Brain-disabling psychiatric medical treatment

Brain-disabling psychiatric medical treatment is based on a theory of Peter Breggin about speculation of brain-disablement and damage due to biopsychiatric treatment
Psychoactive drugs and psychiatric neuromodulation surgeries have become mainstream treatments for psychiatric disorders. The efficacy of these psychiatric treatments are scrutinized due to the controversy that their mechanisms of action work through the disablement and reversal of normal cognitive function. This reaction may be attributed to and not limited by the attempt of the brain to compensate for the introduction of a foreign substance, long-term development of neurological adaptations, or high patient variability. aming and popularizing the theory.
Four main principles
The bases of the brain-disabling treatment theory are built upon a series of conditional neurologically inductive effects. Its sub-principles support common phenomena of the individual user reacting to the biopsychiatric treatment.<ref name="Breggin 2008" /> A main argument of theorists criticizing biopsychiatric treatments and their inefficacies is the extent of varying morphological and psychological side effects that result among users.
Overall biopsychiatric treatments share the following four prominent principles:
# Disruption of normal brain function
# Causes generalized brain dysfunction
# Impairs self awareness
# Impairment of higher human function such as emotional responsiveness
Terms such as and "medication spellbinding" have been given to represent common symptoms that patients can develop due to biopsychiatric therapies. The terminology describes a level of apathy and indifference, as well as impaired self awareness and levels of comprehension that inhibit the user from recognizing negative effects that have occurred within the brain. Psychiatric drugs are believed to defy the claims and standards of the disease-drug model because their effects can be observed in both patients with and without psychiatric disabilities. The disease-drug model supports that a healthy user will only exhibit side-effects, opposed to the desired effects achieved from treating a disorder.<ref name="Breggin 2008" /><ref name="Moncrieff 2007" />
Controversy and ethics
Controversy behind the brain-disabing treatment theories is fueled by the ethical stance of whether or not a patient actually benefits from a biopsychiatric treatment. Most famous from a depression and anxiety standpoint, effects motivate the question of whether the patient is actually feeling better versus that they are unable to feel.
Anti-biopsychiatric treatment theorists encourage only interactive therapies, and suggest that patients undergoing medical therapies experience a deceived sense of relief and yield no actual benefits. Treatments chemically decrease a patient's awareness and sensitivity to his/her environment inhibiting the patient to feel anything at all; this relief is deceptive. Their ethical stance is firmly against medical treatments, which they view destructive to a patient's neurology.
A treatment activist's concern is that psychiatric medical treatment to illnesses are limited outside of "talking therapy," which not all patients benefit from. Treatment activists suggest that medical therapies yielding any improvements on a patient's mental health can be deemed beneficial. Their stances on ethics focus less on neurology and more on a patient's mental well-being and active relief from his/her disorder.
It is recognized that all medications and neurosurgical approaches have side-effects. This compliments the struggle in ethics behind biopsychiatric treatments. Consideration between the pros and cons of temporarily alleviating the patient but allowing susceptibilities to future brain damage must be considered. Psychiatric professionals, under the Hippocratic oath, must converse with patients about each risk and benefit of a treatment.
Psychoactive drugs
Drugs are categorized by the disorder they treat. They are not mechanically customized for the individual user.
Neuroleptics
Neuroleptics commonly act on Dopamine to treat psychological disorders that are correlated with a lack of the neurotransmitter in the frontal and prefrontal cortex. The neuroleptics increase dopamine reuptake through the blocking of dopaminergic receptors, resulting in the saturation of dopamine within the synaptic cleft. In turn, the replenished quantity of dopamine will induce feelings of euphoria and reward. Noted in the brain-disabling theory, a block in dopamine receptors and the flood of dopamine within the synaptic cleft facilitates the degeneration of dopaminergic neurons in the substantia nigra and basal ganglia. This causes a deficiency in the neurotransmitter resulting in continued reliance on the drug through positive feedback. Its effects are achieved by disrupting normal function. Theorists believe that its chemical shift causes an impairment in self awareness and cognitive function.
Antidepressants
The mechanisms behind antidepressants are devised to create a shift in neurotransmitter reuptake patterns, supporting the brain-disabling treatment claim that biopsychiatric treatments disrupt normal brain function. Clinical depression is suggested to be caused by an abnormality in brain function that impairs normalized neurotransmitter patterns. To biopsychiatric theorists, the idea behind antidepressants is to rectify the quantity of neurotransmitter, usually dopamine, norepinephrine, or serotonin, sustainably until this pattern becomes recognized and natural. However, no studies have shown a statistical significance to a lasting effect, supporting the claims of anti-biopsychiatric theorists. A sub principle of the brain-disabling theory describes the brain's attempt at compensating for biopsychiatric interference in an attempt to resist the unfamiliar commanded shifts. This habit of the brain may suggest why sustainable effects of antidepressants are not achievable. It has also been suggested that the changes in serotonin, norepinephrine and dopamine reuptake inhibition through the blocking of their transporters affect the synthesis and degeneration of neuroreceptors. Long-term use has been seen to impact neuroreceptors with degeneration comparable to Parkinsonian-observed symptoms. The mechanisms behind Parkinson's treatments perform similarly, suggesting that these medications indeed disable the brain and hasten degeneration.<ref name="Breggin 2008" /> "Medication spellbinding" is found to be prominent as users may experience an impaired sense of self awareness and apathy, which are desired to lessen the feeling of depression. There is controversy behind whether or not the decrease in feelings of depression are worth an overall sense of apathy.<ref name="Breggin 2008" /><ref name="Healy 2006" />
Anxiolytics
Supporting the brain-disabling theory, anti-anxiety drugs are targeted as a prime treatment that leads to "medication spellbinding." It shares its clinical and toxic effects by suppressing neuronal function through the impairment of the central nervous system. Its effects of an impaired self awareness are desired because the psychological disattachment decreases anxiety by shielding the user from anxiety-inducing comprehension sensitivity. Prolonged use have been recognized to be linked with dementia and amnesia <ref name="DSM IV 2000" /> Psychometric testing on users 6 months past withdrawal suggest that anxiolytics induce significantly lasting effects on an impairment of memory, conceptual comprehension, psychomotor, and proprioception controls.<ref name="Breggin 2008" /><ref name="Lagnaoui 2002" />
Stimulants
Stimulants are more heavily scrutinized by the brain-disabling perspective because they are commonly prescribed to children. Most commonly prescribed are Ritalin, Adderall, Strattera, Concerta, and Dexedrine.<ref name="Breggin 2008" /><ref name="Breggin 2001" />
The principle of the drug-disease model suggests that healthy volunteers will only demonstrate the side effects of a medication due to a lack of impairment in the function that the drug is targeted to treat. Following the brain-disabling treatment principles, theory activists state that its effects are nonspecific since they are found in individuals both with and without disorders. Therefore it causes a disruption in normal brain function.<ref name="Breggin 2008" /><ref name="Moncrieff 2007" /><ref name="Golden 1991" /> Evidence is strengthened since stimulants are heavily abused for performance by healthy individuals. Psychological addiction is common because users feel that their abilities are enhanced due to its effect of optimized focusing. This can also be considered a negative effect because it elicits a behavioral response that can be viewed as making the user more narrow-minded. This has led to the theory naming of a symptom deemed "hung up" because the user can fall into a constant or repetitive thought or action. Obsessive-compulsive reactions have been frequently noted.<ref name="Breggin 2001" /><ref name="Borcherding 1990" /> Ethics behind the risks and benefits of stimulants to the user are widely challenged. The disruptions of normal brain function, natural thought processing, and emotional responsiveness are the desired effects in stimulant use. It can be considered that the user undergoes "medication spell-binding," as they are unaware of negative cognitive changes and feel benefited from these disruptions.
Morphological effects further support the disabling theory. A criticism of stimulants is that while they are prescribed for extended periods of time, no long-term gains have been demonstrated by biopsychiatric and drug companies. Ritalin in particular contains a label stating "Long term effects of Ritalin in children have not been well established." <ref name="Phys desk reference 2007" /> However, abnormal long term dendritic spindle development has been observed in stimulant users. Some stimulants have been liked to a hastening in brain damage which is permanent, due to atrophy caused by the common ingredient Methylphenidate.<ref name="Borcherding 1990" />
Lithium containing drugs
Lithium was widely used for the treatment of mania and depression in the 1940-1970's but has since then significantly decreased in popularity. Although a treatment for depression, some Lithium based medical treatments can cause depression and severe indifference. Its effects allowed psychiatrist Cade to use lithium opposed to surgical lobotomies to control temperamental patients by impairing emotional responsiveness.<ref name="Breggin 2008" />
Because of its potency, therapeutic approaches must be meticulously optimized and routine monitoring is necessary to quickly note side effects.<ref name="Mcknight 2012" /> Lithium toxicity to the central nervous system is severe but gradual. Anti-biopsychiatric theorists believe its delayed onset inhibits patients from recognizing the severity of their own situations and its side effects, which also include disrupted mental function, muscle tremors, and disruptions in gastrointestinal and renal functions. Functions in memory formation have also been seen to be compromised, further offering the patient to a vulnerability of "medication spellbinding" and impaired self awareness. Abnormal brain wave production has also been seen due to lithium usage, and its overall toxic effects on the blood has been shown to cause morphological alterations, such as abnormal brain cell proliferation and growth.<ref name="Lagace 2005" />
It is directly seen to support brain-disablement by impairing emotional responsiveness, causing brain dysfunction, and disrupting cognitive as well as somatic functioning. The effects of Lithium initiated the theory's term of "deactivation" recognized as a chemical lobotomy.
First vs. second generation medications
Second generation neuroleptics are considered to yield less serious side effects, specifically tardive or motor-related symptoms, than first generations. However, controversy surrounds this comparisons. No statistical significance has consistently been observed between the side-effect profiles of atypicals and typicals, as well as any significance in optimized psychiatric treatment.<ref name="Rosenheck 2006" />
Studies done between patients on atypicals or typicals, opposed to those who were drug-free have yielded results showing permanent changes in patient brain morphology. Compared to non drug-users, patients on typical antipsychotics experienced a cluster of excess gray matter in the right lenticular nucleus. There were grey matter reductions in volume spanning of 47, 22, 4, 5, 6, 7, and 31. Atypical antipsychotic users yielded excess grey matter that was localized on both sides of the thalami. The severity in excess grey matter was positively correlated with atypical dosage. The relationship suggests that morphological damage may be predicted and controlled but not necessarily avoided. Studies suggest typicals may be more associated with permanent morphological changes upon the basal ganglia and cortical areas, opposed to atypicals, which influence an enlargement of the thalami.<ref name="Dazzan 2005" /><ref name="Apple 1999" /> Aside from the morphological changes of the brain by both types of antipsychotics, changes in trends of tissue perfusion, water content, and fat have also been observed.<ref name="Dazzan 2005" /><ref name="Weinberger 2002" />
Both generations of drugs do produce morphological changes on the brain, even with short-term treatment.<ref name="Dazzan 2005" /> The morphological changes effect abilities in cognitive function and learning. They both also have been noted to cause increased severity in weight, diabetes, ataxia, and cardiovascular disease.<ref name="de Leon 2009" /><ref name="Matson 2010" /><ref name="WHO 2007" />
Although alterations in brain morphology are observed in different areas of the brain, both treatments produce effects supporting the brain-disabiling treatment theory due to evidence supporting morphological change and dysfunction.
Biopsychiatric therapies
Electroconvulsive therapy
Electroconvulsive therapy (ECT) is a surgical treatment performed on severely depressed patients who are unresponsive to medication. The practice has been linked to permanent brain damage, dysfunction in cognitive processing, chronic headaches, and exemplified depression as a negative feedback symptom.<ref name="Breggin 2008" /><ref name="Sackeim 2007" /> Supporting the disabling's theory by lack of specificity and individual variation, multiple studies considering its efficacy as a treatment have failed to show significant differences between electroshocked patients and placebos.<ref name="Ross 2006" /> It also has been linked with permanent neurological disruption and chronic mental dysfunction. Other supporting side effects are delirium, loss of consciousness, and impaired emotional responsiveness and self awareness. A poor judgement and a flattened sense of self awareness yields the patient to a susceptibility of the theory's "medication spellbinding." The mini seizures induced upon the brain can cause minor head trauma, and damage to the cortical areas of the brain influence personality shifts of irritability and impulsivity. Autopsies have also shown specific hemorrhages and cell death around the electrically stimulated regions of the brain.<ref name="Breggin 2008" /> Studies have also shown direct morphological effects on the central nervous system such as shrunken nerve cells, blood clots in the brain, and prolonged seizures during treatment as well as seizures outside of treatment due to a lack of blood flow.<ref name="Sackeim 2007" />
The chemical lobotomy
The surgical lobotomy is no longer practiced in developed nations. The brain-disabling treatment theory recognizes treatments that can be considered "chemical lobotomies." These include the tranquilizers, often recognizably first generation neuroleptics, that can induce the mimicry of the aesthetic symptoms observed in patients who had lobotomies. The term "deactivation" has been given to describe a phenomena built on severe disinterest and indifference, lack of concern, and drastically reduced emotional reactivity.<ref name="Breggin 2008" /> Chemical lobotomies can influence dysfunction in the frontal lobes or basal ganglia through the impairment of dopaminergic pathways. However, while a psychosurgical lobotomy splices the frontal lobe descending fibers to the deeper layers of the brain, a chemical lobotomy impairs the fibers.<ref name="Breggin 2008" /><ref name="Jackson 2005" />
Remarkable symptoms and side effects
According to the disease and drug-centered model,<ref name="Moncrieff 2007"/> the non-disease related control will only exhibit the side effects of a drug. Recent studies testing several antipsychotics to a control have challenged the model.<ref name="Moncrieff 2007" />
Tardive syndromes
Tardive dyskinesia (TD), dystonia, and akathisia are the most notorious and recognized side effects related to long-term antipsychotic medication use. Tardive dystonia is recognized by severe, repetitive muscle contractions which contort and paralyze the limbs and body into abnormal postures. Repetitive contractions lead to muscle cramping and severe pain. Tardive akathisia is considered a Parkinsonian syndrome, characterized by a restlessness of jittery movements usually in the legs.
This progression of tardive dyskinesia is hastened by pre-existing underlying neurological damage. In general, the development of the syndrome itself represents that neurological damage has already occurred. This suggests that atypical drug use may influence the development of neurological damage as well.<ref name="de Leon 2009" /><ref name="Matson 2003" /> This addresses the main principle that medical treatments cause dysfunction.
Due to the volume of patients who develop motor-related symptoms from neuroleptics, many studies are motivated by questioning the continuing effects of keeping the patient on the medication. It has been seen that removing the patient from the medication can worsen symptoms, and they must be placed back on the medication to lessen the severity. While the development of side effects is due to positive feedback, the continuance and treatment of the developed syndromes are negative. When returned to or maintained on the medication, it has been seen that having TD or akathisia puts the user at significant risk for developing other serious side effects when compared to those who have not developed motor-related syndromes. Further adjustments in neuroleptic dosages contributed to side effects that extended to the cardiovascular, gastrointestinal, excretory, and endocrine related systems, aside from a significant increase in central nervous system syndromes.<ref name="Matson 2010" />
Other "tardive" syndromes are not limited to motor-related effects, such as tardive dysmentia or tardive dysphrenia.
Morphological alterations
Studies have shown correlations between altered brain morphology and psychotropic drug use. Antipsychotics such as Haloperidol and Olanzapine which are used to treat schizophrenia are among the most critically scrutinized. Studies involving patients with first-episode psychosis under the treatment of these medications received MRIs to document any volume changes in the brain that occurred throughout the durations of their treatment, as well as between and after treatments. Results displayed statistically significant associations between Haloperidol use and reductions in grey matter as well as an increase in lateral ventricle volumes, a symptom related to the progression of schizophrenia.<ref name="Lieberman 2005" /> In another study, test groups were devised based on common drug type (typical or atypical) and duration of use, as well as progression of the psychological disorder. Both drug types were associated with unique morphological changes. Correlations were seen between typical drugs and changes in the basal ganglia, while correlations were seen between atypical drugs and enlarged thalami.<ref name="Dazzan 2005" /> Further studies have shown the development of these symptoms in non-schizophrenic controls as well.

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