Bioetica disumana di Maria Gabriella Gatti

Bioetica disumana. L’aborto postnatale

di MARIA GABRIELLA GATTI

Uccidere un neonato non è come fare un’interruzione di gravidanza. Ecco perché è inaccettabile la proposta avanzata in un ciclo di conferenze nelle università italiane, da Alberto Giubilini e Francesca Minerva dell’università di Melbourne

Lo sviluppo della medicina moderna legata alle tecnologie biomediche costituisce una sfida alle tradizionali concezioni razionali e religiose dell’uomo. Le scoperte dell’embriologia e delle neuroscienze hanno aperto una nuova visione dell’ontogenesi, cioè dello sviluppo biologico, che ha radicalmente cambiato anche la nostra concezione della nascita umana. Nessuno attualmente può ignorare che il cervello fetale ha una funzione dei neurotrasmettitori sostanzialmente diversa da quello neonatale. Ciò comporta che il feto, contrariamente al neonato, non prova dolore. Nessuno inoltre può continuare ad ignorare che alla nascita lo stimolo luminoso attiva dei geni ad azione immediata che modificano in toto la fisiologia cerebrale, facendo emergere capacità di pensiero come affermato dalla Teoria della nascita di Massimo Fagioli, inesistenti in utero. Queste conoscenze scientifiche sono il risultato di una ricerca sperimentale che non può essere negata come si faceva ai tempi in cui le dissezioni anatomiche venivano proibite subordinando la biologia alla religione. L’etica astratta del pensiero religioso si opponeva al progresso della conoscenza medica come, a suo tempo, si era opposta alla scienza fisica.Oggi quindi stupisce che un gruppo di filosofi in nome dei valori della bioetica vadano in giro per le università italiane dissertando se il bambino, una volta fuori dall’utero, sia o meno “persona”. Partecipando ad un congresso di bioetica dedicato alla nascita ed alle relative terapie intensive potrebbe accadere che il grande assente sia proprio il neonato nella sua realtà biologica e psichica di cui si fa finta di parlare ma che viene completamente annullato.

Può anche accadere che in talune congreghe di filosofi riunite per affinità ideologiche, si sostenga che il feto è uguale al neonato: se è pertanto legittimo l’aborto fetale lo sarebbe altrettanto il cosiddetto aborto neonatale. Questi esiti paradossali della logica razionale non devono sorprendere. Partendo dalla premessa che la nascita sia solo una parola alla quale non corrisponde nessuna cesura o trasformazione sul piano biologico e psichico, si giunge sia alla conclusione della sacralità del concepito, già “persona fin dallo zigote per i cattolici, in barba ad ogni principio di genetica, sia all’affermazione, da parte dei bioeticisti laici, della assoluta disponibilità della vita del neonato. Siccome quest’ultimo non avrebbe nessuna coscienza di sé esso potrebbe essere tranquillamente soppresso qualora la sua sopravvivenza urtasse con gli interessi della madre. La bioetica cosiddetta laico-utilitaristica, con la tesi di Minerva e Giubilini sull’aborto postnatale, si avvicina pericolosamente alla logica nazista dalla quale pretende di aver preso le distanze a partire dalla dichiarazione dei diritti dell’uomo nel 1948 e dalla condanna della eliminazione delle vite ritenute inutili dal Terzo Reich. Bioeticisti laici e cattolici su una cosa sono d’accordo: sul fatto che la medicina si troverebbe in una condizione di minorità intellettuale e morale necessitando di qualcuno che le chiarisca cos’è la vita umana e la morte umana facendo ricorso alla ragione: quest’ultima, da Platone ed Aristotele fino ai giorni nostri, su questi temi ha sostenuto tutto ed il contrario di tutto. Ha sostenuto per esempio che la donna ed il bambino non sono esseri umani in quanto sprovvisti della ragione. L’altra grande imputata è la tecnologia medica sospetta di poter generare delle mostruosità e di essere incline ad un delirio di onnipotenza e dominio totale esercitato da uomini su altri uomini. Addirittura nel tentativo di screditare la ricerca biologica alcuni si spingono fino a fornire una falsa interpretazione storica della genesi del pensiero medico a partire dalla figura leggendaria di Ippocrate. Si dice, operando una indebita semplificazione e proponendo una ricostruzione riduttiva e parziale, che il discendente di Asclepio avrebbe sostenuto la sacralità della vita in linea con la concezione cattolica attuale. Bisogna ricordare che nel giuramento di Ippocrate è contenuto il principio del non accanimento terapeutico. NelDe morbo sacro che fa parte degli scritti ippocratici si sostiene inoltre che la malattia non ha un’origine divina ma è dovuta a cause naturali individuabili attraverso l’esame clinico. La medicina greca anticipa il metodo di indagine e le forme della razionalità scientifica essendo basata sull’osservazione empirica. Oggi assistiamo al processo per il quale la religione cattolica, forte dei suoi dogmi, e la filosofia con il suo razionalismo laico, vogliono dare dei suggerimenti alla medicina che viene accusata di avere una visione riduttiva dell’essere umano concepito solo come un insieme di meccanismi biologici. Ora il riduzionismo, che è una forma di estremismo, può essere considerato una malattia infantile della biologia. Nessun ricercatore nell’ambito delle neuroscienze sosterrebbe ai giorni nostri le tesi della prima generazione di neuroscienziati, che forti di alcune loro scoperte pretendevano di dire cosa fosse l’uomo o la malattia mentale, partendo da semplici molecole o da meccanismi neuronali elementari.
Il medico oggi che è impegnato nella ricerca sulla realtà umana deve avere la consapevolezza dei procedimenti metodologici che utilizza nel produrre le proprie conoscenze. Questa consapevolezza è parte integrante ed imprescindibile del suo bagaglio culturale. Nessuno potrebbe attualmente svolgere un’indagine scientifica sull’ontogenesi umana con una mentalità positivistica, come ai tempi di Claude Bernard, prescindendo dalla conoscenza dei processi psichici, coscienti e non coscienti che è possibile individuare soltanto facendo riferimento al rapporto fra gli individui che inizia a partire dalla nascita. I neonatologi, che accuratamente i bioeticisti escludono dai loro congressi, non si occupano solo di fisiologia o patologia del corpo, come si vorrebbe far credere, ma rivolgono la loro attenzione alla globalità psicofisica del bambino che venuto alla luce, comincia a fare esperienza di sé e del mondo. Se vogliamo cogliere un’etica nell’agire della medicina essa coincide con la ricerca e l’affermazione della verità relativa alla realtà umana. La verità del neonato, così come la si apprende dalla frequentazione della sala parto e non da solipsistiche meditazioni dietro una scrivania, è nel suo essere un soggetto pensante ed in relazione con il mondo nella sua globalità fin dai primi istanti di vita. A questa conclusione si giunge non solo attraverso l’interpretazione degli esami strumentali che sono in grado oggi di mostrarci in tempo reale le modificazioni del il funzionamento cerebrale ma anche attraverso l’interazione diretta con il bambino che, in accordo con la ricerca psichiatrica, suggerisce la presenza di una interiorità originaria fatta di fantasia, affetti e pulsioni senza parola: nel neonato è presente quel pensiero irrazionale, che si manifesta ogni notte nella creazione dei nostri sogni, come dice lo psichiatra Massimo Fagioli. Quest’ultimo,
con la sua prassi terapeutica pluridecennale ha dimostrato che le immagini oniriche sono un linguaggio dotato di senso. Al contrario il cattolicesimo aveva storicamente condannato i sogni come manifestazione demoniaca mentre Freud aveva voluto vedere in essi solo l’espressione della psicosi e della dissociazione. Freud razionalista e laico era in perfetta sintonia ed accordo con il cattolicesimo nel concettualizzare non solo una colpa o perversione originaria ma anche una totale irrilevanza della nascita come momento costitutivo della vita umana: egli come i cattolici, non riusciva a pensare ad una trasformazione conseguente alla cesura radicale fra stato fetale e stato neonatale nell’atto di venire alla luce. Stupisce nei filosofi bioeticisti laici e cattolici proprio l’ignoranza della ricerca biologica che essi pretenderebbero di regolamentare. Stupisce anche il fatto che dalla storia passata, dalle vicende della cultura del Novecento, che ha visto prosperare la complicità fra le ideologie razionali e la fede nel negare la realtà umana della nascita, non si sia appreso nulla come se ciascuno di noi dovesse essere condannato ad una eterna ripetizione di idee false e superate.

Dsm, la rivolta dei medici

NEWS_91336Articolo interessante, come documentazione storica del problema del DSM.

Interessante è la cricostanza per la quale il DSMIV fu pubblicato nel 1994. L’anno prima c’era stata in America una campagna stampa, mi ricordo una copertina del “Times” dal titolo Freud è morto, che decretava la fine della psicoanalisi freudiana naufragata sotto il peso della sua inconsistenza terapeutica, delle critiche epistemologiche di Grunbaum,Assalto_alla_Verit_pagina_1_di_69_grunbaum
documente della pubblicazione dei carteggi del padre della psicoanalisi. Tutti questi elementi concorrevano a dare della psicanalisi un’immagine molto lontana dalla agiografie edulcorate fra le quali spiccava quella di Ernst Jones e più vicina a quella di un gigantesco imbroglio sostenuto da un’intero apparato istituzionale  e ideologico.images Il DSM si inseriva tempestivamente nel vuoto lasciato dalla” morte di Freud” (morte ovviamente simbolica) che Fritz Lang fin dal 1933 aveva rappresentato come un ipnotizzatore criminale che cercava di imporre ad una intera civiltà il diktat “si prega di chiudere gli occhi”. Già Freud nel 1938 nel suo “Compendio di Psicoanalisi” aveva auspicato l’avvento dell’era farmacologica: la psichiatria organistica nel suo sviluppo a partire dagli anni 80-90 si situa in una linea di continuità con il freudismo con cui condivide l’idea di una incurabilità della malattia mentale. Le corporazioni degli psichiatri cercavano, in quegli anni,  un consenso ed una amalgama  facendo quadrato sul DSM come fosse un manifesto politico piuttosto che un un testo che derivava da approfondite e motivate riflessioni teoriche.

Attualmente il disastro del DSMV coincide con la planetaria crisi economica innescata dalle banche e dalla bolla  del  mercato immobiliare americano: come se la crisi del modello liberista si ripercuotesse sugli aspetti sovrastrutturali della società americana, in particolar modo della psichiatria, incapace  di offrire strumenti di contenimento dell’enorme  malessere sociale ed economico delle fasce di popolazione più deboli negli Usa. Le guerre ingiuste ed inique combattute dagli  States su scala planetaria, in difesa dei loro interessi legati al controllo delle fonti energetiche, hanno indebolito sul piano non solo dell’economia  ma anche dell’immagine il paese. Gli psicofarmaci, come si è scoperto negli ultimi decenni, non solo non possono essere un ‘intervento a lungo termine sulla malattia mentale senza provocare danni iatrogeni rilevanti ma  neppure possono essere somministrati  in modo irresponsabile  ai bambini piccolissimi  senza alterare i processi di sviluppo ed incidere pesantemente sulla realtà psichica di questi ultimi costituendo il punto di innesco di veri e propri episodi psicotici.

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Allen Frances, classe 1942, è un pezzo di storia della psichiatria. Ha presieduto i lavori del comitato scientifico di quel l’American Psychiatric Association (Apa) che, nel 1994, partorì la quarta edizione del Manuale diagnostico e statistico dei disturbi mentali (Dsm-IV): 886 pagine, 297 disturbi. Oggi, capelli bianchi e abbronzatura alla Robert Redford, Frances è un professore emerito che vorrebbe godersi la pensione in California. Invece, è reduce da un giro di conferenze, anche in Italia, dal titolo «Usi e abusi della diagnosi in psichiatria». Oggetto della sua preoccupazione, e delle sue critiche severe, sono i criteri proposti (li trovate su http://www.dsm5.org) per la quinta edizione del Dsm, la cui uscita è prevista nel maggio 2013. Del Dsm-5 (da romana la numerazione è diventata araba, quindi Dsm-5), ha parlato su queste pagine Gilberto Corbellini più di un anno fa («Disturbi mentali, il catalogo è questo», 22 marzo 2010), raccontandone costi e ricavi ed elencando le principali novità: maggior attenzione agli aspetti dimensionali della diagnosi (cioè non solo la presenza/assenza di un sintomo o di un disturbo, ma anche la sua intensità), semplificazione di diagnosi “complesse” quali schizofrenia e autismo, riduzione del numero dei disturbi di personalità, revisione del quadro nosografico delle “dipendenze”, con introduzione di nuove dipendenze comportamentali, per esempio da internet.
Ma cosa preoccupa Frances, al punto da invitare l’intera comunità dei professionisti della salute mentale a firmare una petizione (www.ipetitions.com/petition/Dsm5) e perorare una users’revolt, una ribellione degli utenti del Dsm? Petizione a cui l’Apa, proprio in questi giorni, ha fornito risposte tese più ad appiattire i contrasti che ad affrontare le critiche, attraverso quelle che lo stesso Frances ha definito «formule bizantine» che sostanzialmente ignorano il problema.
Un punto di partenza per descrivere questa rivolta fantapsichiatrica potrebbe essere il mancato coinvolgimento degli psicologi come comunità professionale nella stesura del Dsm-5. La marginalizzazione degli psicologi è un problema delicato dato che questi non solo applicano il Dsm nella pratica clinica, ma conducono anche ricerche sulla base delle sue categorie diagnostiche. Le critiche contenute nella petizione anti Dsm-5 sono infatti sottoscritte da un lungo elenco di divisions dell’American Psychological Association. Poco prima si era mossa in modo simile la British Psychological Society. L’anno scorso, un autorevole cartello di esperti (Shedler, Beck, Fonagy, Gabbard, Gunderson, Kernberg, Michels e Westen) aveva lanciato un allarme sul futuro diagnostico dei disturbi di personalità, una delle diagnosi più importanti nel campo della salute mentale (basti pensare al loro ruolo in ambito forense). In particolare suscitò scalpore, tra noi addetti ai lavori, l’esclusione dal Manuale di alcuni importanti disturbi di personalità, quali il paranoide, lo schizoide, l’istrionico, il dipendente e soprattutto il narcisistico. Tanto che, nel giugno 2011, l’American Psychiatric Association si sentì costretta a reinserire tra le diagnosi almeno quest’ultimo, accogliendo così in parte le osservazioni dei molti clinici che vedevano nella sua eliminazione l’affacciarsi di una pericolosa scollatura tra la realtà clinica e le categorie diagnostiche, oltre che la preoccupante eliminazione di tutte le manifestazioni psicopatologiche non immediatamente riducibili a meccanismi di tipo biologico. Ma il dissenso era ormai diffuso e, proprio dalle pagine dell’American Journal of Psychiatry, questi clinici internazionalmente noti definivano la diagnostica di personalità targata Dsm-5 «un agglomerato poco maneggevole di modelli disparati e male assortiti, che rischia di trovare pochi clinici disposti ad avere la pazienza e la costanza di farne effettivamente uso nella loro pratica». Anche in Italia si è mosso qualcosa: un gruppo di clinici e ricercatori di diversa formazione (Lingiardi, Ammaniti, Dazzi, Del Corno, Liotti, Maffei, Mancini, Migone, Rossi Monti, Semerari, Zennaro) ha voluto inviare all’Apa una lettera con le proprie perplessità sul tema. E anche l’ultima Newsletter dell’Ordine degli psicologi del Lazio presenta un analogo documento critico.
Ricordo che il Dsm è probabilmente il sistema diagnostico in psichiatria più usato al mondo. Se i suoi meriti sono noti, primo tra tutti il tentativo di creare una lingua comune e principi condivisi per descrivere i disturbi mentali, i punti di debolezza dell’imminente Dsm-5 sono sotto i riflettori. Proviamo a riassumerli: 1. «abbassamento delle soglie diagnostiche» col conseguente accresciuto rischio di falsi positivi (viene diagnosticato un disturbo mentale che non c’è) e relativa medicalizzazione (psicofarmaci compresi) di soggetti non clinici; 2. «inserimento di nuove categorie diagnostiche» dubbie, come la «sindrome psicotica attenuata», che sembra peraltro avere un basso potere predittivo rispetto allo sviluppo successivo di una sindrome psicotica vera e propria, e il «disturbo neurocognitivo lieve», diagnosticabile nella maggior parte degli anziani; oppure l’eliminazione del precedente criterio che impedisce di far diagnosi di «depressione maggiore» in presenza di un lutto (per cui sarà più facile diagnosticare come sindromi depressive, e quindi medicalizzare, alcune reazioni di lutto normali); 3. «minore attenzione al peso dei fattori psicologici, sociali e culturali» nella genesi e nell’espressione dei disturbi mentali; 4. «eccessiva polarizzazione medico-organicista», dal punto di vista sia teorico sia clinico

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Secondo Gilberto Corbellini nel DSMV verrà abolita la dizione “schizofrenia paranoide”. Con il gruppo di psichiatri “Progetto psichiatria” abbiamo ultimato in questi giorni un articolo “Breivik e la diagnosi di schizofrenia paranoide” che secondo noi non solo esiste ma ha caratteristiche peculiari che la distinguono dalle altre forme della classica quadripartizione di Eugene Bleuler.

DSM-5

Da Il Sole 24 Ore del 22-03-2010, di Gilberto Corbellini

Articolo: Disturbi mentali, il catalogo è questo

Verso il nuovo manuale. L’associazione psichiatrica americana ha investito 25 milioni di dollari coinvolgendo 600 specialisti per ridisegnare la mappa delle patologie. Siamo vicini al varo finale. L’uscita prevista nel 2013

USA. Dopo undici anni di discussioni e un certo numero di falsi annunci dell’imminente pubblicazione, finalmente la fumata bianca.
Habemus DSM-V. o, quantomeno, si sa verso quali modifiche sono orientati i componenti della task force e dei 13 gruppi che lavorano, coordinati da David Kupfer e finanziati dalla American Association of Psychiatry (Apa), sulle categorie fondamentali delle diagnosi psichiatriche. Il 10 febbraio l’Apa ha pubblicato un draft del DSM-V richiedendo commenti e critiche da parte di tutti gli interessati entro il 20 aprile prossimo. Quindi nei prossimi tre anni, saranno organizzate tre fasi cliniche per testare la validità delle revisioni proposte e l’edizione definitiva sarà acquistabile nel maggio del 2013.
Il DSM o Diagnostic and Statistical Manual of Mental Disorders, è il più diffuso e influente testo di psichiatria nel mondo occidentale. Sulla base di questo strumento, edito dall’Apa, si battezzano e si classificano le malattie mentali, ma soprattutto gli psichiatri e i neurologi diagnosticano e trattano i loro pazienti. Inoltre, le case farmaceutiche progettano e finanziano le sperimentazioni cliniche dei farmaci, e gli enti di ricerca pubblici decidono quali ricerche finanziare.

Ultimo, ma non per importanza, i sistemi sanitari o le compagnie di assicurazione pagano le cure che sono indicate come appropriate. Rappresentando la larghissima diffusione del DSM una fonte di incalcolabile guadagno economico per l’Apa, si comprende l’ingente investimento di 25 milioni di dollari per effettuare la revisione, a cui hanno concorso 600 psichiatri, e anche la decisione di pubblicare un’edizione che probabilmente lascerà insoddisfatti molti, ma che lancia nondimeno una serie di segnali inequivocabili sul cammino che sta percorrendo la psichiatria.
La storia del DSM, dall’I al V, è uno dei capitoli più affascinanti della storia della psichiatria, anzi della storia della medicina del Novecento in generale. Non solo perché è intellettualmente intrigante analizzare i ragionamenti che hanno portato dalle 106 malattie mentali descritte nelle 106 pagine del DSM-1 del 1952 ai 293 disturbi descritti in 886 pagine del DSM-IV del 1994. Ma per il fatto che si tratta di una finestra storica unica sulle difficoltà e i problemi, sia teorici sia pratici, che hanno incontrato i tentativi di fornire alla psichiatria una base scientifica. Cioè una metodologia diagnostica basata sull’eziologia del disturbo clinicamente rilevante, come è nel caso delle definizioni di malattia sviluppate dopo l’avvento della medicina sperimentale o scientifica. […]

L’unico trattamento efficace per superare una condizione di precarietà di natura epistemologica di cui soffre la psichiatria forse sarebbe un salutare pluralismo epistemologico, ispirato però da una rigorosa concezione naturalistica della malattia mentale. Gli avanzamenti delle neuroscienze stanno muovendo in questa direzione, consentendo di tornare a sfruttare euristicamente le teorie per ricondurre i disturbi del comportamento a quello che sono. Cioè alterazioni del funzionamento del cervello.
Dal DSM-IV al DSM-V
– Eliminazione di una serie di sottotipi di schizofrenia (paranoide, disorganizzata, catatonica, eccetera) e maggiore attenzione ai sintomi comuni come allucinazioni e disturbi del pensiero, nonché alla durata e gravità di tali sintomi, nella diagnosi dei disturbi psicotici.
– Introduzione di una diagnosi di depressione ansiosa mista.
– Riduzione da 12 a 5 dei disturbi della personalità. Sono rimasti: borderline, schizotipica, evitante, ossessivo-compulsiva e psicopatica/antisociale.
– Introduzione della categoria di sindromi di rischio, in modo da consentire agli psichiatri di identificare gli stadi precoci di gravi disturbi mentali, come le demenze o le psicosi. […]
– Introduzione della singola categoria diagnostica dei “disturbi autistici” in sostituzione delle attuali diagnosi alquanto indefinite di malattia autistica, malattia di Asperger, disturbo disintegrativo dell’infanzia, e disturbo pervasivo dello sviluppo.
– Introduzione della nuova categoria dei disturbi da dipendenza e simili, in sostituzione della categoria di dipendenza e abuso di sostante.
Questa opzione consente di differenziare il comportamento compulsivo di ricerca della droga dovuto alla dipendenza dalle risposte normali di tolleranzae astinenza.
– Introduzione della categoria delle dipendenze comportamentali, che al momento include solo il gioco d’azzardo, ma dove alcuni vorrebbero includere la dipendenza da internet.
– Aggiunta di una valutazione dimensionale della diagnosi, rispetto al criterio basato solo sulla presenza o assenza di un sintomo, per consentire agli psichiatri di valutare la gravità dei sintomi.

Autismo

im-autistic

Portrait of Allen Frances

Allen Frances, M.D., was chair of the DSM-IV Task Force and of the department of psychiatry at Duke University School of Medicine.


Jul. 19, 2011

 

Autism Generation

hSAN DIEGO – Not long ago, autism was among the rarest of disorders, afflicting only one child in every 2,000-5,000. This changed dramatically with the publication in 1994 of DSM IV (the manual of psychiatric diagnosis widely used around the world). Soon, rates exploded to about 1 per 100. And a large study in South Korea recently reported a further jump to 1 in 38 – an astounding 3% of the general population was labeled autistic. What is causing this epidemic and where are we headed?

This illustration is by Newsart and comes from <a href="http://www.newsart.com">NewsArt.com</a>, and is the property of the NewsArt organization and of its artist. Reproducing this image is a violation of copyright law.
Illustration by Newsart

The natural reaction to any plague is panic. Parents are now fearful that every delay in speech or socialization presages autism. Childless couples decide to avoid having kids. Parents with autistic children are desolate and desperate to determine its cause.

The British physician Andrew Wakefield’s vaccine theory became wildly popular among parents, many of whom began to withhold vaccination (thus subjecting their own and other children to the risk of entirely preventable, and sometimes serious, illnesses). Vaccination seemed a plausible cause because of the fortuitous correlation between getting shots and the onset of symptoms. Wakefield’s work has now been thoroughly discredited as incorrect and dishonest science. But fear of autism is so great, and the reactions to it so irrational, that in some circles Wakefield continues to be revered as a false prophet.

Other factors must be behind the sharp rise in the diagnosis. Before DSM IV, autism was among the most narrowly and clearly defined of disorders. Symptoms had to begin before age three and comprised a striking and unmistakable combination of severe language deficits, inability to form social relationships, and a preoccupation with a very narrow set of stereotyped behaviors. In preparing DSM IV, we decided to add a new category describing a milder (and therefore much more difficult to define and distinguish) form of autism, called Asperger’s Disorder. This seemed necessary because some (still quite rare) children presented with more or less normal language development, but with grave social and behavioral difficulties. We knew that Asperger’s would likely triple the rate of autistic disorders to about 1 per 500-1,000, but this doesn’t explain the new rate of 1 per 38.

A second possible explanation for the explosion in autism is that previously missed cases are now being more accurately diagnosed. This is probably a factor, but again only a minor one.

Perhaps, then, an environmental toxin is causing an epidemic outbreak of autism. This has been the most popular theory, but it, too, is a small factor, at best. There has been no sudden environmental change since 1994 to account for an explosion in rates. This doesn’t entirely disprove an environmental vector, but it does make the odds quite remote – especially since there is a far more plausible explanation.

The most likely cause of the autism epidemic is that autism has become fashionable – a popular fad diagnosis. Once rare and unmistakable, the term is now used loosely to describe people who do not really satisfy the narrow criteria intended for it by DSM IV. Autism now casts a wide net, catching much milder problems that previously went undiagnosed altogether or were given other labels. Autism is no longer seen as an extremely disabling condition, and many creative and normally eccentric people have discovered their inner autistic self.

CommentsView/Create comment on this paragraphThis dramatic swing from under- to overdiagnosis has been fueled by widespread publicity, Internet support and advocacy groups, and the fact that expensive school services are provided only for those who have received the diagnosis. The Korean study, for example, was financed by an autism advocacy group, which could barely contain its enthusiasm at the high rates that were reported.

The Korean study paid no attention to the bias that haunts all epidemiological studies, which always overestimate pathology rates by including as disorder even very mild presentations that do not have clinical significance. It is entirely plausible that 3% of the population may have some smidgen of autism, but it is entirely implausible that so many would have symptoms severe enough to qualify as an autistic disorder. Reported rates should be regarded as an upper limit, not as a true reflection of the rate of actual mental disorder.

Human nature, neurological illness, and psychiatric disorder all change very slowly, if at all. Environmental toxins do not usually just pop out of nowhere to make a condition 100 times more common than it was less than 20 years before. A more plausible scenario is that DSM IV gave autism purchase by introducing a milder form that is close to the extremely populous boundary of normality. Then autism took flight on the wings of definitional diffusion, internet contagion, financial incentive, and naïve interpretation of epidemiological results.

The autism “epidemic” is set to spread further starting in May 2013, when the next revision of the diagnostic manual (DSM 5) will be published. The DSM 5 definition of an “autistic spectrum” will cast an even wider net, capturing many people now considered to be normal or to have another disorder. Their symptoms will not have changed – just the label.

Read more at http://www.project-syndicate.org/commentary/the-autism-generation#Erqrp4S0MGo3GCQk.99

Psichiatria preventiva

Gli articoli di Allen Frances, interessanti come testimonianza del clima in cui vive la psichiatria americana, ovviamente non vanno presi per oro colato ,ma vanno letti in senso critico. La discussione potrebbe vertere su cosa si debba intendere per prevenzione che non credo si possa ridurre ad uno screening diagnostico di tipo descrittivo. L’eliminazione del DSMIV  e V potrebbe essere una misura preventiva importante perché costringerebbe a sviluppare strategie diagnostiche più adeguate. Non è vero quello che dice Allen Frances in un altro suo articolo che la pericolosità dei Mass Murderers non può essere prevista. Non può essere prevista con il DSM ma forse se noi ricorriamo ad una valutazione psicopatologica potremmo essere in grado di  individuare dei soggetti a rischio. In un contesto  socio culturale in cui non esiste una possibilità diagnostica per malattie gravi ma latenti  come la schizofrenia  i comportamenti psicotici prendono delle strade strane e si amplificano anche per l’effetto di fenomeni imitativi come testimonia l’epidemia di mass shooting negli States che si può seguire nei suoi allarmanti risvolti nei media anche in questi giorni.

Edition: U.S.
 psicofarmaci

Preventive Psychiatry Can Be Bad for Our Health

Posted: 01/19/2012 3:58 pm
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Preventive psychiatry may someday be of significant service in reducing the burden of human suffering — but only if it can be done really well. And the sad truth is that we don’t yet have the necessary tools. More people will be harmed than helped if psychiatry stretches itself prematurely to do what is currently well beyond its reach. That’s what is so scary about the unrealistic prevention ambitions of DSM-5, the new manual of mental disorders now in preparation and set to become official in 2013. DSM-5 proposes a radical redefinition of the boundaries of psychiatry, giving it the impossible role of identifying and treating mental disorders in their nascent stages before they have fully declared themselves. Tens of millions of people now deemed normal would suddenly be relabeled mentally disordered and subjected to stigma and considerable risks consequent to inappropriate treatment.

The model fueling the premature DSM-5 hopes for preventive psychiatry has been borrowed from general medicine. In recent decades, the threshold for defining illness has been progressively lowered. Medication is now given for blood pressures or blood sugars, for cholesterols or for levels of bone density that were previously considered well within normal limits. Preventive tests for breast and prostate cancer have been used widely for early detection leading to proactive surgical interventions.

It is ironic that psychiatry wants to jump on this bandwagon just when some of its seeming promise is fading — many previously-ballyhooed preventive medical and surgical procedures are losing their luster. As good as early intervention sounds in theory, in practice the gains afforded by preventive medication often don’t compensate for side effects. And preventive testing may result in more complications than benefits. The once highly-recommended routine testing for early prostate cancer has been abandoned because it is useless in saving lives and promotes unnecessarily-invasive treatments. And routine mammogram testing is now being restricted to a much narrower age range and offered at much less frequent intervals. If the blush is somewhat off preventive medicine, how much more caution is warranted in psychiatry, where the preventive efforts are much less feasible and the possible harm often greater?

All this said, there is no denying the seductive appeal and optimism generated by the prevention model. The storyline is that we can and should identify people destined to have mental disorders early in their course — before symptoms can cause grave distress or impairment. Then, we can intervene early with effective measures that may completely prevent the later development of their symptoms or at least reduce the total lifetime burden of illness. Once people actually get clearly sick, so the argument goes, their brains may be further damaged by the illness, their lives ruined by the secondary effects of having symptoms, and treatments may become less effective. So the secret is to strike before the iron is hot. Preventing symptoms early sounds a lot easier and more efficient than curing them later.

DSM-5 has suggested a number of new disorders intended to initiate the brave new world of early identification and preventive psychiatry. Psychosis risk is the putative prodrome of schizophrenia, minor neurocognitive is the prelude of dementia,and mixed anxiety/depression presages more clearly defined mood and anxiety disorders. DSM-5 would also dramatically reduce the thresholds of existing disorders, turning just two weeks of grief into major depression, normal distractability into attention deficit and the worries of every life into generalized anxiety disorder.

It simply won’t work, in my opinion. Three unavoidable preconditions must all be met before it will make any sense to so dramatically lower diagnostic thresholds in the service of preventive psychiatry. None of these can remotely be achieved, now or for the foreseeable future. First, the patients identified as prodromal must be at considerable risk of actually going on to develop the full-blown disorder. Predicting this precisely enough is currently completely impossible. For every new true “patient” identified correctly as really being at risk, there will be very many who will not progress and would do just fine if instead left to their own devices. Secondly, the preventive interventions must be effective. This has not been documented for any of the DSM 5 candidates. Antipsychotics given before disease onset don’t prevent schizophrenia, cholinesterase inhibitors don’t prevent dementia and time and placebo effect are by themselves so effective in curing many milder conditions that nothing else is necessary. Finally, the prevention must be safe — clearly not the case when most of the currently available real world interventions will consist of medications that have appreciable side effects and risky complications.

The risk/benefit ratio for treating the traditional and clearcut psychiatric disorders is extremely favorable. Most patients experience appreciable benefit and some are totally cured — so the risks that accompany any effective treatment are well worth taking. And once a psychiatric disorder does clearly declare itself, every effort should be made to treat it promptly, thoroughly and for however long it takes. The longer a disorder is allowed to fester or linger, the more impairing it is and more difficult to treat.

But the risk/benefit ratio for the preventive treatment of the proposed pseudo-patients defined by the new DSM-5 proposals tilts badly in the opposite direction — the risks remain just as high and are certainly not worth taking because the benefits are so minimal. The way things add up now is therefore crystal clear. All the possible benefits of preventive psychiatry are unproven and theoretical and off somewhere in the distant future. In contrast, the grave risks are already with us — children are currently getting way too much harmful medication given carelessly for very questionable indications.

And the risk/benefit ratio looks even worse when we consider who will be doing most of the preventive treatment of the new conditions suggested in DSM-5. Recent CDC statistics show that the overwhelming majority of prescriptions for psychiatric drugs are not written by psychiatrists and that most people taking psychotropic medication are never seen by any mental health professional. So although it would be psychiatry introducing the new DSM-5 diagnoses to be used in preventive psychiatry, it will be non-psychiatric physicians who will be assessing most of the patients and providing most of the treatment. Their decisions usually follow 7-minute visits and often reflect only limited training in psychiatric diagnosis and a casual acquaintance with the proper use of psychiatric medicine. Preventive psychiatry is a bad idea in the best of hands, it can be a menace in the worst — an additional excuse for furthering the current practice of wanton overmedication.

Will preventive treatment at least be unsullied by crass commercial interests? Hell no. I know the people preparing DSM-5 and have complete confidence in their sincerity — they are suggesting what I consider to be dangerous changes in the diagnostic system, but for the best intentioned reasons having nothing to do with shilling for drug companies. But the purity of their intentions won’t stop Big Pharma from licking its chops and aggressively exploiting the vast new markets opened by DSM-5. There are always many more potential customers with very mild illness (or no illness at all, suffering from just plain human unhappiness) than there are people with clearcut psychiatric disorders. My last piece warned that our country is already plagued by loose overdiagnosis and careless overtreatment. This has been tirelessly driven by ubiquitous drug company marketing — peddling psychiatric ills in order to help sell their overly-hyped and overpriced pills. Everyday distress transformed into mental disorder is a marketing dream come true.

What is the bottom line? While preventive psychiatry may eventually be the next great advance in our field, it is at least a decade away (and perhaps several decades). We will first need to develop accurate biological tests that require a much deeper understanding of mental disorder than is currently possible and also preventive treatments that are effective and safe. Because the premature new diagnoses introduced by DSM-5 would all cause more harm than good, they should be dropped before the manual becomes official. Preventive psychiatry is the wave of the future, but would be the bane of the present.

Allen Frances is a professor emeritus at Duke University and was the chairman of the DSM-IV task force.

Brain-DisablingTreatments in Psychiatry by Peter Breggin

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Peter Breggin indubbiamente rivela alcuni aspetti negativi del trattamenti farmacologici che non sempre vengono propagandati con la stessa enfasi di quelli positivi, ammesso e non concesso che questi ultimi esistano in un trattamento a lungo termine: in questo senso ciò che dice è degno di essere preso in considerazione ed attentamente valutato. Dove personalmente non seguo Breggin è nel trasformare la sua battaglia contro gli psicofarmaci in uno scontro ideologico che si avvicina molto alle posizioni di Scientology.  in un suo intervento del 2005 egli ringraziava Tom Cruise  di cui  egli condivideva le opinioni e  difendeva l’appartenenza  alla setta.Lo psichiatra americano assomiglia a Beppe Grillo. Egli  si scaglia a testa bassa contro le case farmaceutiche denunciando  giustamente degli abusi ma non propone niente di seriamente alternativo. Le sue proposte sul piano della psicoterapia ad essere gentili sono inconsistenti dato che  secondo lui le malattie nascono da problemi “spirituali”.  La realtà non materiale umana non è ovviamente “spirito” da contrapporre al corpo, salvo non riproporre, in un modo più o meno larvato, un’impostazione fideistica  che si vorrebbe  superare. Il vero nemico da combattere è l’ideologia religiosa  che impedisce alla psichiatria di sviluppare una capacità ed una mentalità atta ad affrontare sul piano della relazione interumana la malattia mentale. Non si possono demonizzare i farmaci e non combattere con altrettanto vigore tanto per fare un esempio  contro le concezioni freudiane infiltrate nella pratica della psicologia e psicoterapia americana. La polemica, peraltro giusta in molte circostanze, contro il trattamento farmacologico è un terreno facile,aperto al sensazionalismo,  che fa leva su componenti persecutorie , come la paura di essere avvelenati o di subire lesioni da parte di medici incompetenti. Rimane la domanda se sia più dannosa una psicoterapia fatta male od un trattamento a base di benzodiazepine od antidepressivi somministrato da uno psichiatra che crede che quella veramente  sia la cura della malattia mentale.

Brain-DisablingTreatmentsi n Psychiatry

DRUGS, ELECTROSHOCI(, AND THE ROLE OF THE FDA

Peter R. Breggin, MD

/7). /;ltj1 LY~

[~I Springer Publishing Company

Contents

Introduction and Acknowledgments …………………………………………….. xi

  1. 1  The Brain-Disabling Principlesof Psychiatric Treatment ……………………………………………………… 1
  2. 2  Deactivation Syndrome (Chemical Lobotomy)Caused by Neuroleptics ……………………………………………………… 14
  3. 3  Neuroleptic-Induced Anguish, Including Agitation,Despair, and Depression …………………………………………………….. 25
  4. 4  Neuroleptic Malignant Syndrome, Tardive Dyskinesia,Tardive Dystonia, and Tardive Akathisia ………………………….. 35
  5. 5  Neuroleptic-Induced Brain Damage, PersistentCognitive Deficits, Dementia, and Psychosis ………………………. 53
  6. 6  Antidepressants, Including Prozac-Induced Violenceand Suicide ………………………………………………………………………… 77
  7. 7  Lithium and Other Drugs for Bipolar Disorder ……………….. III
  8. 8  Electroshock for Depression …………………………………………….. 129
  9. 9  Stimulants and Other Drugs for Children, Including
    an Analysis of Attention-Deficit Hyperactivity Disorder …… 157
  10. 10  Antianxiety Drugs, Including Behavioral Abnormalities

Caused by Xanax and Halcion ., …… ………………………………….. 184

ix

x Contents
11 Drug Companies and the Food and Drug

Administration: Failed Mandates …………………………………….. 208 Bibliography …………………………………………………………………………… 234 Index ……………………………………………………………………………………… 295

CHAPTER 4

Neuroleptic Malignant Syndrome, Tardive Dyskinesia, Tardive Dystonia, and
Tardive Akathisia

This chapter focuses on two well-known neurological disorders caused by the neuroleptics-tardive dyskinesia (TD) and neuroleptic malignant syndrome (NMS), with emphasis on their frequency and their destructive impact on the physical and emotional life of the individual. It also discusses neuroleptic withdrawal syndrome. The next chapter will explore irrevers- ible damage to the brain that primarily affects mental functioning, includ- ing tardive psychosis and tardive dementia. However, as products of neuroleptic neurotoxicity, all these drug-induced abnormalities are clini- cally and neurologically interrelated.

TARDIVE DYSKINESIA

Within a few years after the development of the first neuroleptic, it became obvious that many patients were not recovering from their drug-induced neurologic disorders even after termination of the therapy. Reports were made in the late 1950s. Delay and Deniker (1968) date their awareness

35

36 Neuroleptic Malignant Syndrome and Relnted Disorders

of irreversible neurological syndromes to 1959. By 1968 they were able to provide a vivid review of several varieties, including buccolingual, tnmcal, and variable choreic movements. In 1964 Faurbye (Faurbye, Rasch, Petersen, & Brandborg, 1964) named the disorder tardive dyski- nesia.

As if governed by one mind, psychiatry as a profession refused to give any official recognition to this potential tragedy. Then Crane made it a personal crusade to gain the profession’s recognition of the problem (1973). The American College of Neuropsychopharmacology/Food and Drug Administration Task Force (1973) described the syndrome in a special report. Following 1973, everyone in the profession should have been alerted to the dangers of TD; but too many psychiatrists have contin- ued to act as if it hardly exists.

In 1980, the American Psychiatric Association (APA) published a task force report on TD. In 1985 the FDA took the unusual step of setting specifically worded requirements for a class warning in association with all neuroleptic labeling and advertising (“Neuroleptics,” 1985). In a wholly unprecedented move, in the same year the APA sent out a warning letter about the dangers of tardive dyskinesia to its entire membership (see chapter 11 for further discussion of the FDA’s role).

TD often begins with uncontrolled movements of the face, including the eyes (blinking), tongue, lips, mouth, and cheeks; but it can start with almost any group of muscles. The most common early sign is a quivering or curling of the tongue. Tongue protrusions and chewing movements are also common, and can become serious enough to harm teeth and impair chewing and swallowing. The hands and feet arms and legs, neck, back, and torso can be involved.

The movements displayed are highly variable, and include writhing contortions, tics, spasms, and tremors. The person’s gait can be badly impaired. More subtle functions can be affected and are easily overlooked: respiration (involving the diaphragm), swallowing (involving the pharyn-

and esophageal musculature), the gag reflex, and speech (Yassa & Jones, 1985).

The movements usually disappear during sleep, although I have seen exceptions. They sometimes can be partially suppressed by willpower; frequently are made worse by anxiety; and can vary from time to time (see below).

Many cases of TD appear to be relatively mild, often limited to move- ments of the tongue, mouth, jaw, face, or eyelids. Nonetheless, they are

frequently disfiguring and often embarrassing. Patients have been known to commit suicide (Yassa & Jones, 1985).

The abnormal movements can sometimes become totally disabling. Turner (1971) describes patients who cannot eat and must have their teeth removed in order to facilitate the entry of food into their mouths. He also describes patients who cannot keep shoes on their feet because they wear them out while sitting with the constant foot-shuft1ing activity. I have evaluated a number of cases in which the tardive dyskinesia was wholly disabling, including massive distortions of the position of the neck or body, rocking and swaying, shoulder shrugging, and rotary or thrnsting movements of the pelvis, as well as disturbances of respiration, such as periodic rapid breathing, irregular breathing, and grunting.

Ironically, the disease makes the patient look “very crazy” because of the seemingly bizarre facial and bodily movements. Tragically, this has often led to patients being treated more vigorously with neuroleptics, ultimately worsening their TD.

As in other neurological disorders, the patient may attempt to hide the disorder by adding voluntary movements to the involuntary ones in order to disguise them. For example, to cover up a tendency to move the arms continually, the patient may make grooming movements around the face and hair. This can make it seem as if the individual suffers from a psychological compulsion instead of a neurological disorder. Or the patient may clasp his arms together in order to control the movements, making it seem as if he is trying to psychologically “hold onto himself.”

All the neuroleptics (see chapter 2 for a list) can cause tardive dyskine- sia, including the atypical neuroleptics clozapine (Weller & Kornhuber, 1993) and risperidone (Addington, Toews, & Addington, 1995). The overall adverse effects of the atypical neuroleptics are summarized in chapter 5.

Masking the Symptoms of TD with Continued Neuroleptic Treatment

The symptoms of tardive dyskinesia are masked or suppressed by these drugs, so that the disease symptoms do not fully appear until the patient has been removed from the treatment. For this reason, in addition to using the smallest possible dose for the shortest possible time, whenever possible patients should periodically be removed from their neuroleptics, if only

38 Neuroleptic Malignant Syndrome and Related Disorders

for a short period, to determine if they are developing tardive dyskinesia. Permanent removal from the neuroleptics is a more difficult matter, often requiring many months of gradual withdrawal for the hrain to adjust to the drug-free environment.

Harold Klawans has discussed the dangerousness of trying to control or treat TD with the causative agent. He asserts (in the discussion following Goetz et al., 1980): “Treatment of tardive dyskinesia with neuroleptics themselves is clearly treatment with the presumed offending agent and should be avoided.” He calls it “short-sighted” to use the neuroleptics in the treatment of tardive dyskinesia, and concludes that the therapy “serves to aggravate its pathogenesis.” Unhappily, Klawans himself in the same article too readily recommends reserpine as a helpful agent in the treatment of TD, when it too can cause the disorder.

Nonetheless, I have seen cases of TD that were so disabling that the only recourse seemed to be treatment with a neuroleptic. But two points must be borne in mind about these cases. First, in each instance, the case became so severe because physicians failed to detect the disorder when it first appeared and continued neuroleptic treatment long after it should have been terminated. This has been true in nearly all the most disabling cases I have examined. Second, the individuals in question were overcome with suffering and rendered wholly unable to function by the TD. They and their families made informed decisions to continue the offending agent because the TD was making life unbearable for the patient.

The anticholinergic drugs typically used to ameliorate the symptoms of drug-induced parkinsonism also may aggravate the symptoms of TD (Yassa et al., 1992). They include benztropine (Cogentin), biperiden (Aki- neton), and trihexyphenidyl (Artane, Tremin). These agents are known to worsen similar symptoms in Huntington’s chorea (Hunter, Blackwood, Smith, & Cumings, 1968; Klawans, 1973). At present the role of these drugs in the development or exacerbation of tardive dyskinesia is contro- versial and undetermined, but caution is required in giving them to patients on neuroleptics. Their adverse effects are discussed in chapter 2. These agents are often used to treat acute extrapyramidal symptoms and may be mistakenly prescribed for TD.

Rates of TD

In 1980 the APA produced a detailed analysis of the disease in its Task Force Report: Tardive Dyskinesia. It made clear that TD is a serious,

Brain-Disabling Treatments in Psychiatry 39

usually irreversible, untreatable, and highly prevalent disease resulting from therapy with the neuroleptics. The task force estimated the prevalence rate for TD in routine treatment (several months to 2 years) as at least 10%-20% for more than minimal disease. For long-term exposure to neuroleptics, the rate was at least 40% for more than minimal disease.

Even after the publication of the 1980 task force report and a mountain of confirmatory evidence, some biologically oriented psychiatrists, such as Nancy Andreasen (1984), in The Broken Brain: The Biological Revolu- tion in Psychiatry, continued to misinform the public that tardive dyskine- sia is “infrequent” (p. 210) and occurs in “a few patients” (p. 211).

The more recent APA task force (1992) report cites a rate of 5% per year, cumulative over the first several years of treatment. Jeste and Caligi- uri (1993) estimate the annual incidence rate among young adults at 4%- 5%.

In a recent prospective project emanating from Yale, Glazer, Morgen- stern, and Doucette (1993) reported a long-term evaluation of 362 outpa- tient psychiatric patients who were free of TD at baseline and who were being maintained on neuroleptics. For patients who are starting neurolep- tics, according to projections from their data, the risk of tardive dyskinesia will be 31.8% after 5 years of exposure-a rate of slightly over 6% per year. The risk is 49.4% after 10 years, 56.7% after 15 years, 64.7% after 20 years, and 68.4% after 25 years.

Chouinard, Annable, Mercier, & Ross-Chouinard (1986) followed a group of 136 persons who had already been receiving neuroleptics but had not manifested TD. Over 5 years, 35%-a rate of 7% per year- developed the disorder.

Overall, in relatively young and healthy patients, the cumulative risk of contracting TD when exposed to neuroleptic~ ranges from 4%-7% per year during the first several years o f treatment. Approximately one-third of the patients will develop this largely irreversible disorder within the

first five years of treatment. This represents an astronomical risk for patients and should become part of the awareness of all mental health professionals, their patients, and their patients’ families. Furthermore, we shall find that TD brings with it the additional risk of irreversible cognitive dysfunction and dementia (chapter 5).

There is evidence that rates for tardive dyskinesia are increasing. It may be caused by the growing tendency to use drugs with seemingly more toxic effects on the extrapyramidal system, such as Haldol and Prolixin (see Jeste & Wyatt, 1981). These drugs also come in long-acting

40 Neuroleptic Malignant Syndrome and Related Disorders

intramuscular preparations that do not permit patients to independently lower their own dosages by taking fewer pills than prescribed.

It is unusual for TD to develop in less than 3-6 months’ treatment and standard texts suggest that TD which develops earlier requires special investigation. However, it is not possible to place too much emphasis on one point that has been mentioned by Tepper and Haas (1979) and others (for example, Hollister. 1976): tardive dyskinesia can develop in low-dose, short-tenn treatment. DeVeaugh-Geiss (1979) has seen cases develop in a matter of weeks. I have seen several cases develop at around 3 months of treatment. One patient developed tardive dyskinesia after 1 month of recent exposure, with a history of 2 months’ prior exposure several years earlier. One case which developed in 3 months of constant exposure had a probable history of prior head injury from childhood. In the elderly, many cases may develop within a few weeks (see below).

THE ELDERLY AND
OTHER VULNERABLE POPULATIONS

It is important to remember that medications in general are more likely to cause dysfunction in the elderly (Nolan & O’Malley, 1988). Nowhere is this demonstrated more tragically than in regard to TD.

A study of elderly nursing home patients by Yassa, Nastase, Camille, and Belzile (1988) found that 41 % developed tardive dyskinesia over a period of only 24 months and that none fully recovered. While long-term studies have found a spontaneous dyskinesia prevalence of 1%-5% in the elderly, none of the non-drug-treated controls developed spontaneous dyskinesias during the 2 years. Yassa, Iskander, and Ally (1988) found TD in 45% of an outpatient clinic population with a mean age of 60.

In a more recent study, Yassa, Nastase, Dupont, and Thibeau (1992) followed up patients from a geriatric psychiatric unit who had received neuroleptics for the first time during the hospitalization. Out of 99 patients, 35 (35.4%) had developed TD after a mean exposure of 20.7 months. Of these 35, 21 had moderate TD and 3 had severe. Some had tardive dystonia (see below).

Saltz and his colleagues (1991) found the incidence of TD was 31 % following 43 weeks of cumulative neuroleptic treatment in the elderly. The incidence was higher among patients who had previous electroshock

Brain-Disabling Treatments in Psychiatry 41

treatment. Patients with early signs of parkinsonism developed TD at a faster rate. Of great importance, in this older population, the mean cumula- tive time while taking neuroleptics was very brief, a mere 22.7 weeks. One patient developed TD at 2 weeks.

Jeste, Lacro, Gilbert, Kline, and Kline (1993), in an ongoing prospective study, found that 26% of middle-aged and elderly patients developed TD after 12 months. The authors also reviewed the literature on neuroleptic withdrawal and found “that almost 60 percent of the patients withdrawn from neuroleptics did not relapse over a mean period of 6 months.” They concluded, “it seems feasible to discontinue neuroleptic medication from a select population of older schizophrenic patients, if it is done carefully with adequate monitoring and follow up.” They also experimented with brief 2-week placebo-substituted withdrawal in their own group of pa- tients, both younger and older subjects, and found it relatively benign: none relapsed or required resumption of neuroleptics. They concluded, “Given the heightened risk of TD in older patients, it seems that a trial of neuroleptic withdrawal is warranted in this population.”

Jeste et aI. (1993) emphasize that “The potential seriousness of neuro- leptic-induced TD warrants obtaining competent, informed consent to treatment from patients or guardians.” They recommended that consent be periodically renewed and cited other sources to confirm their position.

In addition to age, prior brain damage probably increases the risk of TD (Breggin, 1983; Chouinard, Annable, Ross-Chouinard, & Nestoros, 1979), although studies are contradictory and not conclusive. McKeith, Fairbairn, Perry, Thompson, and Perry (1992) found that 13 of 16 patients with Lewy body type dementia showed deterioration on neuroleptics, including the development of extrapyramidal features. The authors con- clude, “Severe, and often fatal, neuroleptic sensitivity may occur in elderly patients with confusion, dementia, or behavioral disturbance. Its occur- rence may indicate senile dementia of the Lewy body type . . . ” Pourcher, Cohen, Cohen, Baruch, and Bouchard (1993) found a correlation between TD and prior organic brain disorder.

Relapse, Exacerbation, and Delayed Onset after Termination

TD typically waxes and wanes, both in the course of a day and in the course of weeks or months. Especially in the elderly, both partial remissions and relapses are common (Lacro et aI., 1994).

42 Neuroleptic Malignant Syndrome and Related Disorders

As in many neurological disorders, the manifestations ofTD can worsen during stress and can be somewhat calmed with sedation (Jeste & Caligiuri, 1993). In my experience, anxiety, exhaustion, and other general stresses to the mind and body can temporarily exacerbate the symptoms, while relaxation, when possible, can temporarily reduce them.

With great effort, patients can sometimes suppress some of their symp~ toms for a short time. They can also integrate their movements into more natural-looking actions, such as grooming or smiling, in order to disguise them. One patient with whom I consulted would hide her involuntary facial grimaces by trying to smile. The effect was to make her look even more strange to the casual observer.

Neither the fact that TD waxes and wanes, sometimes in response to stress, nor the patient’s ability to partially suppress it with an exertion of will, should mislead observers into believing that it is psychological or emotional in origin. Too often the early signs of TD are overlooked, denied, or dismissed by physicians on these mistaken grounds.

Christensen, Moller, and Faurbye (1970) have documented that a signif- icant percentage of TD cases may not show up at all until many months or even several years after discontinuation of the treatment. They believe that the symptoms are brought on by the interaction between the damage caused by the drugs and by the aging process. If this is true, then a tragic reality may develop as we observe the evolution of TD in aging populations. I have on occasion seen cases that did not become apparent until several months or more after termination of treatment.

Reversibility Is Rare

In the vast majority of cases, TD is irreversible and there is no effective treatment. One repOlt indicates that among patients with persistent TD, followed for a period of 5 years, 82% showed no overall significant change, 11% improved, and 7% became worse (Bergen et aI., 1989).

Another study followed 49 outpatient tardive dyskinesia cases for a mean of 40 weeks (range 1-59 months) after discontinuation of medication (Glazer, Morgenstern, Schooler, Berkman, & Moore, 1990). Many patients showed noticeable improvement in their movements within the ftrst year after stopping neuroleptics, but only 2% showed complete and persistent recovery. The authors conclude, “A major finding of this study is that complete reversal of TD following neuroleptic discontinuation in chroni- cally treated patients was rare.”

44 Neuroleptic Malignant Syndrome and Related Disorders

underestimated. I therefore reviewed the subject in detail. Fortunately, this is no longer necessary, since it is now well-recognized that children are susceptible to TD at rates no less than adults, and that the disorder is often more virulent in children, because it frequently affects the torso, including posture and locomotion (Breggin, 1983a; Gualtieri & Barnhill, 1988; Gualtieri, Quade, Hicks, Mayo, & Schroeder, 1984; Gualtieri, Schroeder, Hicks, & Quade, 1986). A high percentage of neuroleptic- treated children also develop a permanent worsening oftheir emotional and behavioral problems, psychoses, or dementia (see chapter 5). Physicians should not use neuroleptics for behavioral control in children.

TARDIVE DYSTONIA

It is now apparent that there are at least two related variants of TD, tardive dystonia and tardive akathisia. In a 1988 review of tardive dystonia, Burke and Kang found 21 reports describing 131 patients (for reviews, also see Greenberg & Gujavarty, 1985, and Kane & Lieberman, 1992).

Tardive dystonia involves’ ‘sustained involuntary twisting movements, generally slow, which may affect the limbs, trunk, neck, or face” (Burke et al., 1982, p. 1335). The face and neck are by far the most frequently affected areas of the body. Severe deformities of the neck (torticollis) can cause extreme pain and disability. r have seen several cases affecting the orbital muscles of the eyes (blepharospasm) to the degree that the individual’s vision was impaired, requiring botulin injections to paralyze the muscles. I’ve also seen respiratory and abdominal muscles affected in a painful and debilitating manner.

Tardive dystonia can produce cramplike, painful spasms that temporar- ily prevent the individual from carrying out normal activities. Sometimes the spasms are so continuous that the individual is largely disabled. Dam- age to the joint and skeleton system, including fractures, can occur (Burke & Kang, 1988). The pain and muscle tension, as well as the eff01i to compensate for the spasms, can be exhausting and demoralizing.

The torsions can be worsened by other bodily movements, such as attempts to write or to walk. Sometimes they can be relieved by particular movements, such as touching the chin to relieve torticollis or touching the brow to relieve blepharospasm.

Brain-Disabling Treatments in Psychiatry 43 Physician and Patient Denial of TD

Physicians understandably find it painful to face the damaging effects of their treatments. Sometimes it is difficult for them to confront the damage done to patients by other physicians as well. In addition, physicians may consciously seek to protect themselves or their colleagues by failing to acknowledge or to record obvious symptoms of tardive dyskinesia. I have seen many hospital and outpatient records in which obvious, severe cases of tardive dyskinesia have gone either unrecognized or undocumented, sometimes by several physicians in succession. For example, the nurse’s notes may make clear that the patient is in constant motion, yet the doctor’s physical examination or progress notes will give no indication of the disorder. Even official discharge summaries may fail to record TD in patients who have been demonstrating the disorder throughout the period of hospital or clinic treatment. This denial of the obvious is mirrored within the profession itself, which has been very remiss in recognizing or emphasizing the seriousness of the problem (for an analysis of this history, see Breggin, 1983a; Brown & Funk, 1986; Cohen & McCubbin, 1990; Wolf & Brown, 1987).

Psychiatrists sometimes accuse patients of exaggerating their tardive dyskinesia. In reality, most patients tend to deny the existence or severity of their TD. As discussed in detail in chapter 5, patient denial is caused in part by neuroleptic-induced lobotomy effects and in part by denial associated with brain damage. The mutual denial of TD by physician and patient is an aspect of iatrogenic helplessness and denial-the use of brain-disabling treatments in psychiatry to enforce the patient’s denial of both his personal problems and his iatrogenic brain dysfunction and dam- age (chapter 1).

The Size of the Epidemic

It is difficult to determine the total number of TD cases. Van Putten (see Lund, 1989) estimated 400,000-1,000,000 in the United States. My own earlier estimate is higher, ranging in the several millions (Breggin, 1983). It is no exaggeration to call tardive dyskinesia a widespread epidemic and possibly the worst medically induced catastrophe in history.

Children and TD

When I reviewed the subject in 1983, I was among the first to state that the rate and severity of tardive dyskinesia in children was being vastly

Brain-Disabling Treatments in P5ychiatry 45

As Burke and Kang (1988) point out, tardive dystonia can be mistakenly dismissed as a manifestation of hysteria, psychological in origin: “In this regard it is important to realize that dystonia, like many other neurological disorders, can be influenced transiently by suggestion, placebo, or sedation (e.g., during an amobarbital interview) and such maneuvers cannot exclude a true dystonia.” Also, like many other neurological disorders, it can sometimes be partially controlled by extreme exertions of will.

Tardive dystonia can make an individual appear unsympathetic or bizarre, especially to the uninformed observer who equates the facial grimaces or neck distortions with being “crazy.” As in all the drug- induced dyskinesias, the individual may try to cover up for the disorder with additional movements that make the disorder seem voluntary, and therefore not a product of mental illness. The result can be very confusing or distressing to the observer.

TARDIVE AKATHISIA

Tardive akathisia involves a feeling of inner tension or anxiety that drives the individual into restless activity, such as pacing (see chapter 3 for details). The first report of tardive akathisia I have located in the literature was published by Walter Kruse in 1960. He described three cases of muscular restlessness that persisted at least 3 months after discontinuation of treatment with fluphenazine and trit1upromazine. The “akathisic syn- drome … consisted of inability to sit still, pacing the floor all day, jerky movements of arms and shoulders.” Once again Delay and Deniker (1968) were also among the first clinicians to notice the disorder. In discussing “syndromes persisting after cessation of medication,” they mention “hy- perkinetic” ones. As early as 1977, Simpson more definitively made an association between tardive dyskinesia and akathisia that would not re- spond to treatment.

Gualtieri and Sovner (1989) reviewed the subject of tardive akathisia, cited studies with prevalence rates of 13%-18%, and called it “a signifi- cant public health issue.” Nonetheless, the drug companies have ignored it in the labeling of their products.

The anguish associated with akathisia should not be minimized. Con- sider Van Putten’s (1974) description of a mild, temporary akathisia or hyperkinesia: “Patient feels ‘all nerved up,’ ‘squirmy inside,’ ‘uptight,’

46 Neuroleptic Malignant Syndrome and Related Disorders

‘nervous,’ ‘tense,’ ‘uncomfortable,’ ‘impatient’…. Subjective feeling of ill-being may be accompanied by restless changes in posture.”

One reason that so little attention has been given to the mental disruption associated with the dyskinesias is the tendency to blame the mental compo- nent on the mental illness of the patient. Indeed, it has been commonplace to blame the obvious motor disturbances on the mental illness as well, often resulting in increased treatment, and a worsening of the symptoms, until immobility sets in, masking the entire process.

It takes no great imagination to grasp the suffering of a patient con- demned to a relatively mild tardive akathisia for a lifetime. I have seen cases of this kind that were previously mistaken for severe anxiety or agitated depression. Chapter 3 reviewed research indicating that acute akathisia can drive a patient into psychosis, and to violence and/or suicide. Considering the millions of patients subjected to this torment, the problem takes on epidemic proportions.

Tardive akathisia can be subtle. A woman in her mid-sixties consulted me because of seemingly bizarre feelings that other doctors attributed to her depression and to somatic delusions or hallucinations. She had a feeling of “electricity” going in periodic bursts throughout her body. Although she sat quietly in the office, she spoke of feeling fidgety and driven to move about.

Her hospital and clinic charts disclosed that 2 years earlier she had been treated for approximately 6 months with neuroleptics. The sensation she was describing had first been noted while she was taking the medica- tion. I concluded that she probably had tardive akathisia, a subtle case that did not actually force her to move about. However, because she didn’t show external signs of the disorder, other physicians were reluctant to make the diagnosis. The patient felt “driven to distraction” and even to suicide by the disorder; but after my probable diagnosis, she actually felt somewhat relieved. At least she was being taken seriously.

In 1993, Gualtieri wrote:

In telms of clinical treatment and the public health, however, TDAK [tardive akathisia] is a fact, not a question. It is one more serious side effect of neuroleptic treatment, like TD and the Neuroleptic Malignant Syndrome. Taken together, they define neuroleptic treatment as a necessary evil, a treatment that should be administered with care and caution, and reserved for patients who have no other recourse.

Brain-Disabling Treatments in Psychiatry 47 RESPONSES TO TARDIVE DISORDERS

Physical Exhaustion

Fatigue to the point of exhaustion almost always accompanies tardive disorders of any severity. The patient can be exhausted by the movements themselves, by the effort to hide them, and by increased effort required to cany out daily activities. The primary impact on the brain itself may also produce fatigue. Although the disorders tend to disappear in sleep, they can make it difficult to fall asleep, adding to the exhaustion. Having to contend with the physical pain associated with tardive akathisia (inner torment) and \vith tardive dystonia (muscle spasms) can also wear a person down.

Psychological Suffering

Commonly, patients experience shame and humiliation, often leading to social withdrawal. Even a seemingly mild dyskinesia that affects facial expression can be sufficiently humiliating to cause a person to withdraw from society. So can a speech abnormality that makes a person seem to “talk funny.”

The experience of constant pain from dystonia or inner torture from akathisia can drive a person to suicidal despair. The physical disabilities associated with disorders can also become very depressing to patients.

In a clinical report from the Mayo Clinic by Rosenbaum (1979), depres- sion was found closely linked to tardive dyskinesia. Rosenbaum states, “Almost all patients in our series had depressive symptoms accompanying the onset of tardive dyskinesia,” and he cites other studies confirming his observation.

Tardive dyskinesia patients often feel very betrayed by the doctors who prescribed the medication or who later failed to detect the disorder or to tell the patient about it. Too frequently, perhaps in a self-protective stance toward their colleagues, several psychiatrists in a row will fail to inform the patient or family about the obvious iatrogenic disorder. This can leave patients feeling that they cannot trust psychiatrists. In the extreme, it can create an understandable distrust of doctors in general.

Even a slight or minimal de!,’Tee of tardive disorder can end up seriously impairing an individual’s quality of life.

48 Neuroleptic Malignant Syndrome and Related Disorders

NEUROLEPTIC \VITHDRAWAL SYNDROME

Withdrawal frequently causes a worsening mental state. including tension and anxiety. With those drugs that produce potent anticholinergic effects. such as Thorazine and MeHaril, a cholinergic withdrawal syndrome (cho- linergic rebound) may develop that mimics the flu, including emotional upset, insomnia, nausea and vomiting, diarrhea, anorexia and weight loss, and muscle aches.

Withdrawal symptoms can also include a temporary worsening of dyski- netic effects, both painful and frightening.

While classic addiction to these substances has not been demonstrated, the drugs should be considered addictive in the sense that withdrawal symptoms can make it impossible for patients to stop taking them. For this reason, I have suggested viewing these drugs as addictive (Breggin, 1989a, 1989b).

Because of the withdrawal symptoms, it is often necessary to reduce these drugs at a very slow rate. Sometimes withdrawal seems to be impossible. I have described the principles of withdrawing from psychiat- ric drugs in Talking Back to Prozac.

NEUROLEPTIC-INDUCED PSYCHOSIS AND DEMENTIA

The following chapter will describe irreversible psychosis and dementia associated with the neuroleptics. These may first become obvious as withdrawal effects that make it seemingly impossible to stop the drug therapy.

OTHER NEUROLEPTIC-INDUCED NEUROLOGICAL IMPAIRMENTS

The neuroleptics can produce a variety of other symptoms of central nervous system dysfunction, including abnormal electroencephalogram (EEG) findings, an increased frequency of seizures, respiratory depression, and disturbances of body temperature control (Davis, 1980; Davis & Cole,

Brain-Disabling Treatments in Psychiatry 49

1975). Endocrine disorders, especially in females, may also be of central nervous system origin (Davis, 1980). There is some evidence that auto- nomic dysfunction can become irreversible (tardive autonomic disorders).

NEUROLEPTIC MALIGNANT SYNDROME (NMS)

This devastating disorder was seemingly so bizarre, unexpected, and inex- plicable that physicians for years literally refused to believe their eyes. Seven years after the introduction of the drugs into North America, Leo Hollister (1961) reviewed their side effects for “Medical Intelligence” in the New England Journal of Medicine. In two separate places, he referred to syndromes that probably were NMS. He described a “bizarre” dystonic syndrome that can b e ‘ ‘confused with hysteria, tetanus, encephali- tis or other acute nervous-system disorders; a rare fatality may occur.” Later he mentioned that “other clinical syndromes attributed to central- nervous-system effects of these drugs have resembled acute encephalitis, myasthenia gravis, bulbar palsy or pseudotabes.”

Although NMS was identified in an English-language publication by Delay and Deniker as early as 1968, physicians continued to be reluctant to recognize the syndrome. Delay and Deniker declared it was caused by the neuroleptics, specifically including haloperidol (Haldol) and t1uphen- azine (Prolixin). Any neuroleptic can cause NMS. However, clinicians have found an increased danger with long-acting injectable neuroleptics.

Delay and Deniker were already able to identify many of the compo- nents of NMS, including pallor, hyperthermia, a severe psychomotor syndrome with akinesia and stupor or hypertonicity with varying dyskine- sias. They warn that, at the first suspicion, “one must stop medication immediately and completely.” They were already aware of fatalities. That the syndrome was named and definitively identified in English in 1968 is most remarkable in light of the failure of drug companies to give it formal recognition until compelled to do so by the FDA almost 20 years later (see chapter 11 for further discussion).

Neuroleptic malignant syndrome is characterized by “such symptoms as severe dyskinesia or akinesia, temperature elevation, tachycardia, blood pressure t1uctuations, diaphoresis, dyspnea, dysphagia, and urinary incon- tinence” (Coons, Hillman, & Marshall, 1982). If unrecognized, as too often happens, it can be fatal in morc than 20% of cases. The syndrome

50 Neuroleptic Malignant Syndrome and Related Disorders

frequently leaves the patient with permanent dyskinesias and dementia (see chapter 5).

Most cases develop within the first few weeks of treatment (even within 45 minutes!), but some develop after months or years, or after increased dosage (Gratz, Levinson, & Simpson, 1992).

Estimates for rates of neuroleptic malignant syndrome vary widely but studies indicate that they are very high. Pope, Keck, and McElroy (1986) surveyed 500 patients admitted during a I-year period to a large psychiatric hospital and found a rate of 1.4%. The cumulative rate for patients would be much higher. Addonizio, Susman, and Roth (1986) carried out a retro- spective review of 82 charts of male inpatients and found that prevalence for the diagnosed syndrome was 2.4%. Again, the cumulative rate over repeated hospitalizations or years of treatment would be much higher.

Although it is sometimes called’ ‘rare,” NMS should be described as common or frequent 0/100 is common by FDA standards).

The rates for neuroleptic malignant syndrome, as well as its potential severity and lethality, make it an extreme risk for patients receiving antipsychotic drugs. A risk of this size would probably result in most drugs in general medicine being removed from the market.

I have reviewed cases in which several physicians at a time missed making the correct diagnosis in what seemed, from my retrospective analysis, like an obvious case of NMS. The failure to stop the neuroleptic and to institute proper treatment resulted in severe, permanent impair- ments, or death. The mistaken idea that NMS is rare may contribute to these errors in judgment.

After reviewing episodes of NMS in 20 patients, Rosebush and Stewart (1989) found that most cases fit the following cluster of symptoms: delir- ium, a high fever with diaphoresis, unstable cardiovascular signs, an elevated respiratory rate, and an array of dyskinesias, including tremors, rigidity, dystonia, and chorea.

Patients spoke little during the acute illness and later reported that they had found themselves unable to express their anxiety and feelings of doom. Almost all patients were agitated shOltly before developing NMS, suggesting to the authors that they were undergoing akathisia. The white blood cell count was elevated in all cases, dehydration was common, and lab tests showed a broad spectrum of enzymatic abnormalities, including indications of muscle breakdown.

There is little or nothing about acute NMS to distinguish it from an acute, severe episode of encephalitis, especially lethargic encephalitis

Brain-Disabling Treatments in Psychiatry 51

(also called von Economo’s disease), except for the fact of exposure to neuroleptic therapy. I have previously compared neuroleptic toxicity and lethargic encephalitis in detail (Breggin, 1993; also see chapter 5).

Although Rosebush and Stewart provide insufficient data to draw exact parallels, their NMS patients also suffered chronic impairments similar to those reported in lethargic encephalitis patients. Of the 20 patients, 14 continued to have “extrapyramidal symptoms or mild abnormalities of vitals signs and muscle enzymes at the time of discharge” (p. 721); but we are not told how many of the 14 specifically had persistent extrapyrami- dal signs. In a striking parallel with lethargic encephalitis, three patients displayed persistent parkinsonian symptoms until they were lost to follow- up. One patient, who had mild cognitive impairment prior to NMS, devel- oped a persistent worsening of her dementia.

Neuroleptic malignant syndrome has also been reported with the atypi- cal neuroleptics, clozapine (Anderson & Powers, 1991; DasGupta & Young, 1991) and risperidone (Dave, 1995; Mahendra, 1995; Raitasuo, Vataga, & Elomaa, 1994; Singer, Colette, & Boland, 1995).

NEUROLOGICAL MECHANISMS OF PARKINSONISM AND TD

Drug-induced parkinsonism apparently develops in part, but not wholly, from blockade of dopamine receptors in the basal ganglia, specifically the striatal region or striatum (the caudate and putamen), producing motor retardation, rigidity, and other symptoms. Damage and degeneration in the pigmented neurons of the substantia nigra play a key role. These neurons terminate in the striatum, where, when they are functioning nor- mally, they release dopamine to act on striatal dopamine receptors.

Tardive dyskinesia is a more delayed reaction, probably based on the development of reactive supersensitivity or hyperactivity in these same striatal dopamine receptors following continuous blockade (see American Psychiatric Association, 1980; Fann, Smith, Davis, & Domino, 1980; Klawans, 1973; and chapter 5 in this volume). This supersensitivity of the dopamine receptors becomes most obvious when the drug is reduced or eliminated, terminating the blockade. The overactive, unblocked receptors produce the tardive dyskinesia symptoms. Undoubtedly a great deal more must be learned about the neuropathology of both these drug-induced

52 Neuroleptic Malignant Syndrome and Related Disorders

diseases, which probably involve multiple neurotransmitter system abnor- malities.

CONCLUSION

The widespread use of neuroleptics has unleashed an epidemic of neuro- logic disease on the world. Even if tardive dyskinesia were the only permanent disability produced by these drugs, this would be among the worst medically induced disasters in history. Meltzer (1995) has urged that attempts be made to remove long-term patients from neuroleptics and has attempted to demonstrate its feasibility. Gualtieri (1993), warning about the extreme dangers, has suggested neuroleptics be viewed as a therapy of last resort. I believe the profession should make every possible effort to avoid prescribing them. Although beyond the scope of this book, it is worth ending with a reminder that there is strong evidence that psychosocial alternatives can be more effective in the treatment of both acute and chronic patients labeled schizophrenic (Breggin, 1991a; Breg- gin& Stern, 1996; Karon & Vandenbos, 1981; McCready, 1995; Mosher & Burti, 1989).

Dsm V: a disaster for American psychiatry


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Dsm V: a disaster for American psychiatry

The catastrophic terror, evoked all the time, seems to be the sticking point of the collective psychology in the United States. And there are people who earn inventing diseases

 


Domenico Fargnoli
giovedì 17 gennaio 2013 13:01

Allen J. Frances, Professor Emeritus of Psychiatry at the Duke University and coordinator of the team of experts that in 1994 created the DSM IV (Diagnostic and Statistical Manual of Mental Disorders), regarding the soon to be published new version, the 5th, talked about “a disaster”. With respect to its etymology, the term “disaster” (dis-aster) refers to a calamity, as it could have been the end of the world proposed by the Maya, caused by negative astral influence. The DSM manual, now considered in its various editions a true Bible for psychiatry, has been conceived and written by real people, with real names: on those real people must fall the enormous responsibility for the incalculable damages that the practical applications of DSM criteria – completely devoid of any scientific basis – could cause to the mental health of millions or even billions of people. To exorcize or cancel the sense of guilt about the possible iatrogenic damage, I think that it’s not enough to simply exchange a human event with a natural event, just as schizophrenic patients use to do; or to lose the research of the real causes by referring to horoscopes, destiny and alignment of planets. As the use of particular terms reveals, a catastrophic sense has silently and unnoticeably entered, just like the Trojan Horse, the secret citadels of the powerful lobbies of the A.P.A., pointing out a dangerous flaw in their ideological pseudo-truths. The subject is very present. Freus’d “death” has left, in America, a heavy heritage that negatively influenced psychiatry. Catastrophic fantasies and daydreaming form part of the connective tissue of North American imagination: from the famous 1938 radio show in which Orson Welles announced the war of the worlds and the Earth attacked by Martians, causing a wave of uncontrolled and general panic; to cinema productions like “The Invasion of the Body Snatchers” (Don Siegel, 1956), or like more recent ones: “The Day After Tomorrow” (Roland Emmerich, 2004), “2012” (Roland Emmerich, 2009), the catastrophic terror, perennially evoked and exorcised, seems to be the sensible, aching spot of collective American psychology. Surely Osama Bin Laden had well understood this aspect, when planning the attack to the Twin Towers: a scene that, seen on television, seemed to be taken from a Sci-Fi movie. Sometimes nightmares, or what psychiatrists could define as “socially shared deliriums” are transformed by someone in reality with an enormous amplification of the terrifying effect.

In May 2013 the new edition, revised and corrected, of the DSM, the famous Diagnostic and Statistic Manual of Mental Disorders will be published: even without referring to astrology, it’s been anticipated that for American psychiatry it will represent a true announced catastrophe. According to Allen J. Frances, the present moment – that exactly matches the final approval and the imminent release of the manual – is the worst moment in his multi-decennial activity of study, teaching and clinical research in psychiatry: he encourages patients, physicians, media and naturally psychiatrists to refuse credit to a publication that, in his opinion, has no scientific credibility and that could lead to many and very serious diagnostic mistakes, extremely dangerous for patients due to completely useless prescriptions for drugs. These new diagnoses in psychiatry could well be more dangerous than the medicines, because they deeply affect the circumstance that millions of people could be prescribed psychotropic drugs often by general practitioners and after a very short interview. The introduction of new diagnoses should be done with the same attention that is dedicated to the patients’ health when introducing on the market new drugs. All the new diagnostic categories introduced in the DSMV – from those regarding alimentary abuse (basically everyone who loves eating and good food could be diagnosed with Binge Eating Disorder), to addictions (millions of youths could be diagnosed with Internet Use Gaming Disorder), to autism spectrum (Autism Spectrum Disorder, in which from now on will be included the Asperger Syndrome, that used to be a separate and autonomous diagnosis) – extend the limits of pathology by the tendency to codify many symptoms that are dangerously close to “normality”. There are many other extremely controversial aspects in the DSMV, like the adoption of the definition “Pedophilic Disorder”. The word “disorder” can not, in any case, give a correct idea of the seriousness of this pathology, that in this new edition is considered in such a manner only when the sexual fantasies and impulses create a sense of clinically significant “discomfort” (sic!) or the impairment of working or social activity, as it was already stated in the DSMIV. This definition has a very important consequence: only those who perceive a sense of “discomfort”, a sense of guilt, that is, could be diagnosed as pedophiles, while those with a much more serious illness, those that are completely unemotional could be considered normal because they do not feel any guilt or discomfort, because they maintain an equilibrium. This tendency to identify “normal” and “unemotional” can be found also in the decision – that could also appear in the DSMV, unless last minute changes are adopted – of confusing the pain caused by the loss of someone close, with a clinical depression. Grief excluded depression in the DSMIV, while in the new edition these two situation could coincide. Regardless of the final conclusion of this controversy, that has risen due to many protests from many columnists and important scientific publications, it clearly speaks well about the ideological foundation of American psychiatrists, that consider schizoids, those that are completely unemotional, as perfectly normal and balanced people. The repercussions of this conception are important: every year 2,5 millions of people in the United Stated die, leaving many more people, relatives and friends, in a state of sorrow and grief; if this condition goes on for more than two weeks, these people could easily be diagnosed, especially by general practitioners, a depression – this with great satisfaction, economical also, for pharmaceutical industries. In everyday’s medical practice the false positives of depression diagnoses after a loss, cause absurd situations and clearly show, just by common sense, an admission of complete incompetence.

American psychiatry is absolutely unable to face extremely serious psychotic situations such as Adam Lanza’s mass murdering: in this case schizophrenia hasn’t been diagnosed and aptly treated. A normal and physiological state of grief is considered pathologic and a clear psychotic state isn’t detected. The so called “mass shooting” has become almost epidemic, a sort of unconsciously repeated dramatization of the idea of a violent and hyper rational society (62.000 deaths in just a few years by firearms) that historically has been erected on racism and systematic extermination of native populations. The same war ideology that makes the United States so present in many unfair and useless conflicts, is the origin of a psychiatric emergency in the armed forces: 295 soldiers took their lives just in 2012. The only given response to this dramatic situation is a manual that’s been created with the aim of reinforcing the academic status quo, that is very far from real life and whose main interest is to obtain an economic profit for pharmaceutical sector. According to Frances the motivations that lead to the new edition of the DSM aren’t just of economic nature, tied to a very simple conflict of interests among various researchers paid by different pharmaceutical industries; this conflict, for the scientist, is a lot more of “intellectual” nature: these highly specialized researchers have the natural tendency to value their personal guidelines and ideas, to expand their sectors of study regardless of the practical clinical consequences for the unfortunate patients. It must not be underestimated that A.P.A. invested 25 millions in DSMV, and given that the previous edition has been a worldwide bestseller, a similar result is expected for this new edition as well, not only in terms of profits from the sells, but also in terms of increased popularity and prestige for the researchers – popularity and prestige that can be cashed in on as well. Even if Professor Frances’ critiques appear to be somehow well motivated, they do not decrease his personal responsibility in this announced disaster.

He has been, indeed, the first creator of DSMIV, starting what now appears to be a true psychiatric apocalypse: it must be remembered that the 1994 edition of the manual was labeled as “trash science” in an international survey of experts carried on in England in 2001, as well as being voted as one of the ten worse psychiatric publications of the millennium. It’s false, therefore, to say that there’s a substantial difference between DSMIII and IV, because in the latter, already, it was introduced a clear loss of effectiveness of the diagnosis in favor of its reliability: a group of psychiatrists finds an agreement on a series of atypical behaviours and on the fact that they found a mental disease. The creation of new categories becomes, therefore, a sort of cultural and intellectual game completely devoid of any scientific validity despite its – supposed – reliability that comes from the simple fact of being shared by a large number of experts: this procedure, applied to the real world of clinical practice is a fraud tout court. As it shows, not only Allen J. Frances appears be to be unreliable when not only declaring his non-theoreticism, but also when claiming to have overcome the confusion of diagnoses that ruled psychiatry before the DSMIV; a confusion largely due to the massive presence of Freudian psychoanalysis in America. There’s a precise historical and ideological continuity between the Freudian fraud – submitting patients to analysis without wanting and without being able to be a cure – and DSM in its various versions – proposing diagnostic criteria based on pseudo-scientific assumptions, as those regarding the affirmed genetic nature of schizophrenia, just as an example, very useful to be paid by medical insurances.

Just as Freudians considered all human beings as potential carriers of mental illness, for the fact that in everyone there would be a naturally perverse subconscious and a schizophrenic ideation as the one in dreams; so the A.P.A. now with DSMV sees in normality a state of potential illness: for the psychoanalysis, mental illness, omnipresent in every human being, was latent in the subconscious; at present moment, on the other hand, mental illness is found in the conscious and in the behaviour of so-called normal people that, for example, have the misfortune of losing a relative, therefore getting trapped in the knots of the diagnostic categories of DSM. Personally I will comply with Allen J. Frances advices: I will boycott in every possible way the DSMV, adding that I’ve done exactly the same with III and IV. Just as I did not believe to Mayas’ prophecy about the end of the world, so I don’t believe that the failure of DSMV is a particularly meaningful event in the history of contemporary psychiatry, despite all the hype in the mass media. According to my experience and formation, the true game regarding the future of psychiatry is played on another field: in my professional practice I will keep on using the classification of illnesses that was already present from the start of 20th century in the great theoretical production of the psychopathologists, with the likes of Jaspers, Eugen Bleuler, Minkowsky, Kurt Schneider, Barison.

To my advice, only the critical revision of those diagnostic categories with a psychopathologic derivation, carried on for more than sixty years by Massimo Fagioli, allows us to correctly identify and focus the nature of the pathogenetic processes that we have to face in the practice of psychotherapy. Fagioli’s “Teoria della Nascita” (“Birth Theory”) completely transformed all traditional theoretical views regarding the genesis of mental illness. Starting with Esquirol, throughout 19th and 20th centuries to the present (the last example being Rita Levi Montalcini), it’s been thought that mental illness is tied to a rationality deficit and to a diminished ability to draw together by the conscience. Regression, therefore, would set the subconscious automatisms free, taking into light an irrational ideation that was considered naturally psychotic. Today, though, we know that the generating nucleus of the illness does not reside in conscience, but in a specific unconscious activity, the “Pulsione di Annullamento” (“Annulment Drive”), that was historically discovered by Fagioli: the “Pulsione di Annullamento” is not a natural characteristic with which each human being was born; to the contrary, it derives from a failure in the relations with other human beings. Originally the “Pulsione di Annullamento” comes from an inadequacy in the relation between mother and child: this inadequacy – no matter how we conceive it – affects the child’s vitality right from birth. Only by identifying the generating nucleus responsible for the specific form that mental illness takes, we can get also what is not immediately visible and understandable by the conscience, thus formulating diagnoses that are not only reliable, but also motivated and true. Many other internationally known researchers, such as American Louis A. Sass and Joseph Parnas from Copenhagen University, share this same view, although in a different theoretical reference frame; according to Parnas, only by improving our psychopathologic knowledge, we can fight the reification of the diagnostic categories that is carried on in the various editions of the DSM, the Bible of American psychiatry.

Domenico Fargnoli, psychiatrist

Translation: Dr. Lorenzo Frusteri

Italian version

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The shooters

Film Title: ShooterShooters

Steven Taylor

Several writers of my acquaintance, such as Allen Ginsberg and Ed Sanders, developed the habit of keeping extensive files of press clippings on stories of personal interest. Noam Chomsky, we’re told, does the same thing. An individual news report may mention something in passing that may seem secondary to the main narrative, but when multiple stories collected over time repeat the same seemingly secondary data, important patterns can become apparent.

For example, for many years Ginsberg clipped New York Times articles having to do with the international traffic in narcotics. This collection eventually served as one of the sources for historian Alfred W. McCoy’s definitive study linking the heroin trade to U. S. government agencies, The Politics of Heroin.

Now, amid the sickening media parade endlessly looping, one aspect of the mass shooter phenomenon is continually skipped, but a survey of press reports on the spate of bizarre violence that has arisen since the 1990s reveals a pattern.

In the past few days, following the Newtown murders, various experts have weighed in on the difficulty of profiling the mass shooter type. (An accurate psychological profile, presumably — and hideously problematically — could enable parents, teachers, doctors, and law enforcers to predict which individual is headed toward being the next shooter.)

Despite the difficulty of such profiles and predictions, there are two things that such characters have in common. First, they are mostly young white males. Second, many of the perpetrators are reported to have been taking psychoactive prescription medication.

The website “SSRI Stories: Antidepressant Nightmares” offers a sortable database of more than 4,800 newspaper articles, scientific journal reports, and TV news items linking antidepressant use to cases of extreme violence.

It is important to note that this site is not peddling some conspiracy theory. It is not speculative at all. The website is an index to reputable sources reporting on actual criminal cases, and in all cases reported, prescription meds are implicated.

The articles show that these violent acts were perpetrated by consumers in the 50 billion dollar a year selective serotonin reuptake inhibitor (SSRI) industry. This is a class of drugs whose warning labels and pharmaceutical literature note that a small percentage of SSRI consumers fantasize about and/or exhibit extreme violence.

I was originally tipped to this in July of 2012 in an article by RS regular Jonathan Zap, which he wrote in the wake of the so-called Batman shootings of that summer.

Zap notes as follows.

“Mass shootings, like the one that just happened in Aurora [Colorado], have become a recurrent nightmare that haunts the collective psyche. As the nightmare repeats, we see patterns emerging. One, which we don’t have confirmation on yet in this case, is that the shooter will almost always turn out to be on an SSRI (selective serotonin reuptake inhibitor). For example, Colorado’s other most famous mass shooting, Columbine, was masterminded by 18-year-old Eric Harris who was on the SSRI medication Luvox. Here’s an index of shootings and the SSRI connection someone put together.”

The website Jonathan links us to, “SSRI Stories: Antidepressant Nightmares,” concentrates on reports implicating Prozac (the FDA’s number 2 drug for violence), Zoloft, Paxil (number 3 for violence), Celexa, Lexapro, Luvox, Remeron, Anafranil, Effexor, Cymbalta, Pristiq, and Wellbutrin.images

Here are a few samples of reports from the site, with comments.

“Tim Kretschmer . . . walked into Albertville Secondary in Winnenden, near Stuttgart, at 9.30am on Wednesday armed with a 9mm Beretta he had stolen from his gun enthusiast father and wearing a K4-Schutz bulletproof vest and the black fatigues of Germany’s elite forces, the Kommando Spezialkräfte. . . . He killed nine pupils at Albertville, all but one a girl, and three teachers, all women, in less than 10 minutes. He then shot and killed three bystanders as he tried to escape, before taking his own life after a shootout with police. . . . It emerged that Kretschmer had been suffering from depression . . . and receiving medication for the condition.” –Scotland On Sunday, Edinburgh, March 14 2009.

“Hours before he walked into a Northern Illinois University lecture hall and inexplicably started a shooting rampage that ended five lives and his own, Steve Kazmierczak called one of the people he was closest to and said what would be a final goodbye. . . . [According to his girlfriend] ‘he was anything but a monster. He was probably the nicest, most caring person ever’. . . . [She said] he saw a psychiatrist monthly but stopped taking Prozac a few weeks ago. She said the medicine ‘made him feel like a zombie’.” –Chicago Sun Times, February 8, 2008.

What we might call the “zombie effect” seems to come up in many of these cases. Also common is that the violent behavior tends to occur when the patient is either having the dosage adjusted, or has just stopped taking the pills.

SSRIThe “SSRI Stories” site notes the following.

“The danger of withdrawal from antidepressants and antipsychotics is well documented. The brain tries to compensate for the blockage of the serotonin and dopamine receptors by growing additional receptors for these neurotransmitters. When the medications are discontinued, these additional receptors contribute to an ‘overload’ of serotonin and dopamine flooding the receptor. This is known as ‘supersensitivity psychosis’ and ‘antidepressant discontinuation syndrome’.”

“BEMIDJI, MINN. — Jeffrey Weise had ‘a good relationship’ with the grandfather he shot and killed on Monday as prelude to his deadly assault on students and others at Red Lake High School, according to relatives who are struggling to understand what might have pushed the teenager from sometimes bizarre behavior to mass murder and suicide. . . . They wondered, too, about medication he was supposedly taking for depression, and a recent increase in his prescribed dosage. . . . 60 milligrams a day of Prozac.” –Star Tribune (Minnesota), March 24, 2005.

Consistent with the “zombie effect” noted above, many sources indicate that some perpetrators who survive their crime scenes report being in a dreamlike state in which they feel they are watching their actions but not in control of them. Some of the literature notes sleep disorders, and speculates that the drugs induce a state of waking dream in which one becomes a passive witness to one’s actions. (Christopher Pittman, who killed his grandparents and set fire to their house told his father afterward that it had been like watching a TV show.) Other sources say the shooters do not remember their crimes or do not associate themselves with what occured.

“Huntsville, AL. — 15 year old Hammad Memon is free on bond, awaiting trial on murder charges for the February 2010 shooting death of fellow Discovery Middle School student Todd Brown. . . . Memon has a history of being treated for Attention Deficit Hyperactivity Disorder and Depression. He was being medicated with Zoloft and other drugs for the conditions. . . . Memon’s mother is quoted as saying ‘My son is not normal. He is immature (mentally) for his age. He has become very depressed and withdrawn for the past 2 years, especially in the last 12 months. He does not have insights into what crime he has committed’.” –The Free Republic (Alabama), Feb 5 2012.

“CARTHAGE, NC — Jurors in the Robert Stewart murder trial reached a verdict Saturday. He was found guilty of eight counts of second-degree murder in a shooting rampage at a North Carolina nursing home in 2009. . . . Stewart’s defense lawyers said the 47-year-old was essentially sleepwalking at the time due to taking a combination of prescription drugs. . . . Defense attorney Jon Megerian said Ambien and other drugs in Stewart’s system caused him to be in a zombie-like state of mind when he entered the nursing home. . . . In pleading Stewart’s case, his defense said he was full of remorse, but couldn’t remember anything. –WTVD television, North Carolina.

There have been a number of cases where defendants have been found not responsible for their actions due to the effects of the medication.

“STAMFORD, CT — A Stamford lawyer who shot at a motorist, then broke into his ex-wife’s house was found not guilty by reason of mental disease or defect yesterday. Eric Witlin, 40, will be committed to Whiting Forensic Institute for evaluation until he returns to court July 14. Judge Richard Comerford could commit Witlin for the time he could have been sentenced to prison, a total of 70 years. . . . Two psychiatrists, including one hired by the prosecution, testified that Witlin suffered a psychotic episode brought on by Adderall and Prozac, which were prescribed to treat attention deficit disorder and depression. . . . Senior Assistant State’s Attorney James Bernardi said Witlin’s mental state on the night of the incident was uncontested, since both psychiatrists agreed. –Stamford Advocate, May 20, 2008.

“Anna L. Tang, the troubled former Wellesley student, is finally free to resume her life and has been discharged from court custody. . . . Tang came to the attention of most MIT students in October 2007 when she stabbed her ex-boyfriend, Wolfe B. Styke, then a freshman, in his Next House dormitory room. . . . Tang has bipolar disorder, which she sought help for when she first arrived at Wellesley in 2005. At that time, she was diagnosed with depression and was prescribed an antidepressant. However, as Tang’s psychopharmacologist Michael J. Mufson testified during the trial, bipolar disorder cannot be treated with antidepressants. Doing so creates oscillatory behavior. ­ ‘It made her lows lower and her highs get higher’, Mufson said. That combination of misdiagnosis and mistreatment led to her attack on Styke. Judge Henry found in December that Tang lacked the substantial capacity to conform her actions to the requirements of the law and that she lacked the capacity to appreciate the wrongfulness of her actions. The Tech (MIT student newspaper), Feb 8, 2011.

In other legal news, there have been some 450 suicide-related lawsuits settled out of court by GlaxoSmithKline, the maker of Paxil.
“Since Paxil came on the market in 1992, there have been three separate types of failure to warn lawsuits filed: birth defects, suicide, and addiction. Roughly 150 suicide cases were settled for an average of about $2 million, and about 300 cases involving suicide attempts were settled for an average of $300,000, according to a December 14, 2009 report by Bloomberg News. Glaxo paid an average of about $50,000 each to resolve about 3,200 cases linking Paxil to addiction problems. . . . All total, Glaxo has paid out close to $1 billion to resolve Paxil lawsuits since the drug came on the market in 1992. The company’s provision for all legal matters and other non-tax disputes as of the end of 2008 was listed as $3.09 billion in its annual report.” –Dissidentvoice.org.

To summarize, FDA warnings, court finding, and too many news reports to count make a connection between one of the most widely prescribed drug types and bizarre, ostensibly “inexplicable” violence. And though there are thousands of sources and multiple vectors of association implicating the 50-billion-dollar business in SSRIs to some of the most hideous crimes of our day, the major media continue to spin their wheels about the “unexplainable.” This story needs to go viral. Now.

Image by Carsten Achertzer, courtesy of Creative Commons license.