Neuroleptic Psychological Side Effects
- Akin to being intoxicated with alcohol being
- Unaware anything is amiss with personal behaviour
- To observers it is quite obvious that personal evaluation of behaviour is impaired. (Breggin 2006)
- 20% of patients suffer from akathesia. Braude et al., (1983).
- 20-45% suffer from akathesia Poyurovsky et al., (2001)
- Akathesia is the perpetual inner restlessness & inability of the patient to keep still.
- Highly distressful
- Associated with anxiety and suicide Nelson 2001
- Dementia is associated with TD.
- 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:
- Neurofibrillary Tangles (NFTs) - abnormal clusters of proteins inside the neurons
- Beta -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.)
- Granulovacuolar Degeneration (GVD) - a process which refers to the intraneuronal presence of abnormal membrane bound cavities (vacuoles), containing dense whorls of protein.
- Severe depression occurs with patients on depot neuroleptic medication. (De Alarcon and Carney, 1969).
- 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
Lack of energy
Lack of purpose
Flat affect Affective blunting
Emotional Lack of feeling Reduced emotional range
Motivation Reduced drive Sociality
Reduced initiative Reduced curiosity
Source Lewander (1994)
- 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 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)
SUPER SENSITIVITY PSYCHOSIS (SSP)
- 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.
- 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:
- 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.
- 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)