Is CBT Worthless?

According to a new meta-analysis in Psychological Medicine (Lynch et al., 2009), Cognitive Behavioral Therapy (CBT) is not helpful for those with schizophrenia and bipolar disorder, and any improvements seen in major depression are rather small:

Conclusions: CBT is no better than non-specific control interventions in the treatment of schizophrenia and does not reduce relapse rates. It is effective in major depression but the size of the effect is small in treatment studies. On present evidence CBT is not an effective treatment strategy for prevention of relapse in bipolar disorder.

CBT is a form of psychotherapy that attempts to change the patient's unhealthy thoughts and actions. The patient learns to identify distorted thought patterns and beliefs, and to replace them with more productive ways of thinking and acting. Frequently the treatment is very brief, and also "highly structured, problem orientated and prescriptive, and individuals are active collaborators." The short duration of 5-20 weeks in most cases is appealing to insurance companies. Previous studies have endorsed CBT as one of the most effective treatments for major depression and many other disorders (see this review of CBT meta-analyses by Butler et al., 2006). Recommendations for CBT primarily as an adjunct treatment in schizophrenia are fewer, and have been more common in the UK (Rosack, 2002) than in Canada and the US (but see Rector & Beck, 2002). CBT may have beneficial effects during the depressive phase of bipolar disorder, but previous studies have been variable and inconclusive (Miklowitz & Scott, 2009).

Lately we've been treated to a plethora of articles and press releases saying that antidepressants are worthless and no better than placebo. The present meta-analysis by Lynch et al. (2009) came to the same conclusion about CBT in schizophrenia, and ratcheted down its effectiveness in major depression. The press release is quite blunt:

Cognitive Therapy Is Of No Value In Schizophrenia, Analysis Of Studies Suggests

ScienceDaily (June 26, 2009) — Research co-led by an academic at the University of Hertfordshire, concludes that cognitive behavioural therapy (CBT) is of no value in schizophrenia and has limited effect on depression.

. . .

The results of the review suggest that not only is CBT ineffective in treating schizophrenia and in preventing relapse, it is also ineffective in preventing relapses in bipolar disorder.

The review also suggests that CBT has only a weak effect in treating depression, but it has a greater effect in preventing relapses in this disorder.

The meta-analysis included studies examining the effectiveness of CBT against symptoms in schizophrenia and depression, and in reducing relapse in schizophrenia, depression, and bipolar disorder. Rigorous criteria were used when selecting only well-conducted clinical trials of CBT for inclusion:

The studies were required to use a control intervention that the study investigators either explicitly considered not to have specific therapeutic effects or which might reasonably be regarded as lacking these (e.g. supportive therapy, psycho-education, relaxation). We also included studies comparing CBT to pill placebo (which have only been carried out in major depression). Blindness of evaluations was not specified as a requirement for inclusion, but was examined as a moderator variable. In keeping with the general approach of meta-analysing methodologically rigorous trials, we did not include studies with small sample sizes (less than 10 participants in either group) or studies that were identified by the authors as pilot studies.

Lynch et al. provided a list of excluded studies in their Supplementary Materials, and I imagine there will be much debate in the field over the inclusion and exclusion criteria. The authors end on a cautionary note:

The authors of meta-analyses of CBT for depression seem unperturbed by the fact that they are basing their conclusions on studies that have often been carried out against TAU [treatment as usual] or a waiting list control; that have not always been randomized; that sometimes failed to use diagnostic criteria; and that so far have ignored the moderating effect of blindness altogether. These issues are not trivial; the findings of our meta-analysis could be viewed as an object lesson on the importance of taking such sources of bias into account.

References

Butler AC, Chapman JE, Forman EM, Beck AT. (2006). The empirical status of cognitive-behavioral therapy: a review of meta-analyses. Clin Psychol Rev. 26:17-31.

Lynch, D., Laws, K., & McKenna, P. (2009). Cognitive behavioural therapy for major psychiatric disorder: does it really work? A meta-analytical review of well-controlled trials. Psychological Medicine DOI: 10.1017/S003329170900590X.

Miklowitz DJ, Scott J. (2009). Psychosocial treatments for bipolar disorder: cost-effectiveness, mediating mechanisms, and future directions. Bipolar Disord. 11 Suppl 2:110-22.

Rector NA, Beck AT. (2002). A clinical review of cognitive therapy for schizophrenia. Curr Psychiatry Rep. 4:284-92.

Rosack J (2002). Psychiatrists Assess CBT As Schizophrenia Treatment. Psychiatric News 37:18

Picasso or Prosopometamorphopsia?

Olga Khokhlova, as painted by her husband, Pablo Picasso

The Left Side of Your Face Looks Distorted!

The rare syndrome of unilateral left prosopometamorphopsia -- in which the left half of well-known and unfamiliar faces looks distorted -- was reported by Trojano et al. (2009) in a neuropsychological case study:

D.G., a 24-year-old right-handed housewife with 8 years of formal education, suddenly developed severe migraine, confusional state, and blurred vision, mainly in her right visual hemifield, after child delivery. Consciousness returned normal and migraine subsided in a few hours, but the visual disturbances persisted longer.

Repeated EEG recordings showed theta-wave slowing over posterior regions of the left hemisphere. ... Repeated MR did not disclose pathological areas. Brain SPECT (performed 30 min after the injection of 740 MBq of Tc-99m HMPAO) showed reduced blood flow in the inferior and lateral cortex of the left occipital lobe.

The patient's MRI scan appeared normal but a SPECT (single photon emission computed tomography) scan revealed diminished cerebral blow flow in the left lateral/inferior occipital lobe, as shown below.

Fig. 1 (adapted from Trojano et al., 2009). Axial brain SPECT scans showing reduced blood flow in the inferior and lateral cortex of the left occipital lobe (regional blood flow reduced by 25.8% with respect to contralateral cortex).

D.G. was seen in the clinic 6 months after her stroke, and her right visual field was intact (meaning she did not have damage to the contralateral, or left, primary visual cortex). However,

...she complained that the left half of people's faces (the part on her right side) appeared “out of shape”. D.G. claimed that “the left eye looks elongated towards left ear, the nose appears to be bended towards left cheek and the mouth towards the chin” irrespectively of whether she looked at familiar or unknown people, or even at herself in a mirror. Nonetheless, she reported to be able to recognize relatives and famous people by face, and also to visualise familiar faces in her mind without distortions.

Fig. 2 (Trojano et al., 2009). Patient's drawing of a face to depict her own subjective complaint.

She did not appear to have impairments in other visuospatial perceptual skills, and she could recognize famous faces as well as the control participants did, ruling out prosopagnosia (a face recognition deficit). Interestingly D.G. did not report distortions in the appearance of non-face objects. In a series of experiments, she was impaired in matching pairs of chimeric faces differing in their left halves, but not in a similar condition with chimeric cars. To explain this unusual deficit with a left hemisphere lesion (the right hemisphere is thought to be better at face recognition), the authors speculated that

early stages of face perception proceed in parallel in the two hemispheres and only at late stages the right hemisphere integrates information gathered from both parts of the stimulus to build up an unitary face representation. Replication of such findings and neurofunctional investigations on patients with PMO are warranted to directly verify neural dynamics related to unilateral defects in face processing.

Reference

Trojano, L., Conson, M., Salzano, S., Manzo, V., & Grossi, D. (2009). Unilateral left prosopometamorphopsia: A neuropsychological case study. Neuropsychologia, 47 (3), 942-948 DOI: 10.1016/j.neuropsychologia.2008.12.015.


Pablo Picasso - Weeping Woman - 1937

The Cognitive Dissonance of Zealous Republicans

In a remarkable preliminary study presented at the 2009 Meeting of the Organization for Human Brain Mapping, scientists at Emory University reported that Republicans were less disgusted by images of torture and human rights violations -- i.e., the infamous Iraq prison photos from Abu Ghraib -- than were Democrats (Hamann et al., 2009). Furthermore, the degree of self-reported arousal while viewing the photos was inversely related to the zealousness of support for Bush and Cheney. The authors speculated that this result may reflect the cognitive dissonance necessary for ardent Republicans to blindly support their cause. In addition, neuroimaging results indicated that for the comparison of Iraq prison photos vs. neutral control photos, the insular cortex was less active in Republicans than in Democrats. This brain region is implicated in interoceptive awareness of bodily states (Craig, 2009), and is responsive to scenes and expressions of disgust (Stark et al., 2007).

These findings are very interesting in light of a 2008 Science article by Oxley et al. (summarized in Conservatives Are Neurotic and Liberals Are Antisocial):

I'm sure you've seen the deluge of articles in the popular press saying that social conservatives are great big scaredy cats when it comes to loud noises and aversive pictures...



Newsweek: Spiders, Maggots, Politics

"...in the conservative mind, illegal immigrants may =spiders = gay marriages = maggot-filled wounds = abortion rights = bloodied faces."

Or as Oxley et al. explained in their abstract:

...individuals with measurably lower physical sensitivities to sudden noises and threatening visual images were more likely to support foreign aid, liberal immigration policies, pacifism, and gun control, whereas individuals displaying measurably higher physiological reactions to those same stimuli were more likely to favor defense spending, capital punishment, patriotism, and the Iraq War.

That paper was not without its problems, however, as described in my earlier blog post. Nonetheless, the new observations of Hamann et al. are striking: rabid Bush/Cheney fans showed reductions in

both subjective and FMRI-based aversive responses to Iraqi prison photos... in part because of cognitive dissonance elicited by the conflict between support for partisan policies and aversion while viewing consequences attributed to those policies.

References

Craig AD. How do you feel--now? The anterior insula and human awareness. (2009). Nat Rev Neurosci. 10:59-70.

Hamann S, Blagov P, Harenski K, Kilts C, Westen D (2009). Political Party Affiliation Affects fMRI Responses to Emotional Social Stimuli. 15th Annual Meeting of the Organization for Human Brain Mapping. 230 M-PM.

Oxley DR, Smith KB, Alford JR, Hibbing MV, Miller JL, Scalora M, Hatemi PK, Hibbing JR. (2008). Political attitudes vary with physiological traits. Science 321:1667-70.

Stark R, Zimmermann M, Kagerer S, Schienle A, Walter B, Weygandt M, Vaitl D. (2007). Hemodynamic brain correlates of disgust and fear ratings. Neuroimage 37:663-73.

And as ye would that men should do to you,
do ye also to them likewise.
-Luke 6:31

Myth of the Depression Gene

There never was a single "depression gene", and those patting themselves on the back because of the ceremonial defenestration of that straw man are fooling themselves.



Yes, a new meta-analysis in JAMA (Risch et al., 2009) found that a variant of the serotonin transporter gene (the 5-HTTLPR polymorphic region) is not linked to an increased risk of depression, either alone or in combination with stressful life events. This study examined 14 prior papers, including the now-maligned article by Caspi et al. (2003) in Science.


A depiction of the organization of the serotonin transporter showing the 5HTTLPR region and the positions of several SNPs. Adapted from Heils et al, 1996 and Lesch et al, 1996 by the Genotyping Lab at the University of Colorado.

Contrary to popular opinion, Caspi et al. never said that the single gene 5-HTTLPR is the "prime driver" of depression. Instead, they suggested that it moderates the effects of stressful life events on the risk of depression:

Individuals with one or two copies of the short allele of the 5-HT T promoter polymorphism exhibited more depressive symptoms, diagnosable depression, and suicidality in relation to stressful life events than individuals homozygous for the long allele. This epidemiological study thus provides evidence of a gene-by-environment interaction, in which an individual's response to environmental insults is moderated by his or her genetic makeup.

Caspi et al. (2003) also said the following:

• Evidence for an association between the short promoter variant and depression is inconclusive. Although the 5-HTT gene may not be directly associated with depression, it could moderate the serotonergic response to stress.
• Much genetic research has been guided by the assumption that genes cause diseases, but the expectation that direct paths will be found from gene to disease has not proven fruitful for complex psychiatric disorders.
• Until this study's findings are replicated, speculation about clinical implications is premature.

And the findings did not replicate, which was always a possibility in their view.

Another issue -- the importance of early life experience -- is raised by David Dobbs in The (Illusory) Rise and Fall of the "Depression Gene":

. . .

The headlines are predictable enough, "Sad News for Depression Gene" being perhaps the funnest.

But wait; not so fast. Has an empire crumbled here? A hypothesis evaporated?

You need only look at this briefly, I think, to see that the question addressed by both papers is fairly limited, and does not, crucially, cover variations in how early life experiences might amplify any risk conferred by the short 5-HTT allele. (Caspi & Moffitt clearly did not include such events in theirs excluded such early experiences from some of their analyses, and in fact took measures in some of their measures, such as removing from analysis anyone who suffered depression before age 21, that would be likely to exclude some people who suffered particularly rough early years.. And unless I missed something in reading the Risch paper, it too makes no effort to look at early experience in particular -- and, since it pulled Caspi's data from Caspia, would reflect the same possible filtering out of such early-onset depression cases.)

But does anyone still believe that complex psychiatric disorders are caused by a single gene? I think not. The field of psychiatry genetics is littered with examples of "a gene for schizophrenia" and "the gene for bipolar disorder" that have failed to replicate. Even the most ardent proponents have become more circumspect about the search for genes that predispose one to specific mental illnesses.

Hey oncologists: where's "the gene" for cancer? Neurologists, have you found "the gene" for Alzheimer's disease yet? No? Why not? Because they're complex multidetermined diseases. Does that mean there is no role for genetic contributions to these disorders? Of course not! Here's an editorial by Thomas (2005) in Cancer Epidemiology Biomarkers & Prevention:

Thinking about biochemical pathways has become an increasingly important part of molecular epidemiology. The field is rapidly moving from evaluation of single candidate genes, one at a time, to consideration of entire pathways comprising perhaps dozens of genes and their environmental substrates, even multiple pathways that link up or compete in complex networks. Even in its simplest rendering, for example, dietary folate seems to be a protective factor for colorectal cancer and is involved in at least two distinct pathways... Many proteins critical in folate metabolism are coded for by genes with known polymorphisms. Alcohol and vitamins B6 and B12 also play a role in the folate pathway, and of course other pathways involving metabolism of heterocyclic amines, polycyclic aromatic hydrocarbons, bile acids, and nonsteroidal anti-inflammatory drugs might compete or interact with the folate pathways... To further complicate matters, there is evidence that folate may protect against early precancerous lesions but increase the risk of cancer in those with preexisting lesions.

Why should it be any different for bipolar disorder and major depression? Of course a person's life experiences and their environment influence whether or not they develop depression. Given identical circumstances, some people are more likely to become depressed than others. Why is that?

Clinging to the stubborn view that there is absolutely no biological basis for depression is just as preposterous as saying that stressful life events have no influence whatsoever on one's mental health. Get over it.


References

Caspi A, Sugden K, Moffitt TE, Taylor A, Craig IW, Harrington H, McClay J, Mill J, Martin J, Braithwaite A, Poulton R. (2003). Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene. Science 301:386-9.

Risch N, Herrell R, Lehner T, Liang KY, Eaves L, Hoh J, Griem A, Kovacs M, Ott J, Merikangas KR. (2009). Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression: a meta-analysis. JAMA, 301 (23), 2462-2471.

Thomas DC. (2005). The need for a systematic approach to complex pathways in molecular epidemiology. Cancer Epidemiol Biomarkers Prev. 14:557-9.

HBM 15th Annual Meeting

The 15th Annual Meeting of the Organization for Human Brain Mapping will be held June 18-23, 2009 at the San Francisco Marriott in San Francisco, California.

HBM draws attendance between 1500-2000 attendees each year. Membership in the organization is growing and the meeting continues be one of the most significant neuroimaging conferences for those in the field.

The conference starts on Thursday evening at 6:00pm with the Talairach lecture:

The Talairach Lecture, named after famed neurosurgeon Jean Talairach, is a prestigious honor. Previous lecturers have included: Mahlon Delong, Keiji Tanaka, Brenda Milner, G. Rizzolatti, P. Magistretti, Vernon Mountcastle, Jun Tanji, Eric Kandel, Wolf Singer, Pasko Rakic, Giulio Tononi, Daniel Kahneman, and Michael Gazzaniga.

2009 Talairach Lecture
Morality and the Social Brain
Patricia Churchland, Department of Philosophy, University of California, San Diego, San Diego, CA, USA

Over 2200 posters will be presented, so use the online planner to organize your schedule.

POST-OPERATIVE COMPLICATIONS FOLLOWING THE EXTRACTION OF MEMORY

. . .
Feeling the bonds of language
coming apart in my throat and loins,
I cease attending
to my sacred obligations:
barking, and the gnashing of teeth.

I confess!
I’ve been neglecting
my post-operative physiotherapy
following the extraction of memory.
I’ve even forgotten
the simplest way of collapsing
in exhaustion on the tile floor.

                              10.IV.1973

© 1973, Taha Muhammad Ali
From: Never Mind: Twenty Poems and a Story

© Translation: 2000, Ibis Editions
Translated by Peter Cole, Yahya Hijazi and Gabriel Levin

More Moronic "Mental"

Chris Vance as the unorthodox psychiatrist, Dr. Jack Gallagher and Annabella Sciorra¹as his boss (and ex), Dr. Nora Skoff.

The late David Carradine made a surprise guest appearance Tuesday night on Fox's much maligned new show Mental, playing the main mental patient. His character, Gideon Graham, was a professor ["a national treasure"]² and author of the books Anti-wisdom and the [heavy-handed plot device] Book of Judges. His diagnosis: treatment-refractory catatonia of neuropsychiatric origin following a traumatic injury (being struck by lightning).

According to DSM-IV-TR, catatonia is marked by “motoric immobility, excessive motor activity (that is apparently purposeless and not influenced by external stimuli), extreme negativism or mutism, peculiarities of voluntary movements, or echolalia or echopraxia.” Fink and Taylor (2006) suggest that:

Catatonia, a psychomotor syndrome, is defined in DSM classifications mainly as a subtype of schizophrenia. This identification does not recognize the syndrome’s ubiquitous nature, discourages its recognition in other psychiatric illnesses, and limits treatment to protocols that focus on antipsychotic drugs. We suggest that catatonia be reclassified as an individual abnormal behavior, akin to delirium and dementia.

Professor Graham did not respond to any treatment, including drugs and electroconvulsive therapy (ECT), so the perpetually smirking and supposedly brilliant Dr. Gallagher decides to try transcranial magnetic stimulation (TMS) to awaken him from his stupor. This is not unheard of in catatonic patients, as there are two case studies in the literature that did report some success (Grisaru et al., 1998; Saba et al., 2002). TMS involves the delivery of magnetic pulses to the brain through a specially-designed coil.


BioMag Laboratory, Helsinki University

Depending on the frequency of the pulses, TMS is thought to induce either excitation or inhibition of the brain tissue below. In the case reports of catatonia, the two patients improved following TMS, then their schizophenia was treated with antipsychotic drugs.


The late David Carradine in Mental, being fitted with earplugs prior to receiving TMS. The magnetic coil does indeed make a loud clicking sound, and ear protection is necessary to prevent hearing loss.

The caps being modeled in the two photos above contain electrodes that record brain waves, or EEG activity, in response to the TMS. This is technically difficult because the magnetic pulses produce a strong electrical field which can saturate the amplifiers. Once these methodological hurdles are overcome, Miniussi and Thut (2009) describe the benefits of combining the two in a research setting:

The TMS-EEG integration provides real-time information on cortical reactivity and connectivity through the analysis of TMS-evoked potentials (TEPs), and how functional activity links to behavior through the study of TMS-induced modulations thereof. It reveals how these effects vary as a function of neuronal state, differing between individuals and patient groups but also changing rapidly over time during task performance.

In a clinical setting, TMS has been most commonly used to treat major depression, when administered in a repetitive fashion (rTMS) over the prefrontal cortex (Padberg & George, 2009).³ TMS differs from ECT in that treatment is administered while the patient is awake, and the occurence of seizures (very rare in those without neurological disorders)⁴ is a bad side effect, not the desired outcome.


Mental patient Gideon Graham having violent seizures in response to single-pulse TMS.

But Mental gets it all wrong... very wrong. First, Dr. Gallagher announces that he has conducted some self-experiments on the sly. So when Gideon's daughter, who is a [unconvincing] supermodel, asks "will it hurt?" Gallagher answers from experience that some will feel "a small tapping sensation." Then Gideon is sedated for the procedure, which isn't normally done. Furthermore, the treatment produces violent seizures, convulsions, and writhing. TMS is not supposed to induce seizures; that would be considered an untoward side effect.⁵ And finally they keep turning up the field strength beyond recommended levels. At no point did supermodel daughter sign a consent form for such an experimental procedure. "It looks like an execution," she said... "I hope you people know what you're doing."

But this is TV, right, and other shows with medical themes depict ethical violations all the time, right? [Over-the-top plastic surgery show, Nip/Tuck, I'm thinking of you.] Unfortunately, it's not clear what type of show Mental is supposed to be. Is it supposed to be realistic that the brazen Dr. Gallagher literally pushes the evil drug rep out the door? Funny? Cliched, I would say, and that's one of the major problems. Everyone is a walking stereotype, and some of the plot devices are so painfully concrete and literal-minded that you can see them coming a mile away.

For instance, Gideon Graham was struck by lightning while hiking in the Sierras with his wife during a thunderstorm. He survived, she did not. He was trying to teach his wife a lesson in overcoming her fears, because of course going to the edge of cliff in the middle of a fierce thunderstorm is the best type of exposure therapy. And he hates people who are weak.

Here's Dr. Gallagher's brilliantly insightful theory of Prof. Graham's catatonia:

• Lightning killed the supermodel's mother but not her father - does she blame her father for this fatality? [who wouldn't?]
• TMS treatment is "like an electromagnetic pulse".
• "Did you say TMS made him relive the lightning pulse?" asked his colleague.
• Gideon was working on The Book of Judges...
• Gallagher met with Gideon's tweedy academic colleague, who revealed that the book was dedicated not to his wife but to Vivian, a woman with whom he was having an affair.
• This "brought guilt into his life" - his wife threatened to leave - so Gideon found a way to judge himself.
• In the Old Testament of the bible, Gideon:

is a judge appearing in the Book of Judges... The name Gideon means "Destroyer", "Mighty warrior" or "Feller (of trees)".

Thanks, writers, what subtle and complex points you made here! Gideon feels guilty! He judges the world for taking his wife, and himself for his role in her death! In the end, Dr. Gallagher used the "scared straight" approach, yelling at Gideon, removing all reminders of his life, and accusing him of abandoning his daughter. He sets up one final TMS session, which was rigged to be a sham (unbeknowst to everyone but himself). An angry Gideon has supposed "seizures" (with no external stimulation), wakes up, and reaches out to strangle Gallagher, who says "Where's your lightning now?"

Footnotes

¹ Emmy-nominated for her work in The Sopranos, Annabella Sciorra is by far the best actor in the entire cast.

² This was a clumsily dubbed posthumous tribute to David Carradine.

³ However, Dr Shock isn’t impressed of the efficacy of rTMS in depression and has posted recently on the placebo response of TMS.

⁴ Koo et al. (2008) noted 12 published cases in their review of the literature.

⁵ However, there is an even newer procedure in limited clinical trials called magnetic seizure therapy (MST), which uses TMS to induce seizures (@vaughanbell). It's being tested as a possible alternative to ECT in treating refractory major depression. The show was not depicting MST, though.

References

Grisaru N, Chudakov B, Yaroslavsky Y, Belmaker RH. (1998). Catatonia treated with transcranial magnetic stimulation. Am J Psychiatry, 155:1626.

Miniussi C, Thut G. (2009). Combining TMS and EEG Offers New Prospects in Cognitive Neuroscience. Brain Topogr. Feb 25. [Epub ahead of print].

Padberg F, George MS. (2009). Repetitive transcranial magnetic stimulation of the prefrontal cortex in depression. Exp Neurol. May 3. [Epub ahead of print].

Saba G, Rocamora JF, Kalalou K, Benadhira R, Plaze M, Aubriot-Delmas B, Januel D. (2002). Catatonia and transcranial magnetic stimulation. Am J Psychiatry, 159:1794.

Götterdämmerung Halluzination

Sara Krulwich/The New York Times

Katarina Dalayman as Brünnhilde, in the Metropolitan Opera production of Götterdämmerung.

Musical hallucinations have been reported in the psychiatric literature, most often associated with schizophrenia, depression, and OCD [also with deafness]. The incidence has been estimated to be somewhere between 0.16% to 27% (Schakenraad et al., 2006). They are less commonly observed during confusional states, when visual hallucinations are more typical. Rentrop et al. (2009) have reported an unusual case study of a 74 year old mathematician and opera buff, who presented at the hospital for emergency surgery of the colon. Shortly thereafter...

...he began to suffer from near complete insomnia and mentioned only briefly that ‘this monkey music’ kept him awake. His condition deteriorated and 5 days later he admitted, that he heard complete operas at night from the very first to the last chord, ‘and you know how long these operas are’. He could not offer any explanation as to where these sounds came from, could not distance himself from his elaborate musical perceptions, had no means of interrupting them, and feared the first notes of another overture (which reliably rang out soon after sunset). On examination during daytime he appeared tired and irritable, rather uncooperative with poor concentration, but without overt evidence of a severe confusional state. His medical history was inconspicuous, but it became obvious that he was a dedicated opera-lover with a profound musical expertise, which he had acquired over decades of studying scores and librettos in every detail.

His labs and CT scan appeared to be relatively normal. The patient was started on the atypical antipsychotic drug olanzapine, and after 7 days:

He regained his strength, became friendly, cooperative, and still appeared puzzled about the vivid orchestrations of his musical memory. His neuropsychiatric status was completely normal at discharge.

The authors ended their Letter to the Editor in deadpan fashion:

"...this is (probably) the first report of a patient with a musical hallucinosis of complete operas."

References

Rentrop M, Knebel C, Förstl H. (2009). Opera-hallucinosis. Int J Geriatr Psychiatry 24:432-3.

Schakenraad SM, Teunisse RJ, Rickert MG. (2006). Musical hallucinations in psychiatric patients. Int J Geriatr Psychiatry 21:394–397.



Wagner's Götterdämmerung: The greatest test in opera for singers, conductor, orchestra – and audience