Psicofarmaci e violenza

violenzaNeuroleptic Drugs and Violence


Catherine Clarke SRN, SCM, MSSCH, MBChA.

and Jan Evans MCSP. Grad Dip Phys.

August 19th, 2012



We address the fact that the treatment for Severe Mental Illness (SMI) is neuroleptic medication. One has to give significant thought about the involvement of neuroleptic medications with the tragic circumstances of individuals who have perpetuated a progressive catalogue of catastrophic actions, and the many victims and their families who so sadly are caught up in such tragedies.


It is established that there is an increased risk of violence by people with a mental health diagnosis. A greater risk of violent behaviour (27.6%) has been found for patients who commit substance abuse, compared to non-abusers (8.5%). For patients with schizophrenia, 13.2 % committed at least one violent offence, compared with 5.3% of the general population.1


Violence is reported with command hallucinations: 48% experienced harmful or dangerous actions and this increased to 63% in medium secure units and was significantly higher, 83%, in the forensic population.2


People who are classified as SMI i.e. with schizophrenia or bipolar often experience violent incidents following a diagnosis of SMI, even though they don’t consume alcohol or use street drugs, nor having a past history of violence or command hallucinations to harm others.

Our purpose of this document is to provide a referenced explanation of how neuroleptic medications are a potential cause of violence. We take a physiological perspective concerning pharmacogenetic variants and the disruption of neurotransmitters. In Part 1 we discuss what is known about Neuroleptics and Neurotransmitters; in Part 2, the Neuroleptic Disruption of Neurotransmitters


Part 1


The first part of this document has the following structure:            

·       Violence

  • Neuroleptic Adverse Effects on Behaviour
  • Serotonin Disruption
  • Noradrenaline/Norepinephrine Disruption
  • Acetylcholine Disruption including Neuroleptic Malignant Syndrome and Organophosphate Poisoning

·       Neuroleptic Withdrawal Adverse Effects on Behaviour

·       Neurotransmitter Functioning and Behaviour

·       Increased Prescribing of Neuroleptics as a Risk for Increased Violence



This is an important issue. In three acute psychiatric units in Australia it was reported: “58 % of the incidents were serious violent incidents.”3 In an attempt to address psychiatric violence in the UK, the National Institute for Health and Clinical Excellence (NICE) has a full clinical guideline: Violence. The short-term management of disturbed/violent behaviour in in-patient psychiatric settings and emergency departments.4 Although this addresses many issues, it omits the following potential causes of violence:

  • Neuroleptic medications – due to neuroleptic disruption of neurotransmitter circuits such as dopamine, serotonin, norepinephrine/noradrenaline and acetylcholine.
  • Pharmacogenetics – the issue of inefficient neuroleptic metabolising.


Adverse Effects on Behaviour of Neuroleptics


Neuroleptic toxic adverse reactions are related to behavioural changes such as akathesia, which is known to be a predisposing factor to violence5 and was formally recognised in the late 1970s.6


The symptoms of akathisia, an extreme, involuntary internal physical and emotional restlessness, includes restlessness, agitation and irritability.


When there is an existing precondition of akathisia, any perceived untoward disrespectful attitudes or verbal communications can trigger violence. When patients are agitated or irritable, they are less able to cope with perceived disrespect and are more prone to respond violently.


A marked increase of violence has occurred with patients prescribed moderately high-doses of haloperidol,7 and with Asian patients clozapine played a role in causing aggression and disruptive behaviour.8 Both the older ‘typical’ and the newer ‘atypical’ neuroleptics are associated with adverse behavioural reactions in a study reporting that “the newer antipsychotics did not reduce violence more than perphenazine.”9


Chart Depicting Toxic Behavioural Effects for Typical Neuroleptics:



Typical Neuroleptics



Adverse Reactions Related to Violence

Clopixol Agitation & akathisia
Haloperidol Restlessness, agitation and violence
Stelazine Restlessness
Sulpiride Restlessness & akathisia


 Refs 7, 10 &11


Chart Depicting the Toxic Behavioural Effects for Atypical Neuroleptics:



Atypical Neuroleptics


Adverse Reactions Related to Violence

Abilify Restlessness, agitation and akathisia
Amisulpride Agitation


Akathisia and agitation
Olanzapine Restlessness and agitation
Palperidone/Invega Akathisia and aggression
Quetiapine Akathisia and irritability
Risperidone Agitation
Sertindole Akathisia
Zotepine Akathisia


Ref 10


Observations in prison have also associated neuroleptic treatment with increased aggressive behaviour. Inmates were better able to control their aggression until they were prescribed neuroleptics and then the aggression rate almost tripled.12


Neuroleptic Withdrawal Adverse Effects on Behaviour


There is also the issue of violence experienced during withdrawal. Irritability and agitation is reported in association with neuroleptic withdrawal,13 and a direct reference links akathisia following the withdrawal of a depot in an inpatient setting.14 Irritability, agitation and akathisia need to be recognised as reactions to neuroleptic withdrawal. 

In order to prevent violence in association with akathisia and withdrawal, this process needs to be undertaken by a professional or lay-person who understands the potential problems and can therefore guard against unwittingly appearing at all antagonistic to the patient.

Neurotransmitter Functioning and Behaviour


Fundamentally, human behaviour is determined by neurotransmitter functioning and “A rich literature exists to support the notion that monoamine (i.e. serotonin, dopamine, and norepinephrine) neurotransmitter functioning is related to human aggressive behaviour.”15


Dopamine, serotonin and all other neurotransmitter circuits are interdependent and any disturbance in one will result in an imbalance in them all, disrupting normal functioning. Jackson’s First Law of Biopsychiatry states:  “For every action, there is an unequal and frequently unpredictable reaction.”16


Chronic neuroleptic treatment causes unpredictable behavioural reactions due to dysregulation and disruptions between dopamine, serotonin and acetylcholine neurotransmitters.


Neuroleptics and Serotonin Disruption


Some neuroleptics are known as serotomimetic drugs, affecting serotonin receptors – some block the receptors and some make them more active. “There are 14 different types of serotonin receptors that may be targeted by neuroleptics, with risperidone, clozapine, olanzapine, quetiapine and clopixol especially affecting the serotonin 5-HT2 receptor.”17 


Mental status changes occur in Serotonin Syndrome. This is caused by neuroleptic drugs due to serotonin toxicity.

Animal research indicates that serotonin disruption is associated with increased violence. Reduced levels of a specific serotonin metabolite (5-HIAA) in cerebrospinal fluid has been linked with increased aggression in both dogs and male rhesus macaques18-19 and low concentrations of 5-HIAA in different cultures have been consistently reported to be associated with impulsive destructive behaviours, aggression and violence.20


Since “Impulsive violence is closely linked to serotonergic function and to several brain regions”21 and since impulsivity is also linked with both low and high serotonin levels it is difficult to know which of these changes play the most important role in treatment emergent violence.”17 


The reciprocal interaction between the dopaminergic and serotonergic systems disturbed by either dopaminergic blockers or serotonergic enhancers leads to the disruption of homeostasis.22 Although the serotonin system and its interactions with other neurotransmitters are complex and full information is difficult to find, there are clear research papers, which show that serotonin and aggression are related.


Chart depicting Neuroleptic Serotonin Disruption associated Adverse Toxic Behavioural Effects:

Akathisia Irritability


Arson Aggression
Violent Crime Self Destructiveness
Impulsive Acts Agitation
Hostility Violent Suicide


Ref 23 & 24


Neuroleptics and Noradrenaline/Norepinephrine Disruption


Neuroleptics affect the norepinephrine neurotransmitter and akathisia induction with haloperidol is known to be associated with increased noradrenaline turnover.25- 26


Neuroleptics and Acetylcholine Disruption


An important function of the acetylcholine neurotransmitter is the control of psychological defence mechanisms including fight or flight responses.  Such responses are impulsive and naturally include aggression and violence.


In varying degrees, all neuroleptic drugs have anticholinergic properties. This means that they block and cause disruption to the acetylcholine neurotransmitters. The body compensates and responds by making and releasing more acetylcholine.27


Acetylcholine Disruption and Increased Violence


Aggressive responses such as defensive rage and violence have been linked with excessive acetylcholine in animals28 –30 and a relative acetylcholine increase is associated with neuroleptic drugs due to the disruption of the dopamine-acetylcholine equilibrium.31-32


Since excessive acetylcholine is linked with aggression and violence in animals, it is likely that neuroleptic induced acetylcholine abundance triggers aggression and violence in humans.

Neuroleptic → Disrupted dopamine-acetylcholine equilibrium → Relative acetylcholine increase → Aggression/Violence.


Neuroleptic Malignant Syndrome and Organophosphate Exposure


Neuroleptic Malignant Syndrome (NMS) is an adverse effect of neuroleptics, a potentially fatal condition with up to 76% mortality rate.  Symptoms of NMS include aggression, agitation and violence.27 & 33 New research associates NMS with elevated acetylcholine.34


Organophosphate chemicals form the basis of many insecticides, herbicides and nerve gases. They block the action of the body’s acetylcholinesterase enzyme, which breaks down acetylcholine so it may be processed and recycled. Excessive acetylcholine accumulates in the nervous system if the action of this enzyme is blocked.


Prolonged and repeated exposure to Organophosphates results in Chronic Organophosphate-Induced Neuropsychiatric Disorder (COPIND) e.g. in farmers who handle pesticides, due to chronic Organophosphate Poisoning (OP). COPIND behavioural symptom changes include: Hostility, Anger, Aggression and Violence.35-36  Since OP results in excessive acetylcholine, which is linked with aggression and violence in animals, the behavioural changes in COPIND are highly likely caused by excessive acetylcholine.


The link between Neuroleptic Malignant Syndrome and Organophosphate Poisoning


The symptoms of NMS and OP are similar. In both NMS and OP the replication of symptoms is due to autonomic instability and stems from disruption of the acetylcholine circuits and transmitters of the Autonomic Nervous System, involved with vital involuntary functions.


Autonomic Instability includes profuse sweating, high blood pressure, low blood pressure, respiratory distress, drooling, urinary or faecal incontinence, increased and

decreased heart rate.27

Chart Depicting the Symptom Similarities of NMS and OP



Neuroleptic Malignant Syndrome


Organophosphate Poisoning


Autonomic nervous system disturbance Autonomic Instability

Aggression, agitation and violence

Muscle rigidity Paralysis, Dystonia, Cranial nerve palsy and polyneuropathy                                                                                                                                                                   
Muscle breakdown Weak respiratory and limb muscles
Coma, alterations of consciousness Loss of consciousness
Confusion Dementia, psychosis, anxiety, depression
Fever Seizures


Refs 27 & 33

Conclusion: Organophosphates, Neuroleptics and Violence


Organophosphate Poisoning results in over stimulated acetylcholine neuro-circuits and systems. The action of neuroleptics is similar.  It is generally accepted that Organophosphate Poisoning results in behavioural changes including violence.


Despite research to show that neuroleptics are associated with disrupted acetylcholine, it is not yet generally accepted that neuroleptics are a potential cause of violence.


Antipsychotic/neuroleptic drugs have strong anti-cholinergic properties and long-term use causes behavioural changes, which replicate the same behavioural changes occurring in chronic Organophosphate Poisoning:  


“This adaptation (to psychiatric drugs – author input) replicates the effect of organophosphate poisoning whether by nerve gas, by insecticide, or by anti-Alzheimers pharmaceuticals by over stimulating acetylcholine circuits of the brain.”27  


Increased Prescribing of Neuroleptics


There has been a distinct increase in neuroleptic medications, prescribed as part of treatment for mental health issues.


In the UK between 1998 and 2010, Neuroleptic drug prescriptions increased by an average of 5.1% every year.37 Over twelve years, this is a total increase of 60%.


In England, the approximate number of neuroleptic and depot (injection) prescriptions used by outpatients:

2008 – 7.0 million

2009 – 7.3 million

2010 – 7.6 million

2011 – 7.9 million38


However, due to confidentiality, the data for the number of neuroleptic prescriptions in inpatient settings is not made available. So the actual total increase of neuroleptic prescriptions in the UK is unknown.


Increased Prescribing as a Risk for Increased Violence



As outlined above, neuroleptics are a possible cause of violence. With ever increased prescribing of neuroleptic medications, it is reasonable to expect an increased amount of violent behaviour amongst those with a severe mental health diagnosis.


Since neuroleptic prescriptions are increasing by 300,000 per year in the UK, it is hypothesized that the rise in violence for neuroleptic-treated patients will escalate, whether in the community or in acute wards, secure units, prisons or outpatient units.


Part 2. Neuroleptics and Pharmacogenetics


The second part of this document has the following structure:

  • Introduction to Pharmacogenetics regarding Neuroleptics
  • Pharmacogenetics and Ethnic Black Populations
  • Black Populations and Psychiatric Intensive Care Units
  • Black Populations, detention under the UK Mental Health Act and UK Community Treatment Orders
  •  Pharmacogenetics as an explanation for Black Over-representation in

Psychiatric Intensive Care Units, detentions within the UK Mental

Health Act and Community Treatment Orders


Introduction to Pharmacogenetics with regards to Neuroleptics


Pharmacogenetics is the science of how drugs are broken down and used – i.e. metabolised in the body, mainly in the liver, by the genetically diverse Cytochrome P450 (CYP450) enzyme system and other drug metabolising systems. There are many CYP450 variants that affect therapeutic efficacy and inefficacy of medications.


Extensive Metabolisers are efficient metabolisers, whereby side-effects do not build up. Poor Metabolisers are inefficient metabolisers that have no metabolising activity whatsoever; this means that drug toxicities do build up and cause side effects. Intermediate Metabolisers have approximately 50% drug metabolising capacity and produce lesser side-effects than Poor Metabolisers.39 Ultra Rapid Metabolisers/ Hyperinducers have higher than normal rates of drug metabolism; Those medications which are classified as prodrugs are inactive until metabolised in the body, therefore Ultra Rapid Metabolisers are at increased risk of drug-induced side effects due to increased exposure to prodrug active drug metabolites.40


Neuroleptic drugs are metabolised through CYP450 enzymes e.g.CYP450 1A2, 2D6 and 2C19. A single neuroleptic can necessitate a combination of CYP450 enzymes for metabolisation.

All SMI patients who are Poor and/or Intermediate Metabolisers of neuroleptics, and Ultra Metabolisers of neuroleptic prodrugs; e.g. paliperidone, the active metabolite of risperidone; will inevitably suffer neurological and behavioural changes due to toxicities incurred from the inability to metabolise neuroleptics efficiently. Polypharmacy compounds the toxicities.


CYP450 1A2 Metabolising Pathway and Neuroleptics

CYP450 1A2 enzyme pathway has many variants and metabolises olanzapine and haloperidol and is the major metabolising enzyme for clozapine.


CYP1A2*1C and *1D Poor Metabolisers have been associated with increased clozapine exposure and adverse reactions.41 CYP1A2*1K is also Poor Metaboliser genotype.42


In one study, Asian patients who were prescribed clozapine, experienced aggression and disruptive behaviour who, following clozapine discontinuation, had marked improvement.8 The genotype of the Asian patients in the study is unknown, however since 25% of Asians have CYP1A2*1C Poor Metaboliser genotype,43  it is possible these patients were either CYP1A2*1C, *1D or *1K or a combination of these Poor Metaboliser genotypes.


Additionally15-20% of Asians are Poor Metabolisers for CYP2C19 and 2% are Poor Metabolisers for CYP2D6.44CYP2C19 and CYP2D6 metabolise clozapine as well as CYP1A2; any of these combinations are possible and could have predisposed to disruptive behaviour.

CYP450 2D6 Metabolising Pathway and Neuroleptics


75% of all psychotropic drugs, including neuroleptics, are metabolised via CYP450 2D6.45 CYP450 2D6 is a highly variable enzyme with a significant percentage of the population being Poor, Intermediate or Ultra Metabolisers and is linked with a poor therapeutic response and adverse reactions.


Violence in relation with serotonin toxicity/akathisia has been linked with pharmacogenetic CYP450 2D6 drug metabolising variants.46


Pharmacogenetics and Ethnic Black Populations


Due to genetic variations there is higher incidence of Poor Metaboliser and Ultra Metaboliser status in Black populations, compared with White and Asian populations for the CYP 450 2D6 pathway. “The prevalence of poor metabolizers in Black populations has been estimated from 0 to 19%, compared with consistent reports of   poor metabolizer status in Caucasians (5–10%) and Asians (0–2%).”47


Recalling that 75% of neuroleptic medications are metabolised via CYP450 2D6, the following table shows the variation of metabolising ability in black ethnic populations for CYP450 2D6.



Poor Metabolisers

Ultra Metabolisers

South Africans






African – American







American Black






Ref 48


29% of Ethiopians and 2.4% of North African Americans are Ultra Metabolisers via CYP450 2D6 pathway.48 Furthermore, 10-20% of Africans are Poor Metabolisers and 5% are Ultra Metabolisers via CYP450 2C19.49


Many prescription medications can lead to “serious mental change.”50 Since black populations statistically have difficulty in metabolising general and psychotropic medications and cannabis via the CYP450 pathways, this factor could contribute to  BME groups living in the UK who are more likely to be diagnosed with a Mental Health problem and admitted to hospital.51



Psychiatric Intensive Care Units and Over-representation of Black Populations

In UK Psychiatric Intensive Care Units (PICU), there is clear over-representation of black ethnic patients.52 Another study showed fifty-five percent of PICU admissions came from ethnic minorities(compared with 25.6% of total hospital admissions and 20.9%of the local catchment area population aged between 16 and 65years).53

“TypicalPICU patients are male, younger, single, unemployed, sufferingfrom schizophrenia or mania, from a Black Caribbean or Africanbackground, legally detained, with a forensic history. The mostcommon reason for admission is for aggression management.”54


UK Mental Health Act Detentions and Over-representation of Black Populations

There is also a disproportionately large representation of Black Minority and Ethnic (BME) origin when considering those who are legally detained under the UK Mental Health Act.

The proportion of black and black British people legally detained rose by 9.7%, with a 9% rise in the number of Asian or Asian British and mixed-race people detained for treatment, compared to a 0.3% rise for the overall number of people detained from 2007/8 to 2008/9. This disparity grew and 53.9% of black/black British inpatients spent time compulsorily detained, as did almost half of mixed-race inpatients and over 40% of Asian/Asian British inpatients, compared with 31.8% of all psychiatric inpatients who spent some time detained during the year.55


UK Community Treatment Orders and Black Populations

Legal UK Community Treatment Orders are enforced when patients have received mental health ‘treatment’ i.e. neuroleptics and history of violence; BME Groups have more Community Treatment Orders than white populations.56

“There is a possible relationship for psychiatric in-patients between compulsory detention, disturbed behaviour, depot medication and being black, which is not satisfactorily explained by diagnosis alone.”57


The higher incidence of mental health problems in black populations is most likely due to the higher incidence of Poor, Intermediate and Ultra Metabolisers and the associated problems with metabolising medications.



Neuroleptics can be a cause of violence due to neurotransmitter disruption.


Violence must be considered not simply as an indication of how deeply schizophrenia /bipolar illness can worsen, but as an adverse effect of neuroleptic treatment.


People who are inefficient metabolisers are likely to suffer more severe adverse effects and become violent or aggressive.


BME populations have a higher incidence of inefficient metabolisers and as such a higher incidence of violence leading to PICU admissions and Mental Health Act detentions.


However whatever the nationality, when individuals are Poor and Intermediate Metabolisers and Ultra Rapid Metabolisers for prodrugs, the impact of neuroleptics in triggering akathisia, aggression or irritability can trigger violence indiscriminately.



There is a larger incidence of violence in people with a severe mental health diagnosis than in the general population. The severely mentally ill are invariably treated with neuroleptic medication which itself can be the cause of violence since neuroleptic medications disrupt neurotransmitter functions. This disruption of neurotransmitter functioning can precipitate violent behaviour. Withdrawal of neuroleptic medication – due again to the disruption of neurotransmitters – is also associated with violence.


Pharmacogenetics show that the some people are unable to metabolise neuroleptic medication and this inability can result in further disruption of neurotransmitter functioning with a likelihood of increased violence.

The inability to metabolise neuroleptic medication is particularly prevalent in BME populations. As a consequence this population experience more violence which is confirmed in practice by an over representation of BME individuals, both on Psychiatric Intensive Care Units (PICUs) where a common reason for admission is aggression, and the use of Mental Health Act detentions and Community Treatment Orders.


With the trend towards increased prescribing of neuroleptic medications, a level of increased violence can be anticipated for the future.


There is the possibility of ameliorating the presence of violence in the severely mentally ill by ensuring pharmacogenetics is more fully recognised as a significant factor, and that genotype testing is adopted in order to assess the ability of the individual to metabolise neuroleptic medication. Without this testing,

much of the violence in psychiatry can be laid at the door of  psychiatrists and the  pharmaceutical companies.



Ref 1 Fazel S, et al, (2009)


Ref 2 Birchwood et al. (2011)


Ref 3 Owen C. et al, (1998)


Ref 4


Ref 5 Crowner ML, et al (1990)


Ref 6  GB. Leong, M.D. and JA Silva, M.D. (2003)



Ref 7 John N. Herrera et al (1998)


Ref 8 KA.Mansour, C.Willan and J.Follansbee (2003)


Ref 9 Jeffrey W. Swanson et al, (2008)


Ref 10  Drug Monographs, Prescribing information and UK NICE Guidelines 2007 – 2012. 


Ref 11  Jerome L. Schulte, (1985)


Ref 12 D.G. Workman and D.G. Cunningham (1975) page 65


Ref 13 MIND


Ref 14 Theodore Van Putten, (1975)


Ref 15 Berman ME, Coccaro EF. Neurobiologic correlates of violence: relevance to

criminal responsibility.” Behav Sci Law. 1998 Summer;16(3):303-18. Review.  

Ref16 Jackson, Grace E. MD, Appendix D, Transcript of

            “What Doctors May Not Tell You About Psychiatric Drugs”           

Public Lecture, Centre for Community Mental Health UCE Birmingham June 2004


Ref 17 Jackson Grace E. (2005)  Rethinking Psychiatric Drugs: A Guide for Informed Consent.  Bloomington, IN: Author House.


Ref18 Reisner I, et al, (1996)


Ref 19 Mehlman P, et al (1990)


Ref 20 Brown GL & Linnoila MI (1990)


Ref 21 Muller JL et al (2004)


Ref 22 Odagaki (2009)


Ref 23 Breggin (2003/4)


Ref 24 Pert CB. Ph.D., (2001)


Ref 25 Naveed Iqbal, MD, et al, (2007)


Ref 26 Hall LM et al (1995)


Ref 27 Grace Jackson MD (2009) Drug Induced Dementia. A Perfect Crime Bloomington, IN: Author House.


Ref 28 Siegel A, Bhatt S. (2007)


Ref 29 Stefan M. Brudzynski, et al (1990)


Ref 30 Graeff FG. (1994)


Ref 31 Imperato A. et al, (1993) “Evidence that neuroleptics increase striatal acetylcholine release through stimulation of dopamine D1 receptors” 


Ref 32 Donald W. Black, Nancy C. Andreasen – Introductory Textbook of Psychiatry – (2011) 5th Edition p.544 American Psychiatric Publishing Inc.


Ref 33 Kasantikul D, Kanchanatawan B, (2006)


 Ref 34 Tanya C. Warwick, et al, (2008)


Ref 35 Davies et al, (2000)


Ref 36 Singh S, Sharma N. Neurological syndromes following organophosphate poisoning. Neurol India 2000;48:308.


Ref 37 Trends in prescriptions and costs of drugs for mental disorders in England, 1998–2010 Stephen Ilyas and Joanna Moncrieff (2012)


Ref 38 NHS The Information Centre for Health and Social Care  “Copyright © 2012, Re-used with the permission of the Health and Social Care Information Centre.


Ref 39 Genelex


Ref 40 Genelex


Ref 41 Clinical and Translational Science: Principles of Human Research by David Robertson and Gordon H. Williams Academic Press Inc; 1 edition (16 Jan 2009) Chapter 21 page 303


Ref 42 Aklillu et al, 2003 CYP1A2 allele nomenclature


Ref 43 Todesco et al (2003) 


Ref 44 Asian PM for 2D6 Cozza et al 2003 and Richelson 1997 in Clinical Manual of Geriatric Psychopharmacology  By Sandra A. Jacobson, Ronald W. Pies, Ira R. Katz  Publisher: American Psychiatric Press Inc.; 1 edition (30 Jan 2007) Page 44 & 45


Ref 45 Joan Arehart-Treichel (2005)


Ref 46 Lucire Y, Crotty C, (2011)


Ref 47 Bradford LD, Kirlin WG. (1998).

Ref 48 Benny K. Abraham, C. Adithan  (2001)


Ref 49 Genelex

Ref 50 APRIL, Adverse Psychiatric Reactions Information Link

Ref 51 Mental Health Foundation – Black and Minority Ethnic Communities


Ref 52 Stephen Pereira et al, (2006)


Ref 53 Anthony Feinstein  and Frank Holloway(2002)




Ref 54 Len Bower (2008)


Ref 55 Community Care For everyone in social care “Mental Health Act detentions rise sharply for BME groups”


Ref 56 National Mental Health Development Unit. BME Groups and Mental Health – Presentation and Evidence to the Centre for Social Justice Mental Health Review 18 October 2010.


Ref 57 Violence: The Short-Term Management of Disturbed/Violent Behaviour in Psychiatric In-patients and Emergency Departments Guideline, Appendix 1: Ethnicity review evidence tables. p.447














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?

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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.



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.

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.