Neuroleptic Physical

Adverse Drug Reactions

1
 Contents:
Neuroleptics and Antipsychotics………………………...……….……………………………………...…………....…4
Neuroleptic Adverse Drug Reactions and Pharmacogenetics…………………..….…5
Neuroleptics and Neurotransmitters…………………………………………………………..………...……………7
Neuroleptic Iatrogenic Adverse Reactions:
Body Movement Disorders.….…………………………………………..………….…………………..…. …………..…9
Tardive Dyskinesia….…………………………………………………………....………….………..…….……..……………..10
Parkinsonism…………………………………..……………………………………………..………………………….…….…….….13
Tardive Dystonia……..…………………………………...….…………………………………………………………....….…….15
Oculogyric Crisis…………………………………………………………...………………………………………………………16
Akathesia………………………………………………………...………………………………………….…………………..…….….…19
Endocrine Disorders…………………………………………………………………………………………..………………………21
Metabolic Syndrome……………………..…………………………………………………………..…………………….……22
Sexual Dysfunction Male or Female…………………………………………...…………………….....………23
Osteoporosis……………………………..……….…………………………………………………………………………..…..….…..25
Disruption of Thyroid…..……………………………………………………..…………..….…………………..……....……26

2
 Contents continued…

Cerebro-Vascular and Cardiac Disease …………………………………………….…………………….….27

Neuroleptic Malignant Syndrome.………………………………………………….…………..…...………….……29
Temperature Dysregulation.………………………………………………………………………………………….……...31
Respiratory Disease………………………………………………………………………………………………………...…………32
Agranolocytosis…………………………………………………………………………………………………………...…………….....33
Neuro-degenerative Brain Changes…………………………………………..……….……………….…….…….34
Additional Neuroleptic Iatrogenic Adverse Reactions…………………………..…….…...37
Sudden Unexplained Deaths……………………………..….…………………………………………………………..…39
Tardive Tourettism………………………………………………………………………………………………………………….…43
Conclusion……………………………………………….……………………………………………………………………………..….….…44
Ethics…………………………………………………………………………………………………………….………………….……………….…45
Successful non Neuroleptic Treatments…………………………………...………….…….…………….….46
References………………………………………………………………………………………………………..……………………………....47

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 Neuroleptics and Antipsychotics
The terms ‘antipsychotic’ and ‘neuroleptic’ are used interchangeably in
research papers, although in clinical guidelines and practice, ‘antipsychotic’ is
the most frequently used.
Prior to these terms these medications were known as ‘Major Tranquillisers’.
The term ‘neuroleptic’ was accepted in 1955 and eventually became known as
‘antipsychotic’ by drug companies who used it as a marketing ploy to
influence doctors and patients to believe that the drug’s specific action was to
treat and prevent psychosis. However this ploy puts considerable distance from
numerous other ‘antipsychotic’ actions and the hard reality of what the drug
does to the brain.
Neuroleptic literally means to ‘seize the nerve’, a chilling scenario. For this
reason, throughout this document the word ‘Neuroleptic’ will be used in place
of ‘Antipsychotic.’

4
Neuroleptic Adverse Drug Reactions and Pharmacogenetics

Neuroleptic ADR are caused by the way the drugs act on neurons and
neurotransmitters in the brain and body and are therefore
IATROGENIC. i.e. neuroleptic induced.
ADR are influenced by the genetically predetermined rate of
metabolism known as Pharmacogenetics. When people have the in-
born slower rates of metabolism i.e. Poor Metaboliser or an
Intermediate Metaboliser Genotype profiles, neuro-toxicity increases
which is associated with the severity of ADR. 1, 2

All people who take neuroleptics will be affected by various ADRs,

either within a short or longer period of time.
60% of patients experience severe/very severe side effects.3

5
 Adverse Drug Reactions and Side Effects

In both patient and professional literature, to explain the ‘undesired

effects of medication’, pharmaceutical companies commonly use the
term ‘side effects’. Because the term both minimises and obscures the
cause of ‘side effects’, the term is replaced by Adverse Drug Reactions
(ADRs) in this document.

Many neuroleptic physical ADRs are not found in mainstream literature.

In order to readdress this situation, this document provides up to date
and concise ADR information for mental health and social care
practitioners.

6
 Neuroleptics and Neurotransmitters

It is well known that neuroleptic medication depletes dopamine by

disrupting the dopamine neurotransmitters in the brain.
What is not so well known is that atypical neuroleptic medication disrupts
other neurotransmitters such as serotonin, adrenaline, noradrenaline and
acetylcholine, that play an important role in the maintenance of all body
systems.
It is the balance between all of the neurotransmitters that is important and
this balance is in constant flux to maintain long term stability. If the level
of one neurotransmitter is artificially raised or lowered by medication, all
other neurotransmitters are relatively affected and stability is lost.
Unnatural interference with neurotransmitters by neuroleptics causes
deterioration of physical health and leads to various iatrogenic illnesses.

7
 Physical Functions of Dopamine
Dopamine as a neurotransmitter:
 Co-ordination of voluntary and involuntary movements and
muscular strength.
 Participates in thermoregulation and regulates metabolism.
 Enables the natural regulation of fat and sugar, sleep patterns,
control of hunger, thirst, fatigue, and circadian cycles.

Dopamine as an endocrine neurohormone:

 Participates in the regulation of blood pressure, heart rate, cardiac
output, fluid and sodium balance, gastric motility, lactation, fertility,
and bone strength.4
 Enables the flight and fight responses in the face of danger.5

8
 Introduction to Body Movement Disorders
The Extra Pyramidal System in the brain controls normal body movements
with dopamine playing an important role. Neuroleptics reduce dopamine
causing excessive abnormal body movements.
Neuroleptic Induced Extra Pyramidal Symptoms (EPS):
 Tardive Dyskinesia
 Parkinsonism
 Tardive Dystonia
 Oculogyric Crisis
 Akathesia
These iatrogenic conditions result from adverse structural brain changes.6,7 & 8

Adverse neuroleptic reactions can be due to people's inability to metabolise

psychiatric medication when they have Poor Metaboliser Genotype Enzymes.1

9
 Tardive Dyskinesia (TD)

In 1959 TD was first reported to be linked to neuroleptics.9

TD is due to neuroleptic induced Target Organ Toxicity causing

irreversible damage to the brain cells. TD can appear within 6 months,
is caused by both typical and atypical drugs and the risk increases with
chronic long-term exposure.10, 11, 12

Memory impairment is associated with patients with high TD scores.13

5-HT2C serotonin receptor gene variants are associated with Tardive

Dyskinesia, depending on age, duration of treatment, dose and sex.14

10
 Tardive Dyskinesia (TD)

TD symptoms are disfiguring and include:

 Chewing movements of lower jaw.
 Lip sucking and smacking.
 Blowing in and out and bulging of cheeks.
 Facial grimacing.
 Abnormal tongue movements i.e. the tongue quivers – protrudes.
 Finger movements as though an invisible guitar is played.
 Rocking and swaying of the body.

Body actions are involuntary, potentially irreversible and there is no

proven treatment.

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 Less Well Known Tardive Dyskinesia Symptoms

There are many other "lesser" appreciated symptoms of TD:

 Restless legs (especially at night)
 Poor sleep
 Loss of gag reflex/swallow – can lead to pneumonia
 Unstable blood pressure and heart rate due to autonomic dysfunction.
 Pain syndrome i.e. tardive pain
 Depression.
 Psychosis as the condition progresses.
 Dementia

All the above ‘lesser known symptoms’ are all possible (if not likely) in
Tardive syndromes, largely because of neuroleptic drug treatments, and will be
found if doctors take the time to "think" and ask questions carefully.
(G. E. Jackson MD, Personal Communication)

12
 Parkinsonism

Neuroleptic Induced Extra Pyramidal Symptoms (EPS) manifest in the

same way as they do in Parkinson’s Disease:
 Tremor, ranging from being almost imperceptible to incessant
shaking.
 Hypersalivation: excessive salivation
 Bradykinesia: slowing down of large muscle movement
 Shuffling gait
 Reduced emotional expression
 Rigid stiff muscles

When anti-cholinergic medications are prescribed to alleviate EPS,

patients are then exposed to additional ADRs.

13
 Anti-Cholinergic Adverse Drug Reactions

The role of the Peripheral Nervous System is to connect the Central

Nervous System (brain & spinal cord) to the limbs and organs.

Anticholinergic medications disrupt the Peripheral Nervous System

causing the following ADRs:
Blurred vision Urine retention and Bladder distension
Dry eyes Constipation
Dry mouth Headaches
Increased heart rate Nasal congestion15
Nausea & vomiting16

Anticholinergic (antimuscarinic) medications increase brain damage associated

with cognitive impairment and worsen Tardive Dyskinesia.16, 17

14
 Tardive Dystonia

Dystonia is characterised by involuntary twisting and repetitive

movements, or abnormal postures18, 19, 20 due to dysfunction or over-
activity, in the brain structures that control movement.

These sustained and disfiguring painful muscle spasms include:

 Torticollis- head and neck are twisted to one side
 Retrocollis - head and neck are pulled back between the shoulder
blades
 Blepharospasm - eyelids are forcefully squeezed shut.
 Excessive arching of the back.

15
 Oculogyric Crisis

Oculogyric Crisis is an acute dystonic reaction to certain drugs

including neuroleptics, such as Olanzapine,21, 22 Risperidone, 23
Amisulpiride24 and Clozapine.25

In addition to the acute presentation, it can develop as a recurrent

syndrome.26, 27, 28

Characteristics include rotating of the eyeballs with extreme and

sustained upward deviation accompanied by ocular pain. The eyes
may converge, deviate upward and laterally, or downward.27, 28

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 Associated Dystonic Symptoms with Oculogyric Crisis

Some of these are similar to the symptoms described in Tardive

Dyskinesia, Parkinsonism and Tardive Dystonia as there is a degree of
overlap.

Blepharospasm Respiratory dyskinesia

Periorbital twitches Backwards and lateral flexion of neck
Protracted staring episodes Widely opened mouth
Eye blinking Tongue protrusion
Lacrimation Intensely painful jaw spasm which
Drooling may result in breaking a tooth
Refs 27, 28

17
 Associated Psychiatric Symptoms with Oculogyric Crisis
The clinical spectrum of Oculogyric Crisis is poorly understood, leading to the
frequent mislabel of a psychogenic disorder.27
Vertigo Paranoia Mutism
Anxiety Depression Palilalia
Agitation Recurrent fixed ideas Violence
Compulsive thinking Depersonalization Obscene language
Refs 27, 28

“A wave of exhaustion follows some episodes. The abrupt termination of the

psychiatric symptoms at the conclusion of the crisis is most striking.” 27, 28, 29
Other Symptoms Associated with Oculogyric Crisis
Increased blood pressure & heart rate Facial flushing
Pupil dilation Headache
Refs 27, 28

18
 Akathesia

Neuroleptic induced symptoms of Akathesia are characterized by

unpleasant sensations of inner restlessness that manifest with a
physical inability to sit still or to remain motionless.

Patients have described the feeling as a sense of inner tension and

torment.

Because of the severe negative psychological effects associated

akathesia, it is described in greater detail in:
‘Neuroleptic Psychological Adverse Reactions’30

19
 Conclusion to Body Movement Disorders

Tardive Dyskinesia
Tardive Dystonia
Oculgyric Crisis
Akathesia
Extra Pyramidal Symptoms
- are frequent combinations that make patients look ‘odd’, making
them extremely vulnerable in the public environment.

Abnormal body moments such as TD present an obvious stigma of

'madness' and constitute a severe social handicap ... by causing
embarrassment to the family and friends and apprehension on the part of
the potential employers.31

20
Endocrine Disorders Caused by Neuroleptic Dopamine
Disruption

Metabolic Syndrome
Sexual Dysfunctions
Osteoporosis
Thyroid Disorders

These conditions have a follow on effect causing:

Cerebro Vascular and Cardiac Disease

21
 “Metabolic Syndrome”
Symptoms:
 Cortisolaemia i.e. obesity with excessive abdominal fat
 Diabetes type-2
 Hyperlipidemia i.e. Lipid abnormalities or High Cholesterol
 Hypertension or High Blood Pressure
 Insulin resistant Diabetes.32
Some neuroleptics interfere with appetite regulation networks in the brain
resulting in excessive appetite and massive weight gain associated with
diabetes and heart disease.33
5-HTT (serotonin transporter) and 5-HT2A (serotonin receptor) gene variants
are associated with obesity and tryptophan hydroxylase 2, (TPH2) gene
variants are found to be associated with diabetes.14
The occurrence of metabolic syndrome with typical and atypical neuroleptics is 2-
4 times higher than in people who are not prescribed neuroleptics.34

22
 Sexual Dysfunction Male and Female

Dopamine as a neurohormone acts as a natural brake by inhibiting

excess production of prolactin hormone that is involved in normal
sexual functions i.e. lactation and sexual gratification.35

Dopamine depletion by neuroleptics removes the brake causing

high levels of prolactin hormone, a condition known as
Hyperprolactemia. This condition creates many sexual
dysfunctions.36, 37, 38

23
 Sexual Dysfunction Male and Female
Symptoms of Hyperprolactemia:
MALE FEMALE
Gynecomastia: enlarged breast Galactorrhoea: production and
tissue secretion of breast milk
Galactorrhoea: production and Amenorrhoea: irregular or
secretion of breast milk absent menstruation
Retrograde Ejaculation Loss of Libido
Loss of Libido Anorgasmia
Sterility or damaged sperm DNA Infertility
Erectile dysfunction Birth defects due to damaged
DNA/sperm
Testicular atrophy
Refs 36, 37, 38

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 Osteoporosis
Osteoporosis is associated with neuroleptic induced
Hyperprolactemia.39, 40

Osteoporosis aetiology:
 Long term prolactin-raising neuroleptics pose a high risk of bone
density reduction36
 Reduced bone density in neurolepticized males39
 Risk factor for osteoporosis in young women40

Osteoporosis symptoms:
 Bone pain
 Vulnerability to fractures

25
 Neuroleptic Disruption of Thyroid Production
The thyroid is an endocrine organ and it’s function will inevitably be
disrupted in both the short and long term by neuroleptic drugs in a
similar way to other endocrine disorders caused by neuroleptic
interference.
Limited research indicates thyroid dysfunction is relatively common in
patients with schizophrenia41 and long-term neuroleptic treatment can
induce thyroid autoimmunity associated with hyperprolactinaemia.38
Serum levels of T4 (Thyroxine) have been found to decline after
treatment with neuroleptics, and other psychiatric drugs.42
Both Hyperthyroidism and Hypothyroidism can mimic psychiatric
symptoms which may lead to misdiagnosis with the potential to incur
neuroleptic prescribing.

26
 Cerebro-Vascular Disease
The neuroleptic impact on the endocrine system increases the risk of
microvascular and macrovascular disease,8 causing the following cerbro-
vascular conditions.

Symptoms:
 Hyperlipidemia (High Cholesterol)
 Cerebral Vascular Accidents i.e. Stroke
 Cardiac Rhythm abnormalities
 Heart Failure
 Myocardial Infarction (heart attack)
 Cardiac Death43
 Deep Vein Thrombosis
 Pulmonary Embolus - potentially fatal
 Vascular Dementia

27
 Neuroleptic Cardiotoxicity
Animal studies have demonstrated the cardiotoxic effects of neuroleptic
drugs.44
Neuroleptic drug resulted in cardiac lesions of variable magnitude in
animals, with changes that include thickening of blood vessels, damage
to cardiac muscle fibres, such as disintegration, swelling, fibrotic
scarring45 and cell death (necrosis).46
Based on their discoveries, the authors recommended that patients
receive an ECG (electrocardiogram) and cardiac ultrasound
(echocardiogram) PRIOR to beginning any antipsychotic drug therapy.46
These tests will not prevent the development of neuroleptic
cardiotoxicity.

28
 Neuroleptic Malignant Syndrome (NMS)

This condition is similar to a viral infection of the brain i.e.

Encephalitis.
NMS results from the dysregulation of the sympathetic nervous system47
which is part of the autonomic nervous system, and is vital for the
stability of life functions.

NMS is associated with:

 All neuroleptics, typical and atypical.48, 49
 Rapid and large increases in neuroleptic dose
 Conjunction with other neuroleptics (polypharmacy).

29
 Neuroleptic Malignant Syndrome (NMS)
Clinical Symptoms of NMS:
Hyperpyrexia Generalised muscle rigidity
Altered mental status Sweating
Hypertension Seizures
Hypotension Cardiac arrhythmia
Tachycardia Renal failure
Tremor Respiratory failure
Incontinence Sialorrhea (drooling)
Muscle weakness Dysarthria (speech difficulty)

Mortality rates for NMS, once reported at 20-30% are now estimated at 5-
11.6%. Incidence is probably less now than in the past because of increased
awareness of NMS and efforts at prevention.49

30
 Temperature Dysregulation

Neuroleptics disable thermoregulatory mechanisms50 causing

temperature dysregulation i.e. Hypothermia and Hyperthermia.

Neuroleptics most commonly cause hyperthermia51 although they can

also cause hypothermia. This highlights the complexity of the
temperature regulation system.48

The disruption of normal acetylcholine transmission by neuroleptics

causes Hyperthermia i.e. reduced sweating.

During heat waves, neuroleptic medications increase patients' risk of

death from heat stroke, two fold compared to the general population.52

31
 Respiratory Disease

Dopamine plays a key role in the regulation of the brain’s

respiratory/breathing centre and clearance of excess lung mucous. OK

Neuroleptic dopamine depletion causes:

 Respiratory Dyskinesia - difficulty in breathing.53
 Respiratory Arrest
 Impaired clearance of excessive lung mucous.4
 Impaired recovery from pulmonary oedema due to cardiac disease.4
 Choking and aspiration.53
 Excess mortality among in-patients.54
 Deaths from respiratory disorders gave rise to the highest relative risk
after accidental deaths.54

32
 Agranolocytosis
Clozapine can cause Agranulocytosis which is a blood disorder in which the
total white blood cell (WBC) count falls to a dangerous level. Blood tests are
taken prior to initial prescribing to ascertain the WBC is normal.
In order to prevent fatalities from Agranulocytosis, mandatory blood tests are
taken through out Clozapine prescribing at various time intervals. WBC can
drop spontaneously or due to bacterial infections; patients have to stop
Clozapine immediately, causing emergency hospital admission and change of
neuroleptic medication. Specific antibiotic medications have to be used as
some antibiotics further decrease one type of WBC.
Blood monitoring may prevent neurolepticised people from dying from
agranulocytosis, but it does not prevent iatrogenic blood dyscrasia.
Clozapine has been linked to 950 deaths since being licensed in 1990 —
equivalent to nearly one fatality a week.55

33
 Neuro-degenerative Brain Changes
The book “Drug induced Dementia: A Perfect Crime” presents a
methodical analysis of the scientific and epidemiological evidence
which confirms psychopharmaceuticals as a cause of brain damage and
premature death.8
The Jellinger Study, 1977. Human Autopsies56
46% of patients exposed to neuroleptics displayed prominent injury to
the caudate nucleus, compared with 4% of psychotic patients who had
avoided neuroleptic drugs. The caudate nucleus plays a key role in the
modulation of movement, cognition, and mood.
The brain cell changes showed the brain’s response to chemical injury;
cell death (necrosis), disintegration and inflammation, also found in
systemic lupus patients and Parkinson’s Disease.8

34
 Neuroleptics and Progressive Brain Damage

There are 25 medical articles on brain damage associated with

neuroleptic drug treatment compiled by the late psychiatrist Loren
Mosher, MD.57

Researchers in Denmark found a dose dependent association with brain

shrinkage, estimating the risk of atrophy to be 6.4% for each additional
10 grams of chlorpromazine, or other neuroleptic in terms of equivalent
dose.7, 8

35
 Brain Damage Associated with Poor Outcomes

Neuroimaging Studies of Humans:

Following one year of neuroleptic therapy, patients demonstrated an 8%
increase in lateral ventricle volume, a 1% reduction in total brain
volume, and a 3% reduction in whole brain grey matter.

These brain changes were significant statistically, being clinically

related to poor outcomes in terms of psychotic symptoms, physical
health, social intimacy, and independence. The grey matter changes
corresponded to cumulative neuroleptic dose.8, 30, 58

36
 Additional Neuroleptic Iatrogenic Adverse Reactions

Liver malfunction:
Atypical antipsychotics commonly cause symptomless increase in
aminotransferase liver enzyme levels. Elevated transaminases, which
can be an indicator of liver damage59 have been reported with
olanzapine.60

Kidney failure:
Acute renal failure induced by neuroleptics. 61

Constipation:
Bowel obstructions.62, 63

37
 Additional Neuroleptic Iatrogenic Adverse Reactions

Muscular Weakness:
Loss of muscle power is associated with high neuroleptic dose, in
conjunction with polypharmacy and NMS.64

Sunburn:
Photosensitivity occurs with atypical neuroleptics, i.e. Amisulpride65 and
Clozapine.66 Patients are more prone to increased Sun Sensitivity when
polypharmacy is practised.

Ocular Changes:
Cataracts can occur with Neuroleptics.67

38
 Sudden ‘Unexplained’ Deaths

Many reports are available of sudden deaths of patients who were

medicated with high dosages of neuroleptics. 68, 69,70

Cardiovascular causes of death are most common, accounting for the

majority of sudden and unexpected deaths, thought to result from fatal
arrhythmias. Some neuroleptics prolong the cardiac QTC interval even
at therapeutic doses.71

The risk of sudden cardiac death is elevated at low doses, even among
patients who receive neuroleptic drugs for non-schizophrenic
conditions.4, 72

39
 Sudden ‘Unexplained’ Deaths cont…
 The death of Orville Blackwood in 1991 from heart failure, resulted
from being injected with a cocktail of Promazine and Fluphenazine.73
 In 1990, there were thirteen sudden deaths of patients who were
medicated with Pimozide in the UK.74
 20 people died whilst taking Olanzapine out of 2,500.75
 In 2009 sudden unexplained deaths of psychiatric in-patients were at an
eight year high.76
In England the increase in rates of Sudden Unexplained Deaths is significant.
8.8% per year overall, 7.6% in men and 10.4% in women.77
"We know therefore that the mortality rate among people who are in contact
with specialist mental health services is nearly four times that for the general
population.”78
As more people are diagnosed and treated with neuroleptics, the number of
patient mortalities has increased.79

40
 Conditions Contributing to Premature Death

“When key regions of the brain are destroyed, numerous life-sustaining

functions are affected.” (G. E. Jackson M. D. Personal Communication)

Metabolic Syndrome Hyperthermia – Heat Stroke

Hyperprolactemia Hypothermia
Cardiac Conditions Kidney Failure
NMS Bowel Obstruction
Parkinsonism Cerebro-vascular disease
Respiratory conditions Tardive Dyskinesia & Dystonia

All these conditions leading to premature death result from unnatural

medication interference with the natural life-sustaining functions of the
brain.

41
Premature Death, Parkinsonism and Tardive Conditions
“Parkinson's disease and Tardive Dyskinesia (TD) both contribute to
premature death. The reason for this is that both conditions reflect brain
damage.” (Source G. E. Jackson M. D. Personal Communication)
In a cohort of 608 Asian patients diagnosed with schizophrenia…,
Risk of death was 2.6 times higher among those with TD.80
Sample of 200 patients receiving neuroleptics was assessed in 1995.
Deceased patients had higher average scores for Parkinson syndrome
than those who survived.81
10-year mortality rate among patients with TD.
TD was significantly associated with increase in mortality.82
41% of TD patients died within 10 years vs. 20% of those without TD.83

42
 Tardive Tourettism
Tardive Tourettism has the same symptoms of Tourette’s Syndrome and is
caused by neuroleptics.84, 85

Tourette’s syndrome includes physical and vocal tics, which can either be both
simple and complex.

Physical tics include jerking the head, teeth grinding, rolling eyes and jumping
up and down.

Vocal tics include blowing, squeaking, sniffing, swearing, verbalising

involuntary obscene thoughts, repeating other people’s phrases and
inappropriate language with sexual connotations.86, 87

Tourette’s poses social difficulties and includes low self-esteem,

embarrassment and becoming isolated socially.

43
 Conclusion
The physical Adverse Reactions of neuroleptic medication may be
described as ‘side effects’, but in fact are the main control effects of these
medications acting on the Central Nervous System.
In general medicine, when severe iatrogenic adverse reactions are caused
by common medications, then the ‘offending’ medication is scrutinised and
banned.
However this sanction does not happen within psychiatry. Neuroleptic
adverse reactions are either treated with common medications, - which
patients may or may not be able to break down efficiently, depending on
their genotype profile - dismissed, ignored, or often seen as part of the
psychiatric illness resulting in treatment with further psychiatric
medications. On occasion surgery to rectify the adverse reaction is
performed.

44
 Ethics
Some UK Key Opinion Leaders are insistent that not all neuroleptic
‘side effects’ should be revealed to patients, for fear they may not want
to take neuroleptic medication.
This attitude and practice poses serious ethical questions. The deliberate
hiding of ‘side effects’ information from patients, carers and
professionals is blatant deception and is misleading and disrespectful.
The result is that many people are being coerced into thinking
neuroleptics are safe medications. Nothing could be further from the
truth.
Neuroleptic medications compromise and slowly impoverish peoples’
lives, how their bodies function, their dignity and self respect.
None of this is conducive to social inclusion or the potential of a full
recovery.

45
 Successful Non – Neuroleptic Treatment

There is alternative successful treatment without the use of

neuroleptic medications. This rich and sadly suppressed history of
humanistic alternative treatment has been shown consistently to
present outcomes far superior to those of treatment with
neuroleptic medications.

Successful Non-Neuroleptic Treatments for “Schizophrenia” 88

46
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47
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 Contributors:
Catherine Clarke SRN, SCM, MSSCH, MBChA
Jan Evans MCSP. Grad Dip Phys

November 2011
Revised March 2015

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