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Hearing Voices
March 25, 2007

Commentary on “Can You Live With The Voices In Your Head?” by Daniel B. Smith New York Times Magazine, March 25, 2007 Brian Koehler PhD

Smith (2007), author of Muses, Madmen and Prophets: Rethinking the History, Science and Meaning of Auditory Hallucinations, published by Penquin Press, presents us with a good overview of current psychiatric and psychological thinking on the phenomenology of voices.  It also reveals his lack of knowledge of the psychodynamic approach to auditory hallucinations.

Smith remarks on the current psychiatric viewpoint that the presence and persistence of voices is not only psychosocially toxic, but also neurotoxic.  The former seems definitely to be true in many, but not all, situations, but the latter remains scientifically unproven.  In fact, one could forcibly argue that it is not the symptom itself which can create atrophic processes in various neural regions, but, moreso it is the persistence of profound and chronic fear/stress/social isolation that is etiologic in the observed neural changes in a spectrum of psychiatric conditions, e.g., PTSD, major depression, bipolar disorder, the schizophrenias, etc.  In other words, the symptom and the possible concomitant neural changes may both be downstream to other events, e.g., severe fear/stress/isolation.

As to the potential neurotoxicity of ‘positive’ symptoms in psychosis, I will quote from a recent piece I did commenting on the work of Thomas McGlashan’s article “Is active psychosis neurotoxic?” published in the Schizophrenia Bulletin (vol 32 no. 4 pp. 609-613, 2006):

“First, I shall summarize the McGlashan article. In this article, he approaches the question, which has been taken as dogma by many in our field:  is active psychosis, i.e., the presence of hallucinations and delusions, neurotoxic?  The prevailing viewpoint is that indeed it is and that neuroleptic agents, whether first- or second-generation, are neuroprotective: without their protective coverage, the “schizophrenic brain” will deteriorate further and that there exists a dose-response relationship between frequency of relapse and time to recovery, i.e., every psychotic relapse makes it that much more difficult for the person to achieve stability.  A review of retrospective data in chronic schizophrenia suggests that the deterioration is most apparent in the first three years of active illness.  McGlashan, in commenting on the neuroanatomical research, noted:

The data that have been produced support a picture of reduced synaptic connectivity between brain neurons rather than a reduction in the number of neurons [Neuronal size is known to correlate with the extent of a neuron’s efferent and afferent connections, and therefore reduced neuronal size suggests functional and/or structural dysconnectivity (Cotter 2005- “Stress on the brain: neuropathology and cortisol dysregulation in bipolar disorder” in Bipolar Disorder: The Upswing in Research and Treatment edited by C. McDonald et al for Taylor & Francis )]. Postmortem histopathologic investigations found reduced spine densities and smaller dendritic arbors on the pyramidal cells of the cortex in schizophrenia.  The most replicated postmortem finding has been increased neuronal density in the cortex resulting from reduced neuropil [axons, dendrites, etc.] without neuronal loss….Given the severity that schizophrenic deterioration can reach, the telltale signs of outright neurodegeneration were assumed to exist and were sought for time and again, but to no avail, leading experts in the field to conclude that postmortem neuropathology of schizophrenia yields no specific cell phenotype, no gliosis, and little to no cell loss” (p. 610).

McGlashan gathers together a great deal of research evidence demonstrating that it could not be true that untreated active psychosis is neurotoxic.  The latter does not behave like typical neurodegenerative illnesses, e.g., the DUP{duration of untreated psychosis} effect plateaus (in fact the differences in outcome between a long and short DUP are minimal), we would not see neurodegenerative effects prior to the emergence of positive symptomatology, the relapse-dose effect would continue beyond the window of functional deterioration, etc.  If DUP were neurotoxic, we would expect to observe evidence of neuronal death and/or gliosis as a reaction to neuronal death.  The postmortem brains of persons with schizophrenia show neither gliosis nor loss of neuronal cell numbers for the most part.  McGlashan notes: “Once the plateau is reached, the positive symptoms of schizophrenia neither become more and more severe nor become harder to treat after each relapse” and “Neuropathology, like longitudinal course, does not support the hypothesis that untreated psychosis is neurotoxic”(p. 611).”

Smith’s description of psychoanalytic contributions to understanding psychosis is significantly ill-informed, and lacking in depth.  Firstly, he incorrectly asserts that Freud advised against psychoanalysts from approaching the problem of psychosis.  It is widely known in psychoanalytic circles, that Freud encouraged such exploration (e.g., Freud in his 1925 paper “An autobiographical study”, noted:“...since the analysts have never relaxed their efforts to come to an understanding of the psychosis...they have managed now in this phase and now in that, to get a glimpse beyond the wall.”) and made cogent observations on the psychotic process.  Freud, in his 1911 paper “Psycho-Analytic Notes on an Autobiographical Account of a Case of Paranoia (Dementia Paranoides” analyzed the illness narrative of Daniel Paul Schreber (1903), Memoirs of my Nervous Illness.  Freud emphasized the withdrawal of emotional, libidinal investment in external reality in psychosis which could lead to an internal catastrophe signified in a delusion of world destruction.  The latter is a restitutional attempt at self-cure of the extensive de-cathexis: “The delusional formation, which we take to be the pathological product, is in reality an attempt at recovery, a process of reconstruction” (p. 71).

Freud, in his 1924 paper “Neurosis and Psychosis,” noted: [the ego may be able to avoid collapse] by deforming itself, by submitting to encroachments on its own unity and even perhaps effecting a cleavage or division of itself."

To reduce the significant contribution of psychoanalysts, who tended to spend long periods of time with their patients, meeting with them several times a week for years, to the inflammatory concepts of the “schizophrenogenic mother” and parent blaming just for the sake of parent blaming is unfair and grossly one-sided.  Perhaps very few persons in the field take the time to really immerse themselves in the writings of psychoanalysts working in the field of psychosis over the past 100 years.  So it is particularly dismaying to see the quote from psychiatrist Peter Weiden, at SUNY Downstate Medical Center: “The psychoanalytic approach to psychosis was toxic.”  It would be another state of affairs if Peter Weiden were actually familiar with the depth and range of psychoanalytic contributions to the field of psychosis.  Then, a true dialogue could have a chance of unfolding.

It was refreshing to see the work of friends and colleagues, Marius Romme and his wife Sandra Escher, highlighted.  I think Smith’s descriptions of their work was fairly accurate.  Marius Romme and Sandra Escher do understand “voices” as reflective of the person’s struggle with life problems, i.e., containing meaning, and they are trying to de-stigmatize and contextualize the phenomena of voice hearing.  Jeffrey Lieberman, chair of psychiatry at Columbia University, is quoted as saying “One shouldn’t place too much emphasis on the content of hallucinations.”  This may be appropriate if you understand the voices as epiphenomena arising from neurological dysfunction, e.g., prefrontal-temporal lobe dysconnectivity secondary to problems with neuronal migration and/or other neurodevelopmental factors.  To paraphrase a Biblical saying: if you do not seek, you will not find.  Meaning emerges in a relational context of safety and reliability over time.  And, to paraphrase John Strauss: it may be the biology of meaning more than the biology of perceptual experience that explains these phenomena.  

My experience is that it is not only content, but relational factors between the voice hearer, the voice and the therapist which are significant.  To give one brief example: A person I have been seeing for several months now at a frequency of three times a week chronically hears persecutory voices.  His last therapist would tell him to hit the voices over the head with a hammer, cut their heads off and throw them in the river after setting them on fire.  I refused to reiterate this approach with this individual much to his chagrin.  According to this patient, his therapist would also affirm that he would make a million dollars from his music.  This patient puts a great deal of pressure on me as well to go along with this.  However, my usual response is something like “That would be very good.  You could certainly use the money [he is poor].  But I really don’t know that.  Why don’t you first take it one step at a time?”  Eventually, the voices, according to him, have decreased by approximately half.  He decided to take a different tack with the voices: understand them and not be so destructive towards them (integration of dissociated self-states?).  

In my paper “Auditory Hallucinations: Speaking One’s Dissociated Mind,” I did not fully elucidate the impact and eventual integration of dissociated self-states emerging between therapist and patient, e.g., states of omnipotence and omniscience.  Max Birchwood’s research in the UK demonstrated that the relationship between the voice and the voice hearer parallels the relationships the voice hearer had with peers during adolescence.  CBT therapists center on the reactions of the voice hearer to the voices and also address the nature of the relationship between the two.  Some encourage more of a dialogue.  Most do not believe that talking to the person about her or his voices actually encourages further psychotic decompensation.  The latter viewpoint I encountered in almost every clinical setting I worked in over the past two decades.  I have always felt that this would only serve to increase the person’s isolation and alienation from others.

Brian Koehler

 

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