On the Psychopharmacology of Neuroleptics
Neuroleptics are major tranquilizers, neurological inhibitors, suppressants, and depressants of the central nervous system. Neuroleptics can neither cure nor prevent positive symptoms of schizophrenia, but rather neuroleptics suppress symptoms of schizophrenia or psychosis. Long term preventative or maintenance use of neuroleptics is not justifiable, particularly against the will of the person.
Neuroleptic means “nerve seizing”. Neuroleptics work to treat psychosis by disrupting normal brain function in the reward pathway, and in the mesocortical pathway –connecting to the frontal lobes (the part of our brains that make us human).
All the effects of a neuroleptic may be categorized as follows: mental & physical effects: the total effects of a neuroleptic are not best reduced to only the sum of its target effects and side effects but can instead be categorized as follows: target effects, short-term effects, long-term effects, withdrawal effects; where: target effects:= the mechanisms by which a neuroleptic produces its intended outcome may not be said to be mere “side effects”; these are rather the pharmacological target effects (intended).
Neuroleptics profoundly suppress brain function by occupying/blocking dopamine receptors and inhibiting neuronal function, thereby disrupting communication between neurons along dopaminergic pathways through either (exactly) one of the following mechanisms: antagonism (I.A. = 0%), or inverse-agonism (I.A. < 0%), or partial-agonism (0% < I.A. < 100%), thereby diminishing dopaminergic brain activity. Note: I.A. = intrinsic activity = the relative (%) extent activation of a receptor relative to dopamine receptor(s); where dopamine’s own intrinsic activity on a dopamine receptor: = +100%, by definition.
Neuroleptics block, i.e., put a brake on neurotransmission along dopaminergic pathways including the mesolimbic, i.e., “the reward pathway” and the mesocortical, which is the primary neural pathway to the frontal lobes – the most distinguishable part of the human brain! Neuroleptics block/occupy 70% – 90% of the brain’s dopamine D2 receptors. Thus, neuroleptics may not be said to be normalizing agents in the treatment of anything. Neuroleptics are chemical lobotomizers because they disconnect the frontal lobes from the rest of the brain by profoundly blocking the dopaminergic pathways of the brain, most notably the mesocortical pathway connecting to the frontal lobes via dopamine D2 receptor blockade (with 70% – 90% dopamine D2 receptors occupied at therapeutic doses). Lobotomy, whether surgical or chemical (via neuroleptic) results in dysfunction of the frontal lobes – the part of our brain that makes us human!
Neuroleptics exert their pharmacological target effects by occupying dopamine receptors, inhibiting/deactivating them, resulting in a suppression/reduction of dopaminergic receptor activity, via antagonism, or inverse-agonism, or partial-agonism, in each case dampening down dopaminergic neurotransmission: i.e., disrupting normal brain function along the dopamine pathways: the mesolimbic (i.e., “the reward pathway”), the mesocortical pathway (connecting to the frontal lobes), the nigrostriatal pathway (target of antiparkinsonian agents), and the tuberoinfundibular pathway (endocrine function / hormonal balance). Neuroleptics impair mental functions such as emotions, affect, feelings, cognition, memory, attention, focus; they slow up and dampen down all thinking processes, reducing thought tempo, one’s ability to learn, study, perform on mental tasks and tests, reduce intelligence quotient (IQ) etc.
Neuroleptics do not exert their therapeutic (pharmacological target effects on psychosis (positive symptoms of schizophrenia) by rectifying a brain abnormality, such as a chemical imbalance, nor do they target any physiological process that produces the positive symptoms of schizophrenia, but rather neuroleptics suppress symptoms of schizophrenia by a by a profound slowing up and dampening down of mental processes putting a brake on dopaminergic neurotransmission – they arrest natural brain function.
A neuroleptic induces disorder of diminished motivation, suppresses all thinking processes, degrades a person’s intelligence and executive functional capacity for higher order thinking (ex., complex problem solving, philosophizing, planning/organizing, etc.), incapacitates the mind (i.e., diminishes intelligence, impairs memory, attention, concentration, significantly decreases IQ level), disables the brain, causes significant brain shrinkage as well as a reduction in the number of connections to the pre-frontal cortex, resulting in loss of executive functioning, cognitive impairment, and decline. Moreover, neuroleptics induce “neuroleptic-induced deficit disorder”: a syndrome characterized by the same symptoms that constitute so called “negative symptoms of schizophrenia”; its symptoms include anhedonia (i.e., loss of pleasure), avolition (i.e., loss of will), cognitive impairment, impoverishment of thought & speech, etc.
Neuroleptics cause severe impairment in cognitive function, degrade one’s executive functional capacity, cause disorder of diminished motivation, blunt feelings (ex., pleasure) and flatten emotions, slow up and dampen down thinking processes (ex., slow down thought tempo), cause psycho-sexual dysfunction affecting all phases of sexual functioning including libido (sex-drive), arousal, and orgasm, etc. These are not mere “side effects” or “adverse effects”, but rather the mechanism by which neuroleptic drugs produce their intended outcome. Neuroleptics exert their target (i.e., therapeutic/intended) effects in a global rather than a specific manner: for example, in treating delusions, neuroleptics suppress a person’s general ability to think, and do not just target delusional thoughts specifically.
Benefits/Advantages (non-existent, dubious at best, based on a false narrative of science).
Risks/Harms (causes more harm than good, not in the best interests of the person being involuntarily treated, violates fundamental human and civil rights.)
Neuroleptics are not a cure for schizophrenia and do not even qualify as treatments for it some of the time. Neuroleptics do not treat schizophrenia by rectifying any underlying abnormality: ex., a bio-chemical imbalance such as according to the dopamine hypothesis of schizophrenia, according to which an overactive dopaminergic system is the primary cause of schizophrenia. Neuroleptics are not treatments in the sense of being curative agents, they cannot cure any condition; they are not disease specific treatments for schizophrenia; they are not like antidotes to psychosis. They might work to curb/suppress positive symptoms of schizophrenia/psychosis (ex., delusions, hallucinations), but that depends on the context, what the intended outcome is and who is intending the outcome. Their target effects in treating schizophrenia are slow up and dampen down the dopaminergic neurotransmitter system by blocking/occupying dopamine receptors by antagonism, inverse agonism, or partial agonism, which results in an inhibition of the dopaminergic pathways of the brain. Any effects induced by the pharmacological target effects of neuroleptics cannot be said to be “side effects” because they are the ‘main’ effects and the intended effects; the target effects of a neuroleptic are the mechanisms by which the neuroleptic exerts its main intended effects. No definition for “side effects” could reasonably include the target effects of the neuroleptic. They can, however, be called ‘adverse’ effects in that they are unfavourable effects, which include the disadvantages and risks of treatment with the neuroleptic.
Even while being considered treatments for schizophrenia, under some definitions of treatment, they are however not effective treatments as such; plus, neuroleptics as a class of psychiatric drugs are not much more effective than a placebo but are the most toxic pharmaceutical drugs available by prescription apart from chemotherapy for cancer. There is insufficient evidence for the long-term safety and efficacy of neuroleptics in treating schizophrenia/psychosis. The bulk of research on their safety and efficacy is based on short-term studies (6-8 weeks), and the evidence on their long-term safety and efficacy is lacking: conflicted, at best inconclusive due to some evidence indicating it and other evidence contraindicating it (i.e., indicating against it): i.e., the evidence in favour is conflicted, contradictory, and inconclusive.