Loren Mosher, psychiatrist, refers to the newer atypical neuroleptics
action on the frontal lobes of the brain. Although this action may
result in the patient having fewer EPS side effects, the long-term
effect on the likelihood of inducing dementia is unknown.
It is the frontal lobes where structural changes occur in dementia.
Research by Thomas and McGuire, (1986) showed that subjects with high TD scores had memory impairment.
In America, there are litigations relating to patients who have been
seriously affected by TD and the associated intellectual impairments.
The following studies depict the same brain anatomical changes in patients taking neuroleptics as those with a diagnosis of Alzheimer’s
Disease
The Prohovnik Study
Prohovnik et
al (1993) New York State Office of Mental Health
the researchers identified full blown
Alzheimer’s disease in approximately 30% of the schizophrenic sub group. (Jackson 2009)
The Purohit Study
Purohit et al
(1998) - Pilgrim Psychiatric Centre, NY
“Researchers discovered both a higher
prevalence and greater intensity of plaque and tangle pathology
among the schizophrenic subgroup when compared with age matched controls " (Jackson 2009)
“Is only confirmed by autopsy - a pathologist must identify
specific abnormalities within or around the neurons. In addition to neuronal
death and tissue atrophy (thickening) additional features include:
vNeurofibrillary Tangles(NFTs) - abnormal clusters of proteins inside the neurons
vBeta
-Amyloid Plaques - dense deposits of protein which are found outside the neurons,
forming pleats - called a beta pleated sheet’/compact plaque.(senile plaques - abnormal accumulations of
amyloid (and other proteins) which form outside the neurons - occurring with
normal ageing.)
vGranulovacuolar
Degeneration(GVD) - a process which
refers to the intraneuronal presence of abnormal membrane bound cavities
(vacuoles), containing dense whorls of protein.
DEPRESSION
Severe depression occurs with patients on depot neuroleptic medication. (De Alarcon and Carney, 1969).
DYSPHORIA
Extremely unpleasant and distressing subjective change in mood.
Severe anxiety, agitation, depression and irritability
Impairs psychological therapy (Marder 2005)
Less favourable outcome to treatment both in the long and short term - Singh (1997)
47% of mental health patients experience akathesia, dysphoria and emotional flattening, Windgassen (1991).
NEUROLEPTIC INDUCED DEFICIT SYNDROME (NIDS) A
comparison of the negative symptoms of schizophrenia and the side
effects of the neuroleptic medications show them to be very similar,
Lewander (1994), Schooler (1994). Johnson et al (1994) discovered that
“the dose of the neuroleptic medication was significantly related to
the total score for the negative symptoms, whereas there was no
relationship with positive symptom score. This suggests that negative
symptoms may be induced by neuroleptics”. Thomas (1997).
Psychological Neuroleptic Side Effect Negative Symptom Vigilance Drowsiness Attentional Impairment
Will
Apathy Apathy
Lack of energy
Lack of purpose
Mood
Flat affect Affective blunting
Restrictive effect
Emotional Lack of feeling Reduced emotional range Responsiveness Dysphoria 'Dead inside'
It
has been reported that neuroleptic medications c:
Dull creativity and
interest
More passive behaviour
Less emotional displays in
patients on long-term neuroleptic therapy
Induce a decrease in the
person’s capacity to acquire new responses’. Mayerhoff and Lieberman
(1992).
TARDIVE PSYCHOSIS / WITHDRAWAL / REBOUND PSYCHOSIS AND DEPENDENCY
60%-
80% of patients on depots, 'relapse' if the medication is discontinued,(Johnson 1979).
The Tranter & Healy (1998) study examined the
relapse versus withdrawal problem in drugs used to treat psychosis, and
found that there is strong evidence that discontinuation syndrome
exists.
The above authors refer to evidence associated with
the treatment of TB with Largactil in the 1960’s. When the drug was
withdrawn, five of seventeen subjects had withdrawal symptoms. This
dissipated when the drug was recommenced.
Psychiatrists view
patients when withdrawing from psychotrophic drugs and become
psychotic, as experiencing a ‘relapse’. Psychiatrists generally
perceive that the schizophrenia is worsening, being seen as proof that
the schizophrenic patient is in need of antipsychotic drugs.
All patients who experience psychosis in psychotropic drug withdrawal, have basically gone ‘cold turkey’.
However,
in both scenarios in psychotropic drug withdrawal, the nerve ending
receptors are adjusting to the reduction of the toxic chemicals in the
synapse and a psychosis ensues.
Moncrieffe (2006) Why is it so difficult to stop psychiatric drug
treatment? It may be nothing to do with the original problem.
SUICIDE
Suicide rates are up to 50% higher in neuroleptically treated patients
compared to the general population, Markowe et al., (1967).
Two attempted suicides were recorded by Drake and Ehrlich (1985). Both of these patients suffered from akathesia.
Thomas (1997) notes that intolerable feelings of akathesia together
with the distressing mood changes of dysphoria could cause suicidal
ideation.
Whitaker (2002): records that 12 out of 2,500 people committed suicide whilst taking Olanzapine
60% suicides were taking psychotropic drugs Sweden Trans World News (2007)
Chouinard, G., & Jones, B. D. (1980) has researched into this phenomena.
58% of patients 'relapse' on neuroleptic medication, Crow et al (1986). Moncrieff J (2006)
Samaha et al (2007)
When
the neuroleptic blocks the dopamine transmitter in the synaptic cleft,
the brain responds by trying to compensate. The nerve endings receptors
for the dopamine transmitter increases by 30%, becoming hypersensitive
to the minute traces of dopamine remain in the cleft. The patient
eventually experiences a psychosis. This psychosis is known as SSP -
the anti psychotic drug actually induces the psychosis and is
iatrogenic.
The medical model perspective attributes the SSP to
patients being ‘treatment resistant’ which results in an increasing the
neuroleptic dose and/or mixing various psychotropic drugs together –
the psychotropic cocktail. Because of these patients’ hypersensitivity
to psychotropic drugs their psychological condition deteriorates.
VIOLENCE
High doses of neuroleptic medication present increased patient
violence, Barnes & Bridges, (1998) and Herrera et al., (1998).
The chemical interferes with the patient's rationality, inducing:
Hostility
Verbal aggression
Physical aggression. Increasing the dose of the medication accentuates
aggression: patient distress is thus heightened
Increasing the neuroleptic dose accentuates aggression
DEPENDENCY DSM1V CRITERIA
Tolerance - medication increased to stable level
Withdrawal - creating physiological states
Progressive neglects of interests because of psychoactive substance used.
GENERAL
EPS, TD and Akathesia make patients look ‘odd’. They are extremely
vulnerable in the public environment. These side effects are not
conducive to a patient’s full recovery, as patients loose credibility
in society.
EPS, Akathesia and Tardive Dyskinesia are frequent combinations.
TD worsens when anti-cholinergic drugs are prescribed for EPS - Alexander (1999)
Akathesia, emotional dis-inhibition, liability and psychotic
compensation are treatment rather than disease specific, in that they
happen when these agents have been used in a variety of populations
from health volunteers - Thomas (1997)