The madness behind the bars:prisons as asylums

Goya.-El-caballo-raptor

Domenico Fargnoli

The public does not have the correct perception of the psychiatric emergency involving  Italy which has ties to a more general situation.

Writes Amanda Pustilnik (University of Maryland)

“Today, our largest psychiatric hospitals are prisons. (…) The state prisons spend about $ 5 billion to incarcerate inmates suffering from mental illness, who are not violent. According to the Justice Department 1.3 million individuals with mental illness are incarcerated in state prisons and federal compared with just 70,000 people assisted in psychiatric hospitals ”

Someone  will be put in jail just for mental symptoms and for disturbing public order and not because  he has committed criminal offenses. In July 2004, The House on Comitte Governement Reform has published a study which found that children are incarcerated in the U.S. (including seven years old ) with serious mental illness but not responsible for criminal conduct.

Compared to the Enlightenment ideals that inspired the U.S. Constitution the above situation is paradoxical for the disappearance of the fundamental distinction made by Pinel during the French Revolution: the mentally ill were separated by criminals and freed from the chains. Thus was born a new branch of medicine, psychiatry.

At a distance of more than two centuries we see a reversal of the trend and a  return to confusion between crime and insanity,  to prevalence of the logic of segregation and punishment. The return to   old guidelines is due to the social significance that has taken the disease conceived as a guilty  failure, a lack of control and  sense of personal responsibility. It ‘s the old Christian idea of ​​madness as demonic influence, such as complicity with evil, which reappears in a secularized form.image_sabba_quadro_di_goya

From the religious mentality comes the punitive approach that has prevailed in the U.S., to mental illness. The punishment should reinforce adherence to ‘ethics on which is founded the society and to ensure, by the severity of a penalty, respect for the rules. For the punitive moralistic conception people with mental illness have defects of  will or character that make them incapable of controlling: impose restrictive criteria would help to achieve acceptable behavior and increase the sense of responsibility.

The judge replaces the psychiatrist because the latter considering diseases “disturbs” or questionable diagnostic conventions, cannot give certain criteria of  not imputability. Therefore being mentally “ill” usually does not guarantee, in the U.S., the impunity with respect to violent crimes.

In Europe Anders Breivik was declared sane with DSMIV diagnostic criteria in a trial in which there has been  the tendency to punishment rather than care.

And in Italy? The case of Erika and Omar in Novi Ligure, of Franzoni in Cogne or  killers spouses in  Erba were dominated by a punitive logic unrelated to psychiatry.

Why are we in front of this trend?

Prof. Amanda C. Pustilink does not clarify the essential point that the role played by psychiatric institutions in allowing the moralistic-punitive model of mental illness is affirmed: one hundred years of Freudianism in America have left their mark. Just in the U.S., however, medias  reported the failure of psychoanalysis and  biological psychiatry , successor to Freudianism, prepares for a resounding “disaster”, due to the lack of science, with the new edition of DSMV in May 2013.

American doctors are committed to delivering drugs to a ever-growing population of ‘normal’subjects, using diagnoses that seem ad hoc to further the interests of pharmaceutical companies. The most serious cases are subjected to therapies such as iloperidone taken by Adam Lanza, author of the massacre of Newport, which can amplify the tendency to violence. The prisons act as containers for all sorts of mental illnesses that, in a regime of unprecedented violence and perversion, suffer an aggravation. The effects are devastating on the individual and on society. In Italy, the birthplace of Cesare Beccaria who wanted the penalty rationally commensurate to the crime and was against torture, we are experiencing something similar to what happens in the U.S: the operational  diagnostic models, the abuse of drugs, the use of ECT, damages the credibility of psychiatry and promotes the success of the moralistic model of mental illness. Since doctors are incapable of preventing and treating mental illness management is the responsibility of the latter, the judges and the courts. The law Orsini-Basaglia drained of the asylums about one hundred thousand patients in recent decades, but at the same time, it  filled in a unlikely manner prisons.

There’s an psychiatric emergency within the prisons : according to an epidemiological survey of the Regional Agency of Health prisoners with “psychiatric disorders” are 1137, 33.4% in Tuscany alone. The prison works as a container for mental illness, which is not treated in the circuit of mental health services. With the closure of the asylums were not always created alternative structures so many people are left without control or safety net and ended up in the net of justice. Prisons are infernal. Take over the idea of ​​ruin, the emotional void, humiliation and the ‘marginalization. The psychopathological forms are structured in chronic diseases, difficult to treat. Sexual identity in a context of violence and forced overcrowding, often undergoes a irreversible deconstruction.

Suicide is a dramatic and the frequency, even more than twenty times the norm, is directly related to overcrowding and abuse. How to deal with this situation? On March 31, following the law Marino is expected to close the OPG: the  event has a strong symbolic meaning even if people interested are 1400, out of a total of 66,721 Italian prisoners. The OPG have been the emblem of institutional schizophrenia: individuals with total or partial defect of the mind were subjected to a prison regime in unimaginable poor conditions Not to mention the psychological and physical torture.It is  ‘necessary that  the closure of OPG may be an opportunity not only to propose alternative structures for intervention but an afterthought of psychiatry as a whole. Andrea Zampi, the murderer-suicide  in Perugia was submitted last year in Pisa two cycles of 8 TEC: a “therapeutic intervention ” or a practice without any scientific basis that has aggravated the patient’s condition? Today, psychiatrists do not have the necessary expertise to deal with psychosis with the method of psychotherapy: the drug or the ETC are ineffective and dangerous in the long run. Psychiatry must then make a cultural leap and methodological equipping of new scientific and educational criteria. The experience of ‘Collective Analysis which belongs to the theory of the birth of Massimo Fagioli, is a pilot, almost forty years of care, training and research unique attended by thousands of people and hundreds of psychiatrists, committed to deepening the understanding of psychic reality beyond the  biological reductionism and the morality of reason and religion. Pannitteri Adriana writes in “La pazzia dimenticata ” (L’asino d’oro 2013) ”

<< (…) Mental illness can not be solved simply by throwing down the walls of asylums, but in a more solid  way trying to find out what’s inside the psyche of those who are sick >>

Psicofarmaci e violenza

violenzaNeuroleptic Drugs and Violence

 

Catherine Clarke SRN, SCM, MSSCH, MBChA.

and Jan Evans MCSP. Grad Dip Phys.

August 19th, 2012

Introduction

 

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

 

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

Clozaril

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
Suicidality

Violence

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

 

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

Aggression
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

18.8%

Nigerians

8.6-8.3%

Ghanaians

6%

African – American

3.9%

2.4%

Zimbabwean

2%

Tanzanian

2%

American Black

1.9%

Ethiopians

1.8%

29%

 

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.

 

Synopsis

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.

 

Conclusion

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.

References:

 

Ref 1 Fazel S, et al, (2009) http://www.ncbi.nlm.nih.gov/pubmed/19454640

 

Ref 2 Birchwood et al. (2011)

http://www.biomedcentral.com/1471-244X/11/155/

 

Ref 3 Owen C. et al, (1998) http://ps.psychiatryonline.org/article.aspx?Volume=49&page=1452&journalID=18

 

Ref 4 http://www.nice.org.uk/nicemedia/live/10964/29715/29715.pdf

 

Ref 5 Crowner ML, et al (1990) http://www.ncbi.nlm.nih.gov/pubmed/1973544

 

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

http://library-resources.cqu.edu.au/JFS/PDF/vol_48/iss_1/JFS2002173_481.pdf

 

 

Ref 7 John N. Herrera et al (1998)

http://psychrights.org/research/Digest/NLPs/RWhitakerAffidavit/HerreraNeurolepticsandViolence.PDF

 

Ref 8 KA.Mansour, C.Willan and J.Follansbee (2003)  http://bapauk.com/doc/Deteriorationofpsychosisinducedbyclozapine_41.doc

 

Ref 9 Jeffrey W. Swanson et al, (2008) http://bjp.rcpsych.org/content/193/1/37.full

 

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

 

Ref 11  Jerome L. Schulte, (1985) http://psychrights.org/research/Digest/NLPs/RWhitakerAffidavit/Schulte.PDF

 

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

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2274756/pdf/canfamphys00332-0065.pdf

 

Ref 13 MIND  http://www.mind.org.uk/help/medical_and_alternative_care/making_sense_of_coming_off_psychiatric_drugs

 

Ref 14 Theodore Van Putten, (1975)

http://psychrights.org/research/Digest/NLPs/RWhitakerAffidavit/VanPuttenManyFacesofAkathisia.PDF

 

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

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

http://www.ncbi.nlm.nih.gov/pubmed/9768463  

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) http://www.ncbi.nlm.nih.gov/pubmed/8861609

 

Ref 19 Mehlman P, et al (1990) http://www.ncbi.nlm.nih.gov/pubmed/7522411

 

Ref 20 Brown GL & Linnoila MI (1990) http://www.ncbi.nlm.nih.gov/pubmed/1691169

 

Ref 21 Muller JL et al (2004) http://www.ncbi.nlm.nih.gov/pubmed/15570500

 

Ref 22 Odagaki (2009) http://www.benthamscience.com/cds/samples/cds4-1/0013CDS.pdf

 

Ref 23 Breggin (2003/4) http://www.breggin.com/31-49.pdf

 

Ref 24 Pert CB. Ph.D., (2001) http://ecommerce.drugawareness.org/Ribbon/SSRIMeds.html

 

Ref 25 Naveed Iqbal, MD, et al, (2007) http://www.cnsspectrums.com/aspx/articledetail.aspx?articleid=1262

 

Ref 26 Hall LM et al (1995) http://www.ncbi.nlm.nih.gov/pubmed/7543647

 

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

 

Ref 28 Siegel A, Bhatt S. (2007) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2435345/

 

Ref 29 Stefan M. Brudzynski, et al (1990) http://www.ncbi.nlm.nih.gov/pubmed/2293258

 

Ref 30 Graeff FG. (1994) http://www.ncbi.nlm.nih.gov/pubmed/7916235

 

Ref 31 Imperato A. et al, (1993) “Evidence that neuroleptics increase striatal acetylcholine release through stimulation of dopamine D1 receptors” http://jpet.aspetjournals.org/content/266/2/557.abstract 

 

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)  http://www.ncbi.nlm.nih.gov/pubmed/17214072

 

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

http://www.nature.com/nrneurol/journal/v4/n3/full/ncpneuro0728.html

 

Ref 35 Davies et al, (2000) http://www.national-toxic-encephalopathy-foundation.org/oppest.pdf

 

Ref 36 Singh S, Sharma N. Neurological syndromes following organophosphate poisoning. Neurol India 2000;48:308. http://www.neurologyindia.com/text.asp?2000/48/4/308/1510

 

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

http://bjp.rcpsych.org/content/early/2012/03/10/bjp.bp.111.104257.abstract

 

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.     www.ic.nhs.uk

 

Ref 39 Genelex http://www.healthanddna.com/healthcare-professional/dosing-recommendations.html

 

Ref 40 Genelex http://www.healthanddna.com/healthcare-professional/p450-2d6-genotyping.html

 

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 http://www.imm.ki.se/CYPalleles/cyp1a2.htm

 

Ref 43 Todesco et al (2003) http://www.ncbi.nlm.nih.gov/pubmed/12851801 

 

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)

http://pnhw.psychiatryonline.org/content/40/10/33.1.full

 

Ref 46 Lucire Y, Crotty C, (2011)

http://www.dovepress.com/articles.php?article_id=7993

 

Ref 47 Bradford LD, Kirlin WG. (1998).  http://www.ncbi.nlm.nih.gov/pubmed/11281961

Ref 48 Benny K. Abraham, C. Adithan  (2001)  http://medind.nic.in/ibi/t01/i3/ibit01i3p147.pdf

 

Ref 49 Genelex http://www.healthanddna.com/healthcare-professional/p450-2c19-genotyping.html

Ref 50 APRIL, Adverse Psychiatric Reactions Information Link http://www.april.org.uk/main/index.php?uid=269

Ref 51 Mental Health Foundation – Black and Minority Ethnic Communities 

http://www.mentalhealth.org.uk/help-information/mental-health-a-z/B/BME-communities/

 

Ref 52 Stephen Pereira et al, (2006) 

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=651260

 

Ref 53 Anthony Feinstein  and Frank Holloway(2002)

http://isp.sagepub.com/content/48/1/38.short

 

 

 

Ref 54 Len Bower (2008)

http://www.kcl.ac.uk/iop/depts/hspr/research/ciemh/mhn/projects/litreview/LitRevPICU.pdf

 

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

http://www.communitycare.co.uk/Articles/25/11/2009/113253/mental-health-act-detentions-rise-sharply-for-bme-groups.htm

 

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. www.nmhdu.org.uk/silo/files/bme-groups-and-mental-health-.doc

 

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 http://www.rcn.org.uk/__data/assets/pdf_file/0003/109812/003017_appendices.pdf

 

 

 

 

 

 

 

 

 

 

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.

S

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.

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.