id="AF0012"><institution>Department of Psychiatry, Sir Charles Gairdner Hospital, North Metropolitan Health Service Mental Health – Older Adult Program</institution>,<addr-line>Perth, Western Australia</addr-line>,<country>Australia</country>;</nlm:aff></affiliation></author><author><name sortKey="Lar I, Frank" sort="Lar I, Frank" uniqKey="Lar I F" first="Frank" last="Lar I">Frank Lar I</name><affiliation><nlm:aff id="AF0013"><institution>Department of Psychology: Cognition and Behaviour, University of Liège</institution>,<addr-line>Liège</addr-line>,<country>Belgium</country></nlm:aff></affiliation></author></analytic><series><title level="j">Schizophrenia Bulletin</title><idno type="ISSN">0586-7614</idno><idno type="eISSN">1745-1701</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Much of the research on visual hallucinations (VHs) has been conducted in the context of eye disease and neurodegenerative conditions, but little is known about these phenomena in psychiatric and nonclinical populations. The purpose of this article is to bring together current knowledge regarding VHs in the psychosis phenotype and contrast this data with the literature drawn from neurodegenerative disorders and eye disease. The evidence challenges the traditional views that VHs are atypical or uncommon in psychosis. The weighted mean for VHs is 27% in schizophrenia, 15% in affective psychosis, and 7.3% in the general community. VHs are linked to a more severe psychopathological profile and less favorable outcome in psychosis and neurodegenerative conditions. VHs typically co-occur with auditory hallucinations, suggesting a common etiological cause. VHs in psychosis are also remarkably complex, negative in content, and are interpreted to have personal relevance. The cognitive mechanisms of VHs in psychosis have rarely been investigated, but existing studies point to source-monitoring deficits and distortions in top-down mechanisms, although evidence for visual processing deficits, which feature strongly in the organic literature, is lacking. Brain imaging studies point to the activation of visual cortex during hallucinations on a background of structural and connectivity changes within wider brain networks. The relationship between VHs in psychosis, eye disease, and neurodegeneration remains unclear, although the pattern of similarities and differences described in this review suggests that comparative studies may have potentially important clinical and theoretical implications.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Macpherson, F" uniqKey="Macpherson F">F Macpherson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bleuler, E" uniqKey="Bleuler E">E Bleuler</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Waters, F" uniqKey="Waters F">F Waters</name></author><author><name sortKey="Woods, A" uniqKey="Woods A">A Woods</name></author><author><name sortKey="Fernyhough, C" uniqKey="Fernyhough C">C Fernyhough</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jablensky, A" uniqKey="Jablensky A">A 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Schizophr Bull</journal-id><journal-id journal-id-type="iso-abbrev">Schizophr Bull</journal-id><journal-id journal-id-type="hwp">schbul</journal-id><journal-id journal-id-type="publisher-id">schbul</journal-id><journal-title-group><journal-title>Schizophrenia Bulletin</journal-title></journal-title-group><issn pub-type="ppub">0586-7614</issn><issn pub-type="epub">1745-1701</issn><publisher><publisher-name>Oxford University Press</publisher-name><publisher-loc>US</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24936084</article-id><article-id pub-id-type="pmc">4141306</article-id><article-id pub-id-type="doi">10.1093/schbul/sbu036</article-id><article-categories><subj-group subj-group-type="heading"><subject>Supplement Article</subject></subj-group></article-categories><title-group><article-title>Visual Hallucinations in the Psychosis Spectrum and Comparative Information From Neurodegenerative Disorders and Eye Disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Waters</surname><given-names>Flavie</given-names></name><xref ref-type="corresp" rid="c1">*</xref><xref ref-type="aff" rid="AF0001"><sup>1</sup></xref><xref ref-type="aff" rid="AF0002"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Collerton</surname><given-names>Daniel</given-names></name><xref ref-type="aff" rid="AF0003"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>ffytche</surname><given-names>Dominic H.</given-names></name><xref ref-type="aff" rid="AF0004"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Jardri</surname><given-names>Renaud</given-names></name><xref ref-type="aff" rid="AF0005"><sup>5</sup></xref></contrib><contrib contrib-type="author"><name><surname>Pins</surname><given-names>Delphine</given-names></name><xref ref-type="aff" rid="AF0005"><sup>5</sup></xref></contrib><contrib contrib-type="author"><name><surname>Dudley</surname><given-names>Robert</given-names></name><xref ref-type="aff" rid="AF0006"><sup>6</sup></xref><xref ref-type="aff" rid="AF0007"><sup>7</sup></xref></contrib><contrib contrib-type="author"><name><surname>Blom</surname><given-names>Jan Dirk</given-names></name><xref ref-type="aff" rid="AF0008"><sup>8</sup></xref><xref ref-type="aff" rid="AF0009"><sup>9</sup></xref></contrib><contrib contrib-type="author"><name><surname>Mosimann</surname><given-names>Urs Peter</given-names></name><xref ref-type="aff" rid="AF0010"><sup>10</sup></xref></contrib><contrib contrib-type="author"><name><surname>Eperjesi</surname><given-names>Frank</given-names></name><xref ref-type="aff" rid="AF0011"><sup>11</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ford</surname><given-names>Stephen</given-names></name><xref ref-type="aff" rid="AF0012"><sup>12</sup></xref></contrib><contrib contrib-type="author"><name><surname>Larøi</surname><given-names>Frank</given-names></name><xref ref-type="aff" rid="AF0013"><sup>13</sup></xref></contrib><aff id="AF0001"><sup>1</sup><institution>Clinical Research Centre, Graylands Hospital, North Metropolitan Health Service Mental Health</institution>,<addr-line>Perth, Western Australia</addr-line>,<country>Australia</country>;</aff><aff id="AF0002"><sup>2</sup><institution>Centre for Clinical Research in Neuropsychiatry, School of Psychiatry and Clinical Neurosciences, the University of Western Australia</institution>,<addr-line>Perth, Western Australia</addr-line>,<country>Australia</country>;</aff><aff id="AF0003"><sup>3</sup><institution>Northumberland, Tyne and Wear NHS Foundation Trust, Bensham Hospital, Gateshead and Newcastle University</institution>,<addr-line>Newcastle Upon Tyne</addr-line>,<country>UK</country>;</aff><aff id="AF0004"><sup>4</sup><institution>Institute of Psychiatry, King’s College London</institution>,<addr-line>London</addr-line>,<institution></institution><country>UK</country>;</aff><aff id="AF0005"><sup>5</sup><institution>Laboratoire de Neurosciences Fonctionnelles & Pathologies, Université Droit & Santé (UDSL), Univ Lille Nord de France and Centre Hospitalier Universitaire (CHU Lille), Hôpital Fontan</institution>,<addr-line>Lille</addr-line>,<country>France</country>;</aff><aff id="AF0006"><sup>6</sup><institution>School of Psychology, Newcastle University</institution>,<addr-line>Newcastle Upon Tyne</addr-line>,<country>UK</country>;</aff><aff id="AF0007"><sup>7</sup><institution>South of Tyne Early Intervention in Psychosis Service, Northumberland, Tyne and Wear NHS Foundation Trust</institution>,<addr-line>Newcastle Upon Tyne</addr-line>,<country>UK</country>;</aff><aff id="AF0008"><sup>8</sup><institution>Parnassia Psychiatric Institute</institution>,<addr-line>The Hague</addr-line>,<country>The Netherlands</country>;</aff><aff id="AF0009"><sup>9</sup><institution>Department of Psychiatry, University of Groningen</institution>,<addr-line>Groningen</addr-line>,<country>The Netherlands</country>;</aff><aff id="AF0010"><sup>10</sup><institution>University Hospital of Old Age Psychiatry</institution>,<addr-line>University of Bern, Bern</addr-line>,<country>Switzerland</country>;</aff><aff id="AF0011"><sup>11</sup><institution>Ophthalmic Research Group, School of Life and Health Sciences, Aston University</institution>,<addr-line>Birmingham</addr-line>,<country>UK</country>;</aff><aff id="AF0012"><sup>12</sup><institution>Department of Psychiatry, Sir Charles Gairdner Hospital, North Metropolitan Health Service Mental Health – Older Adult Program</institution>,<addr-line>Perth, Western Australia</addr-line>,<country>Australia</country>;</aff><aff id="AF0013"><sup>13</sup><institution>Department of Psychology: Cognition and Behaviour, University of Liège</institution>,<addr-line>Liège</addr-line>,<country>Belgium</country></aff></contrib-group><author-notes><corresp id="c1">*To whom correspondence should be addressed; Clinical Research Centre, Graylands Hospital, Private Mail Bag 1, Mount Claremont 6010, Perth, Western Australia, Australia; tel: <phone>(+61 8) 6346 6650</phone>, fax: <fax>9384 5128</fax>, e-mail: <email>Flavie.waters@health.wa.gov.au</email></corresp></author-notes><pub-date pub-type="ppub"><month>7</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>13</day><month>6</month><year>2014</year></pub-date><pub-date pub-type="pmc-release"><day>13</day><month>6</month><year>2014</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
<volume>40</volume><issue>Suppl 4</issue><fpage>S233</fpage><lpage>S245</lpage><history><date date-type="received"><day>23</day><month>11</month><year>2013</year></date><date date-type="rev-recd"><day>12</day><month>2</month><year>2014</year></date><date date-type="accepted"><day>12</day><month>2</month><year>2014</year></date></history><permissions><copyright-statement>© The Author 2014. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center.</copyright-statement><copyright-year>2014</copyright-year><license license-type="creative-commons" xlink:href="http://creativecommons.org/licenses/by/3.0"><license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/3.0/">http://creativecommons.org/licenses/by/3.0/</ext-link>), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>Much of the research on visual hallucinations (VHs) has been conducted in the context of eye disease and neurodegenerative conditions, but little is known about these phenomena in psychiatric and nonclinical populations. The purpose of this article is to bring together current knowledge regarding VHs in the psychosis phenotype and contrast this data with the literature drawn from neurodegenerative disorders and eye disease. The evidence challenges the traditional views that VHs are atypical or uncommon in psychosis. The weighted mean for VHs is 27% in schizophrenia, 15% in affective psychosis, and 7.3% in the general community. VHs are linked to a more severe psychopathological profile and less favorable outcome in psychosis and neurodegenerative conditions. VHs typically co-occur with auditory hallucinations, suggesting a common etiological cause. VHs in psychosis are also remarkably complex, negative in content, and are interpreted to have personal relevance. The cognitive mechanisms of VHs in psychosis have rarely been investigated, but existing studies point to source-monitoring deficits and distortions in top-down mechanisms, although evidence for visual processing deficits, which feature strongly in the organic literature, is lacking. Brain imaging studies point to the activation of visual cortex during hallucinations on a background of structural and connectivity changes within wider brain networks. The relationship between VHs in psychosis, eye disease, and neurodegeneration remains unclear, although the pattern of similarities and differences described in this review suggests that comparative studies may have potentially important clinical and theoretical implications.</p></abstract><kwd-group><title>Key words:</title><kwd>visual hallucinations</kwd><kwd>schizophrenia</kwd><kwd>psychosis</kwd><kwd>cognition</kwd><kwd>imaging</kwd></kwd-group><counts><page-count count="13"></page-count></counts></article-meta></front><body><sec sec-type="intro" id="s1"><title>Introduction</title><p>Hallucinations are defined in different ways by different philosophical traditions.<sup><xref rid="CIT0001" ref-type="bibr">1</xref></sup> In the clinical domain, a visual hallucination (VH) is a visual percept, experienced when awake, which is not elicited by an external stimulus. It contrasts with a visual illusion which is elicited by an external stimulus but differs from the percept normally associated with the stimulus. VHs occur in a wide-range of organic and psychiatric conditions, as well as in the absence of any demonstrable pathology. These experiences have been well described and researched in the context of organic disorders, particularly eye disease and neurodegenerative conditions such as dementia with Lewy bodies (DLB) and Parkinson’s disease (PD), but VHs have been largely neglected in psychiatric disorders and delirious states and in nonclinical populations.</p><p content-type="indent">Although the diagnostic manuals for mental disorders list hallucinations as a primary characteristic symptom in psychotic disorders, <italic>auditory</italic> hallucinations are the symptoms that clinicians commonly ask about. One explanation lies in the traditional beliefs that VHs are more common in organic states than in psychosis.<sup><xref rid="CIT0002" ref-type="bibr">2</xref></sup> It is also often difficult to decide whether the full criteria for the presence of VHs have been fulfilled when a range of other perceptual abnormalities are reported.</p><p content-type="indent">In this article, we review the available evidence with regards to the prevalence, phenomenology, clinical characteristics, and assessment methods for VHs in the psychosis spectrum alongside studies of cognition, brain imaging, electrophysiology, and treatment (cognitive behavioral and pharmacological). Given the lack of available literature on other psychiatric disorders, our focus is on schizophrenia, affective psychosis (ie, bipolar and depressive disorders), and nonclinical population groups (who experience VHs outside of the context of any psychiatric or somatic disease). The psychosis evidence is compared with evidence related to eye and neurodegenerative disease in the hope that similarities and differences between different clinical contexts will help our understanding of the underlying mechanisms of VH and its treatment.</p><p content-type="indent">To our knowledge, this is the first review of VH in psychosis. For the first time, a cross-disciplinary and cross-diagnostic examination of VH is also presented. Our broad aim is to provide a useful base for future studies on the topic and specifically to achieve a clearer understanding of VH in psychiatric illness and greater clarity regarding the assessment of VH for use in clinical practice and research.</p><p content-type="indent">Parts of this article were presented in Durham at the 2nd International Consortium on Hallucination Research (ICHR) 2013 conference.<sup><xref rid="CIT0003" ref-type="bibr">3</xref></sup></p></sec><sec id="s2"><title>Epidemiology</title><sec id="s3"><title>Psychosis</title><p>The centrality of VH in psychosis has been put into question by studies which show that auditory, and not visual, hallucinations are among the cardinal symptoms of schizophrenia which are common in all cultures.<sup><xref rid="CIT0004" ref-type="bibr">4</xref></sup> VHs, however, appear to be more frequent in schizophrenia than commonly thought.</p><p content-type="indent"><xref ref-type="table" rid="T1">Table 1</xref> describes studies that have provided the point prevalence of VH in schizophrenia. Estimates vary widely from 4% to 65%, reflecting variations in population and ascertainment methods. Out of 29 studies that have addressed this issue (5873 participants), the weighted mean prevalence of VH in schizophrenia is 27% (SD = 9). For comparison, the weighted mean of auditory hallucinations as provided by the same studies is 59% (range: 25%–86%; SD <italic>=</italic> 15), ie, twice as frequent as VH, although it is possible that clinician biases toward auditory hallucinations have skewed the results.</p><table-wrap id="T1" position="float"><label>Table 1.</label><caption><p>The Comparative Point Prevalence of Visual and Auditory Hallucinations in Schizophrenia</p></caption><table frame="vsides" rules="groups"><thead><tr><th align="left" rowspan="2" valign="bottom" colspan="1">Authors</th><th align="left" rowspan="2" valign="bottom" colspan="1"><italic>n</italic></th><th align="left" colspan="2" valign="bottom" rowspan="1">Modality of Hallucinations</th></tr><tr><th align="left" valign="bottom" rowspan="1" colspan="1">Visual (%)</th><th align="left" valign="bottom" rowspan="1" colspan="1">Auditory (%)</th></tr></thead><tbody><tr><td rowspan="1" colspan="1">Bowman and Raymond (1931)<sup>5
</sup></td><td rowspan="1" colspan="1">1408</td><td rowspan="1" colspan="1">22</td><td rowspan="1" colspan="1">53</td></tr><tr><td rowspan="1" colspan="1">Arnold (1949)<sup>6
</sup></td><td rowspan="1" colspan="1"><sup>a</sup></td><td rowspan="1" colspan="1">14</td><td rowspan="1" colspan="1">78</td></tr><tr><td rowspan="1" colspan="1">Feinberg (1962)<sup>7
</sup></td><td rowspan="1" colspan="1">19</td><td rowspan="1" colspan="1">4</td><td rowspan="1" colspan="1">84</td></tr><tr><td rowspan="1" colspan="1">Malitz et al (1962)<sup>8
</sup></td><td rowspan="1" colspan="1">100</td><td rowspan="1" colspan="1">9</td><td rowspan="1" colspan="1">50</td></tr><tr><td rowspan="1" colspan="1">Vitols et al (1963)<sup>9
</sup></td><td rowspan="1" colspan="1">110</td><td rowspan="1" colspan="1">13</td><td rowspan="1" colspan="1">35</td></tr><tr><td rowspan="1" colspan="1">Goldberg et al (1965)<sup>10
</sup></td><td rowspan="1" colspan="1">270</td><td rowspan="1" colspan="1">18</td><td rowspan="1" colspan="1">45</td></tr><tr><td rowspan="1" colspan="1">Mott et al (1965)<sup>11
</sup></td><td rowspan="1" colspan="1">50</td><td rowspan="1" colspan="1">24</td><td rowspan="1" colspan="1">66</td></tr><tr><td rowspan="1" colspan="1">Small et al (1966)<sup>12
</sup></td><td rowspan="1" colspan="1">50</td><td rowspan="1" colspan="1">30</td><td rowspan="1" colspan="1">66</td></tr><tr><td rowspan="1" colspan="1">Chapman (1966)<sup>13
</sup></td><td rowspan="1" colspan="1"><sup>a</sup></td><td rowspan="1" colspan="1">40</td><td rowspan="1" colspan="1"><sup>a</sup></td></tr><tr><td rowspan="1" colspan="1">Holmboe and Astrup (1967)<sup>14
</sup></td><td rowspan="1" colspan="1">255</td><td rowspan="1" colspan="1">25</td><td rowspan="1" colspan="1">79</td></tr><tr><td rowspan="1" colspan="1">Jansson (1968)<sup>15
</sup></td><td rowspan="1" colspan="1">293</td><td rowspan="1" colspan="1">13</td><td rowspan="1" colspan="1">25</td></tr><tr><td rowspan="1" colspan="1">Goodwin et al (1971)<sup>16
</sup></td><td rowspan="1" colspan="1">45</td><td rowspan="1" colspan="1">59</td><td rowspan="1" colspan="1">82</td></tr><tr><td rowspan="1" colspan="1">Eggers (1973)<sup>17
</sup></td><td rowspan="1" colspan="1"><sup>a</sup></td><td rowspan="1" colspan="1">44</td><td rowspan="1" colspan="1">71</td></tr><tr><td rowspan="1" colspan="1">McCabe (1976)<sup>18
</sup></td><td rowspan="1" colspan="1">40</td><td rowspan="1" colspan="1">20</td><td rowspan="1" colspan="1">36</td></tr><tr><td rowspan="1" colspan="1">Young (1974)<sup>19
</sup></td><td rowspan="1" colspan="1">20</td><td rowspan="1" colspan="1">45</td><td rowspan="1" colspan="1"><sup>a</sup></td></tr><tr><td rowspan="1" colspan="1">Zarroug (1975)<sup>20
</sup></td><td rowspan="1" colspan="1">69</td><td rowspan="1" colspan="1">47</td><td rowspan="1" colspan="1">62</td></tr><tr><td rowspan="1" colspan="1">Ciompi and Müller (1976)<sup>21
</sup></td><td rowspan="1" colspan="1"><sup>a</sup></td><td rowspan="1" colspan="1">18</td><td rowspan="1" colspan="1">58</td></tr><tr><td rowspan="1" colspan="1">McCabe (1976)<sup>18
</sup></td><td rowspan="1" colspan="1">25</td><td rowspan="1" colspan="1">20</td><td rowspan="1" colspan="1">52</td></tr><tr><td rowspan="1" colspan="1">Deiker and Chambers (1978)<sup>22
</sup></td><td rowspan="1" colspan="1">28</td><td rowspan="1" colspan="1">64</td><td rowspan="1" colspan="1">86</td></tr><tr><td rowspan="1" colspan="1">Huber (1979)<sup>23
</sup></td><td rowspan="1" colspan="1"><sup>a</sup></td><td rowspan="1" colspan="1">33</td><td rowspan="1" colspan="1">75</td></tr><tr><td rowspan="1" colspan="1">Ndetei and Singh (1983)<sup>24
</sup></td><td rowspan="1" colspan="1">51</td><td rowspan="1" colspan="1">43</td><td rowspan="1" colspan="1">43</td></tr><tr><td rowspan="1" colspan="1">Ndetei (1984)<sup>25
</sup></td><td rowspan="1" colspan="1">141</td><td rowspan="1" colspan="1">15</td><td rowspan="1" colspan="1">41</td></tr><tr><td rowspan="1" colspan="1">Winokur et al (1985)<sup>26
</sup></td><td rowspan="1" colspan="1">140</td><td rowspan="1" colspan="1">32</td><td rowspan="1" colspan="1">78</td></tr><tr><td rowspan="1" colspan="1">Phillipson and Harris (1985)<sup>27
</sup></td><td rowspan="1" colspan="1">73</td><td rowspan="1" colspan="1">62</td><td rowspan="1" colspan="1">44</td></tr><tr><td rowspan="1" colspan="1">Bracha et al (1989)<sup>28
</sup></td><td rowspan="1" colspan="1">43</td><td rowspan="1" colspan="1">56</td><td rowspan="1" colspan="1">42</td></tr><tr><td rowspan="1" colspan="1">Owens and Slade (1989)<sup>29
</sup></td><td rowspan="1" colspan="1"><sup>a</sup></td><td rowspan="1" colspan="1">29</td><td rowspan="1" colspan="1">63</td></tr><tr><td rowspan="1" colspan="1">Mueser et al (1990)<sup>30
</sup></td><td rowspan="1" colspan="1">117</td><td rowspan="1" colspan="1">14</td><td rowspan="1" colspan="1">71</td></tr><tr><td rowspan="1" colspan="1">Jablensky et al (1992)<sup>4
</sup></td><td rowspan="1" colspan="1">1288</td><td rowspan="1" colspan="1">30</td><td rowspan="1" colspan="1">55</td></tr><tr><td rowspan="1" colspan="1">Bauer et al (2011)<sup>31
</sup></td><td rowspan="1" colspan="1">1238</td><td rowspan="1" colspan="1">34</td><td rowspan="1" colspan="1">79</td></tr><tr><td rowspan="1" colspan="1">Total: 29 studies, <italic>n</italic> = 5873 participants</td><td align="center" rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">Weighted mean = 27%</td><td rowspan="1" colspan="1">Weighted mean = 59%</td></tr><tr><td rowspan="1" colspan="1"></td><td align="center" rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">SD = 9.73</td><td rowspan="1" colspan="1">SD = 15.30</td></tr></tbody></table><table-wrap-foot><fn fn-type="other"><p><italic>Note</italic>: <sup>a</sup>Not assessed or missing data.</p></fn></table-wrap-foot></table-wrap><p content-type="indent">Psychotic symptoms such as hallucinations and delusions are also a common feature of affective disorders including bipolar disorder.<sup><xref rid="CIT0006" ref-type="bibr">6</xref></sup><xref ref-type="table" rid="T2">Table 2</xref> shows that out of 12 studies that differentiated between different modalities of hallucinations, the weighted mean frequency of VH is approximately 15% (range: 6%–27%, SD <italic>=</italic> 9). Similarly to schizophrenia, the rates of VH in bipolar disorder are approximately half that of auditory hallucinations (28%).</p><table-wrap id="T2" position="float"><label>Table 2.</label><caption><p>The Comparative Prevalence of Visual Hallucinations and Auditory Hallucinations in Bipolar and Affective Disorder</p></caption><table frame="vsides" rules="groups"><thead><tr><th align="left" rowspan="2" valign="bottom" colspan="1">Authors</th><th align="left" rowspan="2" valign="bottom" colspan="1"><italic>n</italic></th><th align="left" rowspan="2" valign="bottom" colspan="1">Diagnosis</th><th align="left" colspan="2" valign="bottom" rowspan="1">Modality of Hallucinations</th></tr><tr><th align="left" valign="bottom" rowspan="1" colspan="1">Visual (%)</th><th align="left" valign="bottom" rowspan="1" colspan="1">Auditory (%)</th></tr></thead><tbody><tr><td rowspan="1" colspan="1">Bowman and Raymond (1931)<sup>5
</sup></td><td rowspan="1" colspan="1">1009</td><td rowspan="1" colspan="1">Mania</td><td rowspan="1" colspan="1">9</td><td rowspan="1" colspan="1">17</td></tr><tr><td rowspan="1" colspan="1">Rosenthal et al (1966)<sup>32
</sup></td><td rowspan="1" colspan="1">79</td><td rowspan="1" colspan="1">Mania</td><td rowspan="1" colspan="1">21</td><td rowspan="1" colspan="1">30</td></tr><tr><td rowspan="1" colspan="1">Winokur (1969)<sup>26
</sup></td><td rowspan="1" colspan="1">100</td><td rowspan="1" colspan="1">Mania</td><td rowspan="1" colspan="1">9</td><td rowspan="1" colspan="1">21</td></tr><tr><td rowspan="1" colspan="1">Goodwin et al (1971)<sup>16
</sup></td><td rowspan="1" colspan="1">28</td><td rowspan="1" colspan="1">Primary affective disorder</td><td rowspan="1" colspan="1">72</td><td rowspan="1" colspan="1">82</td></tr><tr><td rowspan="1" colspan="1">Taylor and Abrams (1975)<sup>33
</sup></td><td rowspan="1" colspan="1">52</td><td rowspan="1" colspan="1">Mania</td><td rowspan="1" colspan="1">23</td><td rowspan="1" colspan="1">47</td></tr><tr><td rowspan="1" colspan="1">Rosenthal et al (1980)<sup>34
</sup></td><td rowspan="1" colspan="1">32</td><td rowspan="1" colspan="1">Mania</td><td rowspan="1" colspan="1">25</td><td rowspan="1" colspan="1">30</td></tr><tr><td rowspan="1" colspan="1">Winokur (1984)<sup>26
</sup></td><td rowspan="1" colspan="1">122</td><td rowspan="1" colspan="1">Bipolar disorder</td><td rowspan="1" colspan="1">9</td><td rowspan="1" colspan="1">14</td></tr><tr><td rowspan="1" colspan="1">Black and Nasrallah (1989)<sup>35
</sup></td><td rowspan="1" colspan="1">467</td><td rowspan="1" colspan="1">Acute bipolar disorder</td><td rowspan="1" colspan="1">6</td><td rowspan="1" colspan="1">13</td></tr><tr><td rowspan="1" colspan="1">Mueser et al (1990)<sup>30
</sup></td><td align="center" rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">bipolar disorder</td><td rowspan="1" colspan="1">25</td><td rowspan="1" colspan="1">75</td></tr><tr><td rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">37</td><td rowspan="1" colspan="1">Severe affective disorder</td><td rowspan="1" colspan="1">10</td><td rowspan="1" colspan="1">17</td></tr><tr><td rowspan="1" colspan="1">Keck et al (2003)<sup>36
</sup></td><td rowspan="1" colspan="1">352</td><td rowspan="1" colspan="1">Mania</td><td rowspan="1" colspan="1">22</td><td rowspan="1" colspan="1">25</td></tr><tr><td rowspan="1" colspan="1">Baethge et al (2005)<sup>37
</sup></td><td rowspan="1" colspan="1">33</td><td rowspan="1" colspan="1">Manic/mixed type with hallucinations</td><td rowspan="1" colspan="1">27</td><td rowspan="1" colspan="1">54</td></tr><tr><td rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">32</td><td rowspan="1" colspan="1">Depressed type with hallucinations</td><td rowspan="1" colspan="1">25</td><td rowspan="1" colspan="1">59</td></tr><tr><td rowspan="1" colspan="1">Tillman et al (2008)<sup>38
</sup></td><td rowspan="1" colspan="1">549</td><td rowspan="1" colspan="1">BPD</td><td rowspan="1" colspan="1">26</td><td rowspan="1" colspan="1">57</td></tr><tr><td rowspan="1" colspan="1">Total: 12 studies, <italic>n</italic> = 2892</td><td align="center" rowspan="1" colspan="1"></td><td align="center" rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">Weighted mean = 15%</td><td rowspan="1" colspan="1">Weighted mean = 28%</td></tr><tr><td rowspan="1" colspan="1"></td><td align="center" rowspan="1" colspan="1"></td><td align="center" rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">SD = 9.75</td><td rowspan="1" colspan="1">SD = 18.11</td></tr></tbody></table><table-wrap-foot><fn fn-type="other"><p><italic>Note</italic>: BPD = bipolar disorder.</p></fn></table-wrap-foot></table-wrap><p content-type="indent">Overall, these data challenge the assumption that VHs are atypical or uncommon in psychosis.</p></sec><sec id="s4"><title>Subclinical Symptoms in the General Community</title><p>Occasional hallucinatory experiences are fairly common in community-living individuals. However, community and epidemiological studies rarely report the prevalence rates for VH specifically and independently from other hallucinatory experiences, with few exceptions. <xref ref-type="table" rid="T3">Table 3</xref> (A) shows that the weighted mean for VH in the general community is 7.3% (SD = 5, based on 6 studies).</p><table-wrap id="T3" position="float"><label>Table 3.</label><caption><p>The Comparative Prevalence of Visual Hallucinations and Auditory Hallucinations in the General Community (A) and After Excluding Hallucinations Arising From Drug-Taking or Physical Illness (B)</p></caption><table frame="vsides" rules="groups"><thead><tr><th align="left" valign="bottom" rowspan="1" colspan="1"></th><th align="left" valign="bottom" rowspan="1" colspan="1"><italic>n</italic></th><th align="left" valign="bottom" rowspan="1" colspan="1">Visual Hallucinations (%)</th></tr></thead><tbody><tr><td align="left" rowspan="1" colspan="1">(A) General population</td><td align="center" rowspan="1" colspan="1"></td><td align="center" rowspan="1" colspan="1"></td></tr><tr><td rowspan="1" colspan="1"> Eaton et al (1991)<sup>39
</sup></td><td rowspan="1" colspan="1"> 810</td><td rowspan="1" colspan="1">8</td></tr><tr><td rowspan="1" colspan="1"> Tien (1991)<sup>40
</sup></td><td rowspan="1" colspan="1">18572</td><td rowspan="1" colspan="1">14</td></tr><tr><td rowspan="1" colspan="1"> Ohayon (2000)<sup>41
</sup></td><td rowspan="1" colspan="1">13057</td><td rowspan="1" colspan="1">3.2</td></tr><tr><td rowspan="1" colspan="1"> Waters et al (2003)<sup>42
</sup></td><td rowspan="1" colspan="1"> 562 (university students)</td><td rowspan="1" colspan="1">10</td></tr><tr><td rowspan="1" colspan="1"> Larøi and Van der Linden (2005)<sup>43
</sup></td><td rowspan="1" colspan="1"> 236 (university students)</td><td rowspan="1" colspan="1">32</td></tr><tr><td rowspan="1" colspan="1"> Kessler et al (2005)<sup>44
</sup></td><td rowspan="1" colspan="1"> 9282</td><td rowspan="1" colspan="1">6.3</td></tr><tr><td rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">Total: 6 studies, <italic>n</italic> = 42519</td><td rowspan="1" colspan="1">Weighted mean = 7.35%</td></tr><tr><td rowspan="1" colspan="1"></td><td align="center" rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">SD = 5.08</td></tr><tr><td colspan="2" rowspan="1">(B) Excl drug-taking and physical illness</td><td align="center" rowspan="1" colspan="1"></td></tr><tr><td rowspan="1" colspan="1"> Eaton et al (1991)<sup>39
</sup></td><td rowspan="1" colspan="1"> 810</td><td rowspan="1" colspan="1">4</td></tr><tr><td rowspan="1" colspan="1"> Tien (1991)<sup>40
</sup></td><td rowspan="1" colspan="1">18572</td><td rowspan="1" colspan="1">7</td></tr><tr><td rowspan="1" colspan="1"> Van Os et al (2000)<sup>45
</sup></td><td rowspan="1" colspan="1"> 7076</td><td rowspan="1" colspan="1">2–6</td></tr><tr><td rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">Total: 3 studies, <italic>n</italic> = 26 458 participants</td><td rowspan="1" colspan="1">Weighted mean = 6%</td></tr><tr><td rowspan="1" colspan="1"></td><td align="center" rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">SD: 1.73</td></tr></tbody></table></table-wrap><p content-type="indent">Little is known about what distinguishes visual hallucinators from non-hallucinators in the general population, but evidence suggests that factors such as intoxication and withdrawal from substances such as alcohol, cannabis and cocaine, and other physical states such as physical illness and stress are linked to VH.<sup><xref rid="CIT0046" ref-type="bibr">46</xref>,<xref rid="CIT0047" ref-type="bibr">47</xref></sup> Importantly, when research criteria exclude hallucinations arising from drug-taking or physical illness, the weighted percentages of hallucinations in the community reduce to 6% (see <xref ref-type="table" rid="T3">table 3</xref>, B).</p></sec><sec id="s5"><title>Eye Disease and Neurodegenerative Conditions</title><p>For comparison, it is helpful to understand the epidemiology of VH in other disorders in which VHs are common. The frequency estimates for VH in PD range from 15% to 40% (comparable to those in psychosis), and the frequency roughly doubles for PD dementia (PDD) (30%–90%) and DLB (60%–90%).<sup><xref rid="CIT0048" ref-type="bibr">48</xref>,<xref rid="CIT0049" ref-type="bibr">49</xref></sup> In age-related eye disease, between 10% and 60% of patients experience complex VH, depending on the severity of visual loss. The most common eye disease associated with VH is age-related macular degeneration.<sup><xref rid="CIT0050" ref-type="bibr">50</xref>,<xref rid="CIT0051" ref-type="bibr">51</xref></sup> VHs are the diagnostic criterion for Charles Bonnet syndrome (CBS). Such observations have prompted many authors to suggest that VH arise because of dysfunctions involving visual processing.</p></sec></sec><sec id="s6"><title>Demographic and Clinical Characteristics</title><sec id="s7"><title>Gender</title><p>Contradictory data have emerged regarding a VH gender pattern in psychosis or organic illness.<sup><xref rid="CIT0005" ref-type="bibr">5</xref>,<xref rid="CIT0037" ref-type="bibr">37</xref>,<xref rid="CIT0052" ref-type="bibr">52</xref>,<xref rid="CIT0053" ref-type="bibr">53</xref></sup> By contrast, studies in PDD and DLB do not report different frequencies of VH by gender, although it is important to consider the gender ratio in these disorders which are more common in men than women.</p></sec><sec id="s8"><title>Age Risk Factor and Longitudinal Course</title><p>With regards to age as a risk factor for VH in psychosis, some studies have demonstrated evidence that VH are more common in younger, compared with older, individuals with schizophrenia,<sup><xref rid="CIT0031" ref-type="bibr">31</xref>,<xref rid="CIT0053" ref-type="bibr">53</xref></sup> although negative findings exist.<sup><xref rid="CIT0016" ref-type="bibr">16</xref></sup> A similar inconsistency is found in the eye disease literature with only 3 of 9 studies investigating age and VHs reporting a weak association.<sup><xref rid="CIT0051" ref-type="bibr">51</xref></sup></p><p content-type="indent">By contrast, in nonclinical populations, the prevalence of VH is maximal in adolescence, and late adulthood, between which times the frequencies decrease.<sup><xref rid="CIT0040" ref-type="bibr">40</xref>,<xref rid="CIT0054" ref-type="bibr">54</xref></sup> One explanation for increased frequency of VH with age is that the prevalence of most chronic disorders increases with age, as does the prevalence of neurodegenerative disorders and age-related eye disease. In further support, the prevalence of death-bed visions among the dying may be as high as 50%.<sup><xref rid="CIT0055" ref-type="bibr">55</xref></sup></p><p content-type="indent">Thus, there appears to be a bimodal distribution of VH in the population with one peak in late adolescence and early adulthood, which is associated with psychosis, and a second increase in late life associated with eye and brain disease.</p><p content-type="indent">With regards to the longitudinal course, it is believed that hallucinations in schizophrenia tend to decrease as individuals age,<sup><xref rid="CIT0056" ref-type="bibr">56</xref></sup> although it is important to note that the risk of schizophrenia also declines with age.</p></sec><sec id="s9"><title>Clinical Characteristics of VH</title><p>The presence of VH in psychosis has often been linked to a more severe psychopathological profile<sup><xref rid="CIT0030" ref-type="bibr">30</xref>,<xref rid="CIT0057" ref-type="bibr">57</xref></sup> and to a less favorable prognosis.<sup><xref rid="CIT0018" ref-type="bibr">18</xref></sup> In patients with bipolar disorder, Baethge et al<sup><xref rid="CIT0037" ref-type="bibr">37</xref></sup> found that hospitalization for individuals with hallucinations (all modalities) averaged 17% longer than those who did not hallucinate.</p><p content-type="indent">In the general community, a link between VH and anxiety (OR = 5.0)<sup><xref rid="CIT0041" ref-type="bibr">41</xref>,<xref rid="CIT0058" ref-type="bibr">58</xref></sup> and psychotic pathology (OR = 6.6)<sup><xref rid="CIT0041" ref-type="bibr">41</xref></sup> has been reported. The important role of negative emotions in VH is illustrated in studies showing that stress and bereavement are linked to VH. For example, hallucinations of a dead spouse are common grief reactions in older adults.<sup><xref rid="CIT0059" ref-type="bibr">59</xref></sup></p><p content-type="indent">The literature in neurodegenerative disease is consistent with this view of greater psychopathology in VH, with studies showing poorer response to treatment, greater mortality and morbidity, major depressive syndrome, and a move to institutional care.<sup><xref rid="CIT0060" ref-type="bibr">60</xref>,<xref rid="CIT0061" ref-type="bibr">61</xref></sup></p><p content-type="indent">Thus, in both younger patients with psychosis and older patients with neurodegenerative disease, VHs are associated with poorer functioning and outcome. The same is not true of eye disease (eg, CBS) where the symptoms improve over time without progressive loss of cognitive function.</p></sec><sec id="s10"><title>Association With Other Symptoms</title><p>In schizophrenia, VHs typically co-occur in association with other hallucinations and other sensory modalities.<sup><xref rid="CIT0016" ref-type="bibr">16</xref>,<xref rid="CIT0028" ref-type="bibr">28</xref>,<xref rid="CIT0030" ref-type="bibr">30</xref>,<xref rid="CIT0062" ref-type="bibr">62</xref></sup> For example, it has been reported that co-occurring visual and auditory hallucinations occur in up to 84% of individuals with schizophrenia.<sup><xref rid="CIT0030" ref-type="bibr">30</xref></sup> Furthermore, early evidence suggested VH never occurred in psychosis without the presence of auditory hallucinations (either at the same time—multimodality hallucinations—or on different occasions).<sup><xref rid="CIT0062" ref-type="bibr">62</xref></sup> In Oorschot et al’s<sup><xref rid="CIT0057" ref-type="bibr">57</xref></sup> sample of individuals with mixed psychosis, VHs occurring alone were rarer than auditory hallucinations occurring alone. As shown in <xref ref-type="table" rid="T1">table 1</xref>, auditory hallucinations predominate over VH in terms of their relative prevalence.</p><p content-type="indent">Hallucinations in multiple modalities have also been noted in individuals with severe depression<sup><xref rid="CIT0063" ref-type="bibr">63</xref></sup> and with mixed psychiatric diagnoses,<sup><xref rid="CIT0064" ref-type="bibr">64</xref></sup> as well as in nonclinical adults and adolescents (<italic>n</italic> = 355, 11–13 years).<sup><xref rid="CIT0065" ref-type="bibr">65</xref></sup> Such co-occurrences of auditory/VHs suggest a common hallucinatory mechanism which, in combination with specific sensory dysfunctions, determines the modality of hallucinations.</p><p content-type="indent">It is important to note, however, that “simultaneous” (or “fused”) auditory and VHs are not a frequent occurrence.<sup><xref rid="CIT0016" ref-type="bibr">16</xref></sup> In most cases, they are experienced at different times (eg, an auditory hallucination one day and a VH the next). Furthermore, when simultaneous auditory/VHs do occur, they are typically unrelated<sup><xref rid="CIT0066" ref-type="bibr">66</xref></sup> (eg, seeing the devil while hearing the voice of a relative inside one’s head), suggesting that the mechanisms for auditory and VHs in these disorders must be partly independent, though with some overlap.</p><p content-type="indent">By contrast, a different pattern can be observed in organic disease. In PD, VHs predominate over auditory hallucinations,<sup><xref rid="CIT0067" ref-type="bibr">67</xref></sup> and in CBS, the absence of hallucinations in other modalities is a diagnostic criterion. Where eye disease co-occurs with dementia, auditory hallucinations and delusions may appear as the dementia progresses, as is the case in PD<sup><xref rid="CIT0068" ref-type="bibr">68</xref></sup> or dementia alone.<sup><xref rid="CIT0069" ref-type="bibr">69</xref></sup> In these disorders, auditory and VHs very rarely occur at the same time.</p><p content-type="indent">Overall, the relative proportion of auditory to visual modality hallucinations seems to differentiate the psychosis spectrum from organic conditions.</p></sec></sec><sec id="s11"><title>Phenomenological Features of VH</title><sec id="s12"><title>Psychosis</title><p>There are few systematic or comprehensive studies of VH as dimensional experiences in psychosis. Exceptions include Goodwin et al,<sup><xref rid="CIT0016" ref-type="bibr">16</xref></sup> Gauntlett and Kuipers,<sup><xref rid="CIT0064" ref-type="bibr">64</xref></sup> and Dudley et al.<sup><xref rid="CIT0070" ref-type="bibr">70</xref></sup> For the following review, information was drawn from these and other studies.<sup><xref rid="CIT0012" ref-type="bibr">12</xref>,<xref rid="CIT0016" ref-type="bibr">16</xref>,<xref rid="CIT0028" ref-type="bibr">28</xref>,<xref rid="CIT0053" ref-type="bibr">53</xref>,<xref rid="CIT0062" ref-type="bibr">62</xref>,<xref rid="CIT0071" ref-type="bibr">71</xref>,<xref rid="CIT0072" ref-type="bibr">72</xref></sup></p><sec id="s13"><title>Perceptual Qualities.</title><p>VHs in psychosis are reported to have the physical properties of real perceptions. They are often life-sized, detailed, and solid. They are projected into the external world in most cases and are typically “anchored in external space,” either just beyond the reach of individuals or further away. VHs often have 3 dimensional shapes, with depth and shadows, and distinct edges. VH can be colorful or in black and white. Images are often described as dynamic with the contents changing in size, shape, and movement but may also be static.</p></sec><sec id="s14"><title>Temporal Aspects.</title><p>The frequency of hallucinatory episodes varies from rare to frequent, and episodes can last several seconds to several minutes. VH may be experienced during both day and night.</p></sec><sec id="s15"><title>Content.</title><p>Fully formed VHs are more common than unformed visual experiences and distortions. Complex VHs often comprise images of people (walking, family), faces, animals, objects, or events (eg, visions of fires) taking place in front of the individual. In contrast to hallucinations in organic conditions, a common theme is of visions with frightening content (bugs, dogs, snakes, distorted faces), and these are linked to distress. Unlike VH in PD, visions of dead people are rare, although visions of God, angels, the devil, saints, and fairies are common.</p></sec><sec id="s16"><title>Reality.</title><p>VHs are perceived to be real and “definitely present” in a concrete sense. In further support for the subjective reality of the experience, a majority of individuals undertake some activity directly related to the vision—such as moving toward the vision, hitting at the vision, or moving away. In the case of distressing images, individuals may act to keep themselves safe.</p></sec><sec id="s17"><title>Sense of Control.</title><p>A lack of control over the content and appearance is a prominent feature of VH in psychosis. Individuals are surprised when VHs occur and are generally helpless to change or stop them. In general, individuals believed that visions are experienced only by themselves.</p></sec><sec id="s18"><title>Onset and Triggers.</title><p>The onset of VH has been linked to stress, tiredness, loneliness, and relationship problems in psychiatric individuals. Other psychological triggers include negative emotions, and they may co-vary with levels of anxiety.</p></sec><sec id="s19"><title>Reactions.</title><p>A mixture of positive and negative images may be experienced. Reactions vary and can include pleasure, happiness and reassurance, or indifference. Images can also evoke fright, depression, sadness, or hopelessness. While the <italic>content</italic> of VH is often impersonal or unrelated to the person, images are often interpreted to have personal implications. Many individuals believe that the content of visions must be acted upon, for fear of a negative event occurring as a consequence. This differs from hallucinations in organic conditions, where VHs are not generally perceived to be real.</p></sec><sec id="s20"><title>Beliefs and Appraisals.</title><p>VHs may be believed to arise from an external source, particularly of supernatural origin. Images of powerful religious figures are often perceived to be visions intended as a sign for the person to act and as a threat to their physical or psychological wellbeing. This can also impact on the individual’s belief system and can be used as evidence for their delusional beliefs.</p><p content-type="indent">Overall, such rich phenomenology of VH in psychosis points to true hallucinatory experiences and not only misperceptions. This close examination of VH characteristics also reveals remarkable similarities with auditory hallucinations with regards perceptual quality, contents, lack of control, beliefs, appraisals, and reactions.</p><p content-type="indent">With regards a comparison with organic disorders, broadly speaking, the form and character of VH in psychosis is similar to those seen in eye disease and neurodegeneration. Although there is a notable lack of studies making direct comparisons, there are several characteristics that distinguish VH in psychotic disorders from other disorders, namely frightening contents, emotional reactions, and appraisals of personal significance; a lack of illusions (common in neurodegenerative disease) and simple VHs (common in eye disease) also differ.</p></sec></sec><sec id="s21"><title>Subclinical Symptoms in the General Community</title><p>Nonclinical individuals in the community report vivid VH, where objects are real and uncontrollable, but often of brief duration.<sup><xref rid="CIT0073" ref-type="bibr">73</xref></sup> The features of VH in nonclinical samples are broad-ranging and include unformed VH (such as dots, flashes of light and other unformed shapes) and formed VH (people and faces, but also aliens).<sup><xref rid="CIT0065" ref-type="bibr">65</xref></sup> In contrast to VH in psychosis, hallucinated images in nonclinical populations are less likely to involve complex scenes but more likely to show people.<sup><xref rid="CIT0052" ref-type="bibr">52</xref></sup></p><p content-type="indent">These VH clinical features are similar to that of auditory hallucinations in nonclinical populations, which also tend to be brief and mostly neutral or pleasant in content.<sup><xref rid="CIT0074" ref-type="bibr">74</xref></sup></p></sec><sec id="s22"><title>Eye Disease and Neurodegenerative Conditions</title><p>For comparison with the above, the most detailed accounts of visual content are found in the eye disease literature (CBS).<sup><xref rid="CIT0075" ref-type="bibr">75</xref></sup> The commonest contents are of simple hallucinations, followed by images of people or animals (50%–80%), patterns (55%), faces often described as grotesque and cartoon-like (40%), landscapes or inanimate objects (20%). They are usually colorful. Unlike in psychosis, VHs in CBS are not generally perceived to be real or to have personal meaning. Only in a third of the cases is the content negative. Once individuals understand they are a common feature of poor vision, anxiety about VH generally decreases. This differs from psychosis, where lack of insight may contribute to distress about these experiences. Other dimensional features related to clarity, frequency, temporal factors, and appearance are similar to those in psychosis.<sup><xref rid="CIT0076" ref-type="bibr">76</xref></sup> In PD, VHs mostly consist of people who may be familiar or not, and alive or deceased (73%), animals (33%), and objects (19%) which may appear briefly and move sideways (passage hallucination).<sup><xref rid="CIT0049" ref-type="bibr">49</xref></sup> The contents are fairly stereotyped and repetitive but may last for hours at a time. Experiences appear to be real and outside voluntary control but are not often perceived as frightening. In dementia, VHs tend to be of fairly mundane content, including unfamiliar or small figures, faces, animals, and objects/machines, and are rarely distressing.<sup><xref rid="CIT0069" ref-type="bibr">69</xref></sup></p><p content-type="indent"><xref ref-type="fig" rid="F1">Figure 1</xref> (adapted from ffytche<sup><xref rid="CIT0077" ref-type="bibr">77</xref></sup>) provides an overview of VH in different clinical settings, where a range of clinical conditions (columns) are cross-tabulated with VH content and related phenomena (rows). Comparing the phenomenology of VH in psychosis with other conditions suggests that they are most similar to VH in cortical and subcortical disorders (red box) but differ in the relative predominance of auditory and VHs. Whether this is an important neurobiological distinction is unclear, and the boundary of the grouping has been left open as indicated by the dashed line.</p><fig fig-type="figure" id="F1" position="float"><label>Fig. 1.</label><caption><p>Visual perceptual symptoms and their clinical contexts.<sup><xref rid="CIT0077" ref-type="bibr">77</xref></sup></p><p>A range of clinical conditions (columns) are cross-tabulated with visual hallucination (VH) content and related phenomena (rows). For each condition, the percentage of individuals with VHs reporting a given content is coded red (>20%), pink (10%–20%), or white (not reported or < 10%). The prevalence of each symptom in psychosis is taken from.<sup><xref rid="CIT0064" ref-type="bibr">64</xref></sup> For auditory hallucinations, (+) indicates higher prevalence than VH and (−) indicates lower prevalence than VH (figure adapted from ffytche<sup><xref rid="CIT0077" ref-type="bibr">77</xref></sup>). Visual experiences in schizophrenia best match the phenomena reported in the red box derived from PD, AD, DLB, and peduncular lesions—but not the green (eye and visual pathway pathology) and blue (serotonergic syndrome) boxes.
</p></caption><graphic xlink:href="schbul_sbu036_f0001"></graphic></fig></sec></sec><sec id="s23"><title>The Assessment of VHs</title><p>It is often difficult to distinguish VH from related visual phenomena such as illusions, distortions, and misperceptions that co-occur with VH in psychosis and other conditions. The relationship between what is seen and what is actually present in the environment is complex and poorly understood with internal models and top-down inference interacting with visual inputs. The match between what is perceived and what is present is closest for veridical perception (our day-to-day visual perceptual experience), tenuous for illusions, and absent for hallucinations; however, there are no sharp dividing lines between categories. Based on a working definition of hallucinations,<sup><xref rid="CIT0078" ref-type="bibr">78</xref></sup> the key features to elicit in an assessment of VH are (see <xref ref-type="boxed-text" rid="B1">Box 1</xref>):</p><list list-type="order"><list-item><p>They must be experienced in full consciousness (rules out sleep-related VH, fever, delirium, and hypnosis).</p></list-item><list-item><p>Not elicited by an external stimulus (excludes visual distortions and illusions).</p></list-item><list-item><p>The experience has a sense of reality to resemble a veridical perception (must have physical properties of real perceptions and be located in external space; note that this does not mean that VH must be perceived to be real or that insight must be lacking).</p></list-item><list-item><p>The subject does not feel s/he has direct and voluntary control (rules out visual imagery).</p></list-item></list><boxed-text id="B1" position="float"><caption><title>Box 1. A Diagnostic Algorithm for Visual Hallucinations and Related Phenomena<sup><xref rid="CIT0079" ref-type="bibr">79</xref></sup></title></caption><sec id="b1"><title>Question 1: Are the visual phenomena experienced (a) during sleep, (b) on the border of waking and sleeping, or (c) while awake?</title><list list-type="simple"><list-item><p>a) During sleep</p></list-item><list-item><p> Rule out: dream</p></list-item><list-item><p> Possibility 1: incubus phenomenon</p></list-item><list-item><p> Possibility 2: visual sleep start</p></list-item><list-item><p>b) On the border of waking and sleeping</p></list-item><list-item><p> Possibility 1: hypnagogic hallucination</p></list-item><list-item><p> Possibility 2: hypnopompic hallucination</p></list-item><list-item><p>c) While awake</p></list-item><list-item><p> Go to Question 2</p></list-item></list></sec><sec id="b2"><title>Question 2: Are the visual phenomena perceptual in nature? (ie, with physical properties comparable with sensory perceptions)</title><list list-type="simple"><list-item><p>No Rule out: imagery</p></list-item><list-item><p>Yes Continue with Question 3</p></list-item></list></sec><sec id="b3"><title>Question 3: Do they constitute (a) images without a representation in the outside world, (b) images with a representation in the outside world, or (c) distortions?</title><list list-type="simple"><list-item><p>a) Without representation in the outside world (visual hallucinations):</p></list-item><list-item><p> Go to Question 4</p></list-item><list-item><p>b) With a representation in the outside world (visual illusions):</p></list-item><list-item><p> Go to Question 5</p></list-item><list-item><p>Distortions (metamorphopsias): </p></list-item><list-item><p> Go to Question 6</p></list-item></list></sec><sec id="b4"><title>Question 4: Are the hallucinations (a) simple in nature, (b) geometric, (c) complex, or (d) compound (ie, multimodal) in nature?</title><list list-type="simple"><list-item><p>a) Simple hallucinations</p></list-item><list-item><p> Rule out: physiological phenomena such as blue-field entoptic phenomenon, macular star pattern, or mouches volantes (uncomplicated)</p></list-item><list-item><p> Determine: type and context</p></list-item><list-item><p>b) Geometric hallucinations</p></list-item><list-item><p> Determine: type and context</p></list-item><list-item><p>c) Complex hallucinations</p></list-item><list-item><p> Determine: type and context</p></list-item><list-item><p>d) Compound hallucinations</p></list-item><list-item><p> Determine: type (ie, sensory modalities) and context</p></list-item></list></sec><sec id="b5"><title>Question 5: Are the illusions attributable to (a) physical reality, (b) the perceptual system, or (c) mental associations?</title><list list-type="simple"><list-item><p>a) Physical illusions</p></list-item><list-item><p> Determine: type and context (never pathological!)</p></list-item><list-item><p>b) Physiological illusions</p></list-item><list-item><p> Determine: type and context</p></list-item><list-item><p>c) Cognitive illusions</p></list-item><list-item><p> Determine: type and context</p></list-item></list></sec><sec id="b6"><title>Question 6: Do the distortions have (a) a peripheral or (b) a central origin?</title><list list-type="simple"><list-item><p>a) Peripheral metamorphopsias</p></list-item><list-item><p> Determine: type and context</p></list-item><list-item><p>b) Central metamorphopsias</p></list-item><list-item><p> Determine: type and context</p></list-item></list></sec></boxed-text></sec><sec id="s24"><title>Cognition</title><p>Cognitive processes of VH in psychosis have rarely been investigated. In organic disorders, hallucinations are held to reflect disorders within distributed perceptual systems. The Perceptual and Attentional Deficit model advocates for a combination of impaired visual processing and attention in VH in neurodegenerative disorders and eye disease.<sup><xref rid="CIT0080" ref-type="bibr">80</xref></sup> Diederich et al’s<sup><xref rid="CIT0081" ref-type="bibr">81</xref></sup> contemporaneous PD-developed interactive model similarly proposes a combination of poor visual input and processing with defective central visual monitoring. More recently, Shine et al’s Attentional model<sup><xref rid="CIT0082" ref-type="bibr">82</xref></sup> proposes that hallucinations occur in PD when there is underactivity in dorsal attentional networks in the presence of ambiguous percepts. Each of these models, therefore, proposes that combined attentional and visual perceptual problems lead to VH.</p><p content-type="indent">In psychosis, however, perceptual processes are usually believed to be intact or even overactive. It has been suggested that VH in psychosis may be best understood in terms of the intrusion into awareness of subconscious images or highly vivid mental imagery, as modulated by personal, social, or psychological variables.<sup><xref rid="CIT0058" ref-type="bibr">58</xref></sup> In support, an increase in the salience of imagery has been found in schizophrenia individuals with VH.<sup><xref rid="CIT0045" ref-type="bibr">45</xref></sup> Other cognitive deficits found in psychotic VH include source-monitoring impairments, such as difficulties making internal/external and self/other discriminations<sup><xref rid="CIT0083" ref-type="bibr">83</xref></sup> and confusion regarding whether the source of material was real or imagined.<sup><xref rid="CIT0084" ref-type="bibr">84</xref></sup> Such source-monitoring deficits are also commonly found in auditory hallucinations<sup><xref rid="CIT0085" ref-type="bibr">85</xref></sup> and may lead to these events being believed as real.</p><p content-type="indent">Personal, social, and cultural contributors to VH have not yet been systematically investigated, although top-down mechanisms (which include expectations, personal meaning-making, and social context) may influence dynamic attentional processes by biasing the competition between potential perceptions toward objects and persons that have personal and social relevance. In support for this view, stress and bereavement are linked to the onset of VH. Further support comes from cognitive models of psychosis<sup><xref rid="CIT0078" ref-type="bibr">78</xref></sup> that propose that key influences of personal events, social/cultural context, and expectations have the ability to activate percepts in the absence of external stimulation.</p><p content-type="indent">Altogether, mechanisms of VH in psychosis are not well understood. Interesting similarities with the literature on auditory hallucination exist, including source-monitoring deficits and the strong influence of top-down mechanisms. By contrast, evidence for visual processing difficulties which feature strongly in models of VH in the organic literature<sup><xref rid="CIT0077" ref-type="bibr">77</xref></sup> is lacking.</p></sec><sec id="s25"><title>Brain Imaging and Electrophysiology</title><p>In the field of psychosis, a study conducted in individuals with first-episode psychosis (<italic>n</italic> = 15 with VH) showed per-hallucinatory activity within visual association cortex, while the vividness of VH was linked to activity within the primary visual cortex.<sup><xref rid="CIT0086" ref-type="bibr">86</xref></sup> Activity in the visual association cortex during VH has also been demonstrated in single case studies in schizophrenia.<sup><xref rid="CIT0087" ref-type="bibr">87</xref>,<xref rid="CIT0088" ref-type="bibr">88</xref></sup> Concerning the organic literature, dysfunctions of higher visual processing areas during or between VH episodes have been found in Alzheimer’s disease,<sup><xref rid="CIT0089" ref-type="bibr">89</xref></sup> DLB,<sup><xref rid="CIT0090" ref-type="bibr">90</xref>,<xref rid="CIT0091" ref-type="bibr">91</xref></sup> and CBS<sup><xref rid="CIT0092" ref-type="bibr">92</xref></sup> within the ventral and the dorsal visual pathways involved in object recognition and visuospatial memory<sup><xref rid="CIT0093" ref-type="bibr">93</xref>,<xref rid="CIT0094" ref-type="bibr">94</xref></sup> as well as the frontal lobes.<sup><xref rid="CIT0095" ref-type="bibr">95</xref></sup> Furthermore, structural changes in these areas were independent of cognitive function and age.<sup><xref rid="CIT0096" ref-type="bibr">96</xref></sup> Overall, symptom-capture studies in these populations showed that the location of the per-VH activity correlated with the phenomenological content of the hallucinatory experiences (ie, color-specialized cortex if in color, face-specialized cortex if faces are experienced, etc).</p><p content-type="indent">Connectivity studies have much relevance for the study of VH, given that dysconnectivity is a prominent model for psychosis, which could also apply to specific symptoms such as hallucinations.<sup><xref rid="CIT0097" ref-type="bibr">97</xref></sup> The dysconnectivity hypothesis suggests that the existence of impaired connectivity between different brain regions is responsible for abnormal functional integration within neural networks. In support for dysconnectivity, using diffusion tensor imaging, Ashtari and collaborators showed that adolescents suffering from early-onset schizophrenia with a history of VH exhibited lower fractional anisotropy, potentially reflecting a loss in white matter integrity, in the left inferior longitudinal fasciculus which connects temporal and occipital cortices, when compared with individuals without VH.<sup><xref rid="CIT0098" ref-type="bibr">98</xref></sup></p><p content-type="indent">The hippocampal complex (HC) is also of considerable interest with regards to VH in both neurodegeneration and psychosis. The HC has been shown to be atrophied in individuals with PD and VH,<sup><xref rid="CIT0099" ref-type="bibr">99</xref></sup> and it appears to occupy a key place within the networks involved in VH in psychosis.<sup><xref rid="CIT0100" ref-type="bibr">100</xref></sup> For example, a recent multimodal connectivity study, combining functional connectivity, tract-based spatial statistics, and shape analysis of the HC, confirmed differential connectivity patterns of this structure in individuals with schizophrenia. Moreover, this abnormal connectivity depends on the sensory-modality of hallucinatory experiences involved and was particularly obvious with visual areas in patients with VH.<sup><xref rid="CIT0097" ref-type="bibr">97</xref></sup> In addition, a symptom-capture study of VH in schizophrenia<sup><xref rid="CIT0087" ref-type="bibr">87</xref></sup> reported cortical activity in the HC, although this was not reported in CBS.<sup><xref rid="CIT0092" ref-type="bibr">92</xref></sup></p><p content-type="indent">A particular subtype of functional connectivity studies focuses on spontaneous fluctuations at rest. It has already been used in the field of auditory hallucinations to test the hypothesis of disrupted intrinsic connectivity as a pathological mechanism.<sup><xref rid="CIT0101" ref-type="bibr">101</xref></sup> Jardri and colleagues’ study confirmed a dynamic interaction between association sensory cortices and the default-mode network (DMN) for patients with multisensory hallucinations, including VH.<sup><xref rid="CIT0086" ref-type="bibr">86</xref></sup> Sensory and DMN networks were found to be anticorrelated during the experience of hallucinations; furthermore, the DMN spatial and temporal instability persisted during non-hallucinatory periods.<sup><xref rid="CIT0086" ref-type="bibr">86</xref></sup> Impaired interactions with the DMN have also been suggested in the pathophysiology of VH in PD,<sup><xref rid="CIT0082" ref-type="bibr">82</xref></sup> but contrary to what has been proposed in first-episode psychosis in which the DMN seems primarily and intrinsically affected, these authors proposed an external DMN interference through aberrant interactions with ventral and dorsal attentional networks.</p><p content-type="indent">Fewer studies have investigated the electrophysiology of VH. Spencer and colleagues found reduced visual cortex activation as measured by a negative evoked potential component (NI) and increased gamma band phase locking associated with VH in schizophrenia, consistent with an underlying visual cortical hyperexcitability and reduced responsiveness to external visual stimulation in this subgroup.<sup><xref rid="CIT0102" ref-type="bibr">102</xref></sup> Indices of hyperexcitability and reduced responsiveness have also been found in PD (a delayed P100 evoked potential component)<sup><xref rid="CIT0103" ref-type="bibr">103</xref></sup> and post-lysergic acid diethylamide VH (occipital theta coherence).<sup><xref rid="CIT0104" ref-type="bibr">104</xref></sup> The electrophysiology of VH capture is consistent with brain imaging studies in suggesting activation of visual association cortex as measured by coherence<sup><xref rid="CIT0105" ref-type="bibr">105</xref></sup> or theta/alpha desynchronization.<sup><xref rid="CIT0106" ref-type="bibr">106</xref></sup></p></sec><sec id="s26"><title>Comparative Psychopathology</title><p>What are the implications of the similarities and differences between VH in psychosis spectrum, eye and neurodegenerative disease outlined above? It is clear that there is an absence of evidence in many areas, and that direct comparative work is required. VHs in psychosis most closely resemble VH in neurodegeneration, and the association of auditory and VHs in these conditions suggests the 2 modalities of hallucination share a common pathophysiological mechanism. Dysfunctions in attentional and executive/top-down mechanisms are also common in both neurodegenerative and psychotic conditions, as are occipital cortex and HC involvement during hallucinations.</p><p content-type="indent">However, the differing predominance of auditory and visual modalities in neurodegenerative disease and psychosis, the phenomenological differences at the levels of emotional reactions and appraisals, and the differing dysconnectivity and visual processing profiles suggest there are also important differences. Perhaps the same pathological mechanism has differential effects on the visual and auditory systems in psychosis and neurodegenerative disease, depending on the presence/absence of specific co-occurring sensory dysfunctions. Such comparative insights have potentially important implications for treating VH as they provide a rationale for importing approaches found effective in one clinical context to another.</p></sec><sec id="s27"><title>Treatment Approaches</title><sec id="s28"><title>Cognitive Behavioral Therapy</title><p>Cognitive behavioral therapy has an established, though modest, evidence base for the treatment of psychosis (referred to as CBTp). However, evidence for its use in VH rests mainly on case studies.</p><p content-type="indent">Recently, O’Brien and Johns<sup><xref rid="CIT0107" ref-type="bibr">107</xref></sup> described an individual who had visions of snakes and who held beliefs that she was at risk of harm from these snakes. CBT that included a graded exposure approach to help reduce fear and escape reaction showed some benefit which was maintained at 3 months. Whether this is helpful with other visual experiences is unclear, although studies show that the appraisals and beliefs should be a core target for treatment.<sup><xref rid="CIT0070" ref-type="bibr">70</xref>,<xref rid="CIT0108" ref-type="bibr">108</xref></sup></p><p content-type="indent">Collerton and Dudley<sup><xref rid="CIT0109" ref-type="bibr">109</xref></sup> developed a model drawn from a cognitive model of auditory hallucinations and panic and which targets appraisal and reactions to VH. Given that avoidance, escape and safety-seeking behaviors are common but unhelpful strategies, the aim of treatment is for people to recognize that they are safe, and that the fear may be real but the danger is not. The therapy includes psychoeducation about VH, reality testing and normalization, as well as understanding of triggers. Imagery exposure and transformation strategies are used to attempt control over the experience. A case series (under review) describes the use of this treatment approach in 4 people with psychosis with distressing VH.</p><p content-type="indent">Overall, evidence for the effectiveness of CBT for VH is limited. The treatment of VH may be improved by addressing trauma and stress as a key feature of VH presentation, and with the development of sensitive and specific outcome measures that match the goals of treatment.</p></sec><sec id="s29"><title>The Pharmacological Management of VH</title><p>There is limited evidence for specific pharmacological treatments for VH in psychosis. Antipsychotics are typically used, but some studies have reported that VHs were not linked to treatment effects<sup><xref rid="CIT0028" ref-type="bibr">28</xref>,<xref rid="CIT0110" ref-type="bibr">110</xref></sup> or even that VHs may be a marker of neuroleptic resistance.<sup><xref rid="CIT0010" ref-type="bibr">10</xref></sup> Clozapine has been reported as effective for VH in PD,<sup><xref rid="CIT0111" ref-type="bibr">111</xref></sup> but studies in schizophrenia are lacking.</p><p content-type="indent">The literature drawn from organic disease suggests the different approaches that might be considered. For example, for individuals with visual impairment, treatment of the eye condition can reduce the risk of VH.<sup><xref rid="CIT0112" ref-type="bibr">112</xref></sup> The case report literature has highlighted a range of medications that may help reduce VH, but there is currently a lack of clinical trial data. For example, drugs increasing cholinergic activity are thought to reduce the risk for VH. The AchE-I (rivastigmine, donepezil, and galantamine) are beneficial when treating behavioral and psychological symptoms of dementia<sup><xref rid="CIT0113" ref-type="bibr">113</xref></sup> and PD<sup><xref rid="CIT0114" ref-type="bibr">114</xref></sup> and have been reported to help in schizophrenia.<sup><xref rid="CIT0114" ref-type="bibr">114</xref></sup> Other drugs have been used in organic conditions (antidepressants, memantine, or anticonvulsants) but have not been examined in psychosis.</p><p content-type="indent">In sum, there is a lack of systematic studies, but this overview suggests new possibilities for treating VH in psychosis.</p></sec></sec><sec sec-type="conclusions" id="s30"><title>Conclusion</title><p>Altogether, this article reviewed the available evidence on the prevalence, phenomenology, clinical characteristics, assessment methods, cognition, brain imaging, electrophysiology, and treatment approaches for VH in the psychosis spectrum.</p><p content-type="indent">There are significant potential benefits to making direct comparisons of VH in organic and psychotic illness. These include informing our understanding and theoretical models of VH in schizophrenia and across diagnostic categories, informing hypothesis-driven questions for research, and suggesting new possibilities for therapeutic interventions.</p><p content-type="indent">This is the first review of VH in psychosis to incorporate data using different methodological perspectives and different population groups. One open question is whether VHs in psychosis have the same pathological mechanisms as VH in eye or organic conditions. From the evidence, it is clear that they are not as closely associated as they might appear. They show some similarities in clinical presentation and form, and in cognitive mechanisms, but differences in age, emotional content and appraisal, pathological profile, and neuroimaging findings might argue for different causal pathways. There is also little evidence one way or the other on whether visual perception in psychosis is as impaired as it is in other disorders.</p><p content-type="indent">This review also aided our understanding of hallucinations across different modalities, and particularly auditory hallucinations. As seen above, auditory hallucinations and VH frequently co-occur, although not necessarily simultaneously. One possibility suggests a set of core pathological mechanisms in addition to specific modality-dependent dysfunctions. Alternatively, the same pathological mechanism has differential effects on the visual and auditory systems in psychosis and neurodegenerative disease, depending on the presence/absence of specific co-occurring sensory dysfunctions. Clearly, direct comparisons are needed testing the compatibility of theoretical models developed in the 2 modalities of hallucinations (see key future directions in <xref ref-type="table" rid="T4">table 4</xref>).</p><table-wrap id="T4" position="float"><label>Table 4.</label><caption><p>Future Directions</p></caption><table frame="vsides" rules="groups"><tbody><tr><td valign="bottom" rowspan="1" colspan="1"></td><td valign="bottom" rowspan="1" colspan="1">Future Studies Should Seek to Pursue the Following Research Questions</td></tr><tr><td rowspan="1" colspan="1">i)</td><td rowspan="1" colspan="1">What is the frequency of VH in psychosis, as assessed using prospective, rigorous, and detailed investigations? What is the relationship of VH with hallucinations in other modalities (eg, temporal relationship, similarities in content and emotional themes)?</td></tr><tr><td rowspan="1" colspan="1">ii)</td><td rowspan="1" colspan="1">Are “fused” multimodality hallucinations characteristic of schizophrenia or do they occur in other disorders? Is there a close relationship between VH and voices in fused hallucinations, such that there is a match between the vision and the verbal output? Is the acoustic information closely linked to the speaker’s characteristics (sex, age, emotional characteristics)? Are there reports of fused hallucinations of animals (eg, dogs barking), and environmental scenes (eg, car with engine running, water falls), in addition to fused hallucinations of persons (person talking)?</td></tr><tr><td rowspan="1" colspan="1">iii)</td><td rowspan="1" colspan="1">What are the similarities and differences in the VH profile of individuals with psychosis compared with other psychiatric/neurological conditions at the level of phenomenological characteristics, risk factors, triggers, cognition, psychology, social and brain factors, as assessed using direct comparisons?</td></tr><tr><td rowspan="1" colspan="1">iv)</td><td rowspan="1" colspan="1">Are the same brain regions and networks activated during VH in psychosis also activated during VH in other conditions? Are the changes in brain structure, function, and connectivity predisposing to VH the same across different conditions?</td></tr><tr><td rowspan="1" colspan="1">v)</td><td rowspan="1" colspan="1">What are the mechanisms involved in hallucinations in different modalities? Is there a set of core pathological mechanisms in addition to specific modality-dependent dysfunctions? Alternatively, is there one pathological mechanism that has differential effects on visual and auditory systems?</td></tr><tr><td rowspan="1" colspan="1">vi)</td><td rowspan="1" colspan="1">What is the compatibility of verbal (language based) models of auditory hallucinations which focus on deviations in language areas, with models of <italic>visual</italic> hallucinations?</td></tr><tr><td rowspan="1" colspan="1">vii)</td><td rowspan="1" colspan="1">What are the mechanisms by which distress and negative mood contribute to both visual and auditory hallucinations?</td></tr><tr><td rowspan="1" colspan="1">viii)</td><td rowspan="1" colspan="1">What is the predictive value of non-clinical VH (especially for those first observed in childhood/adolescence), as assessed using longitudinal epidemiological study designs?</td></tr><tr><td rowspan="1" colspan="1">ix)</td><td rowspan="1" colspan="1">Are there different subtypes of VH and which type is most often associated with poorer prognosis and functioning?</td></tr><tr><td rowspan="1" colspan="1">x)</td><td rowspan="1" colspan="1">Research into the treatment for VH in individuals requiring care is urgently needed, examining the efficacy of existing and new interventions in large samples</td></tr></tbody></table><table-wrap-foot><fn fn-type="other"><p><italic>Note</italic>: VH = visual hallucination.</p></fn></table-wrap-foot></table-wrap></sec><sec><title>Funding</title><p>F.W. is supported by a National Health and Medical Research Grant (634329) and funding from North Metro Health Service Mental Health (Graylands Hospital).</p></sec></body><back><ack><title>Acknowledgment</title><p>The authors have declared that there are no conflicts of interest in relation to the subject of this study.</p></ack><ref-list><title>References</title><ref id="CIT0001"><label>1.</label><mixed-citation publication-type="book"><person-group person-group-type="author"><name><surname>Macpherson</surname><given-names>F</given-names></name></person-group><article-title>The philosophy and psychology of hallucination: an introduction</article-title>. 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