DRUG THERAPY
DRUG THERAPY FOR SCHIZOPHRENIA: TYPICAL AND ATYPICAL ANTIPSYCHOTICS.
THE BIOLOGICAL APPROACH TO MENTAL DISORDERS
The biological approach attributes mental disorders to abnormalities in the brain, such as neurotransmitter imbalances. For instance, schizophrenia is believed to be caused by an abnormal dopamine metabolism.. Drugs used to treat this condition work by blocking dopamine receptors, which reduces the neurotransmitter's activity, improving symptoms. These drugs also help by inhibiting reuptake and promoting the breakdown of dopamine molecules after release
KEY TERMS
CHEMOTHERAPY: Drug therapy
NEUROTRANSMITTER: is a chemical that allows neurons in the brain to communicate, they do this by producing a bridge across the synapse between the axon terminals and dendrites; this process allows the continuation of the nerve impulse to progress.
DOPAMINE: a neurotransmitter.
DOPAMINE FUNCTION: Dopamine plays a crucial role in various brain functions, including behaviour and cognition (thinking), voluntary movement, motivation, punishment and reward, pleasure, and focus. It is key to the brain's reward system, influencing mood and decision-making
PSYCHOTROPIC DRUGS: A psychotropic drug is any substance that affects behaviour, mood, thoughts, or perception. It serves as an umbrella term for a wide range of drugs, including both prescription medications and commonly misused substances. Psychotropic drugs can alter the chemical processes in the brain, affecting the way individuals think and feel.
PHARMACEUTICAL PSYCHOTROPIC DRUGS
There are several types of legal, prescription psychotropic medications used to manage various mental health conditions. These are broadly categorised into five main types:
Antidepressants: Medications that help alleviate symptoms of depression by influencing neurotransmitters like serotonin, dopamine, and norepinephrine. Common examples include Prozac (fluoxetine) and Sertraline.
Anti-anxiety medications: These reduce symptoms of anxiety, often by enhancing the effects of GABA (a calming neurotransmitter). Examples include Valium (diazepam) and Xanax (alprazolam).
Stimulants: These are commonly used to treat ADHD and narcolepsy, increasing dopamine and norepinephrine to improve focus and alertness. Examples include Ritalin (methylphenidate) and Adderall (amphetamine).
Antipsychotics: Used to treat disorders like schizophrenia and bipolar disorder, these medications work by blocking dopamine receptors to reduce psychotic symptoms. Examples include Risperidone and Clozapine.
Mood stabilisers: These are used to manage mood fluctuations, particularly in bipolar disorder. Common examples include Lithium and Valproate.
AGONISTS/STIMULANTS: Agonists, or stimulants, are drugs that enhance the activity of neurotransmitters in the brain by increasing their production, release, or preventing their reuptake. This results in more of the neurotransmitter being available in the synapse, leading to amplified effects on brain function. Agonists work by binding to specific receptors, mimicking the action of naturally occurring neurotransmitters, and increasing the intensity of their signals.
Agonists affect a variety of neurotransmitters, including dopamine, serotonin, norepinephrine, and acetylcholine, depending on the specific drug.
ILLEGAL AGONISTS AKA ILLEGAL PSYCHOTROPIC DRUGS are often street drugs that stimulate neurotransmitter activity in the brain. Some examples include:
Cocaine: Increases dopamine and norepinephrine availability by blocking their reuptake, leading to heightened euphoria and energy.
Crack cocaine: A more potent form of cocaine, with similar effects on dopamine levels.
PCP (Phencyclidine): Mimics the action of glutamate, affecting perception, mood, and cognition.
LSD: Primarily affects serotonin receptors, causing intense alterations in sensory perception and mood.
Amphetamines (speed) and methamphetamine: Increase the release of dopamine and norepinephrine, resulting in enhanced alertness and euphoria.
Ecstasy (MDMA): Stimulates serotonin, dopamine, and norepinephrine activity, leading to heightened mood and emotional connectivity.
Cannabis (THC): Mimics the action of natural cannabinoids, impacting memory, coordination, and pleasure.
Heroin: Acts as an opioid agonist, stimulating endorphin receptors, producing intense pleasure and pain relief.
LEGAL AGONISTS AKA LEGAL PSYCHOTROPICS ( see above). There are several agonists used in medical settings that enhance neurotransmitter availability to treat various conditions. Some examples include:
L-dopa: Prescribed to Parkinson’s disease patients to increase dopamine levels in the brain, helping to improve motor function.
Methadone: An opioid agonist used in pain management and addiction treatment, acting on endorphin receptors to relieve pain and reduce withdrawal symptoms.
Prozac (fluoxetine): A selective serotonin reuptake inhibitor (SSRI), it increases serotonin availability in the brain to treat depression and anxiety.
Valium (diazepam): A GABA agonist, enhancing the effects of GABA, an inhibitory neurotransmitter, to reduce anxiety, muscle spasms, and seizures.
ANTAGONIST/BLOCKERS Antagonists are drugs that block the availability or action of neurotransmitters in the brain by preventing their binding to receptors. They are typically used to treat conditions like psychosis, as they reduce excessive brain activity caused by neurotransmitters such as dopamine.
LEGAL ANAGONISTS:: Antipsychotics/Neuroleptics: These are dopamine antagonists that block dopamine receptors, reducing excessive dopamine activity associated with conditions like schizophrenia and psychosis.
Chlorpromazine (Thorazine): A typical antipsychotic used to reduce hallucinations and delusions.
Risperidone: An atypical antipsychotic used to treat schizophrenia and bipolar disorder.
Clozapine: Another atypical antipsychotic, often used for treatment-resistant schizophrenia.
Naloxone: An opioid antagonist that reverses the effects of opioid overdose by blocking opioid receptors.
Beta-blockers (e.g., Propranolol): These block adrenaline receptors, used for treating anxiety and heart conditions
ANTIPSYCHOTICS: Antipsychotic drugs are antagonists that block neurotransmitter availability in the brain, particularly dopamine. These are primarily used to manage symptoms of psychosis and schizophrenia by reducing excessive neurotransmitter activity.
Typical Antipsychotics: Block dopamine receptors (D2) and are effective in treating positive symptoms of schizophrenia (e.g., hallucinations and delusions). Example: Chlorpromazine (Thorazine).
Atypical Antipsychotics: Block both dopamine and serotonin receptors, making them more effective for treating both positive and negative symptoms of schizophrenia (e.g., avolition, anhedonia). Examples: Risperidone, Clozapine, Olanzapine.
NEUROLEPTICS: NEUROLEPTICS: Another term for antipsychotics. Neuroleptics and antipsychotics are often used interchangeably, but there are subtle differences between them, primarily related to the dopamine receptors they target (e.g., D1, D2, D3 receptors).
Neuroleptics are typically older, typical antipsychotics, like Hariperidol, which primarily target D2 receptors.
FIRST GENERATION ANTIPSYCHOTIC DRUGS are referred to as "typical" or "conventional antipsychotics" and were introduced in the 1950s. These drugs primarily work by reducing dopamine activity in the brain, specifically targeting D2 receptors. They are effective at reducing the positive symptoms of schizophrenia, such as hallucinations and delusions, but are less effective in addressing negative symptoms.
SECOND GENERATION ANTIPSYCHOTIC DRUGS are referred to as atypical antipsychotics. These are newer antipsychotics, developed in the 1990s, that target both dopamine and serotonin receptors. Unlike typical antipsychotics, they are effective at reducing both the positive symptoms (such as hallucinations and delusions) and the negative symptoms.
HYPO AND HYPER-: These two prefixes are easily confused as they sound similar, but they have, in fact, more or fewer opposite meanings. Hyper- means over, excessive, more than normal, as in such words as hyperbole (extravagant and obvious exaggeration) and hyperactive (abnormally or pathologically active). Hypo means low, under, beneath, down, or below normal, as in hypoglycaemia (low blood sugar) and hyposensitivity (under sensitivity). Regarding neurotransmitters, a hyper neurotransmitter system means too much neurotransmitter is being secreted into the synapses within a certain neural circuit. Because of this, it produces over-stimulation of the cells and causes an exaggeration of functions.
TARDIVE DYSKINESIA: is a difficult-to-treat form of Dyskinesia (disorder resulting in involuntary, repetitive body movements) that can be Tardive (having a slow or belated onset). It frequently appears after long-term or high-dose use of typical antipsychotic drugs. Tardive Dyskinesia is characterized by repetitive, involuntary, purposeless movements, such as grimacing, tongue protrusion, lip-smacking, puckering and pursing of the lips, and rapid eye blinking. Rapid movements of the extremities may also occur. Impaired movements of the fingers may also appear. For comparison, patients with Parkinson's disease have difficulty moving, while patients with Tardive Dyskinesia have difficulty not moving.
AGRANULOCYTOSIS: A lowered number of white blood cells (remember these are vital for fighting infection and made in the bone marrow. Agranulocytosis may be asymptomatic, or it may clinically present with sudden fever, rigours and sore throat. Infection of any organ may be rapidly progressive (e.g., pneumonia, urinary tract infection). Septicaemia may also progress rapidly. Neutrogena and Agranulocytosis are associated with gum diseases, such as gingival bleeding, saliva increase, halitosis, osteoporosis, and destruction of periodontal ligament Causes: Many drugs have been associated with Agranulocytosis, including some antipsychotics (the atypical antipsychotic Clozapine. Clozapine users in the US must be nationally registered to monitor low white blood cell counts.
NEUROLEPTIC MALIGNANT SYNDROME: (NMS) is a life-threatening neurological disorder most often caused by an adverse reaction to Neuroleptic or Antipsychotic drugs. It generally presents with muscle rigidity, fever, autonomic instability, and cognitive changes such as delirium, and is associated with elevated Creatine Phosphokinase (CPK). The incidence of the disease has declined since its discovery (due to proactive prescription habits), but it is still dangerous to patients being treated with antipsychotics. Because of its unpredictability, there is no one set course of action to treat the syndrome, but generally, removal of the antipsychotic drug treatment, along with medical management, leads to a positive outcome.
TYPICAL ANTIPSYCHOTICS: DISCOVERY AND FIRST DRUG TREATMENTS FOR SCHIZOPHRENIA
The discovery of typical antipsychotics in the 1950s marked a major milestone in the treatment of schizophrenia. This breakthrough came about by accident, when doctors observed that certain antihistamines administered before surgery reduced surgical shock by making patients more relaxed and less fearful. These sedative effects prompted pharmaceutical companies to explore the tranquilising properties of antihistamines more deeply.
Researchers found that it was the phenothiazine nucleus in antihistamines that was responsible for these calming effects. Building on this discovery, the French chemist Paul Charpentier synthesised a new derivative of phenothiazine called Chlorpromazine. When Chlorpromazine was initially prescribed, it was given to patients exhibiting severe agitation or disruptive behaviour, but it soon became apparent that the drug was highly effective at calming patients with schizophrenia.
The mechanism behind Chlorpromazine’s effectiveness is linked to its ability to block dopamine receptors in the brain, specifically D2 receptors. This finding led to the formulation of the dopamine hypothesis, which proposed that the symptoms of schizophrenia are caused by an excess of dopamine activity in key areas of the brain, such as the subcortical and limbic regions. The ability of Chlorpromazine to block these dopamine receptors directly supported this theory.
Dopamine is a neurotransmitter that helps relay signals between neurons by crossing the synapse, allowing communication between brain cells. In schizophrenia, excess dopamine in the synapses leads to overstimulation of neurons, which manifests as the hallucinations, delusions, and disordered thinking seen in psychosis. Chlorpromazine and other typical antipsychotics work by reducing this overstimulation, thereby managing the psychotic symptoms.
Kapur expanded this further by explaining that dopamine acts as a “fuel” for the cognitive distortions that people with schizophrenia often exhibit. According to Kapur, individuals with schizophrenia are prone to jumping to conclusions or adopting extreme interpretations of reality, and the excess dopamine in their brain further inflames these tendencies. By blocking dopamine receptors, drugs like Chlorpromazine effectively "douse the flames" of these psychotic tendencies, though they do not change the underlying cognitive patterns.
ANALYSIS SPECIFIC TO TYPICAL ANTIPSYCHOTICS
The development of Chlorpromazine and other typical antipsychotics was the first significant step towards using drug treatments as a primary intervention for schizophrenia, providing a biological basis for controlling the symptoms of the disorder. This discovery not only revolutionised the management of schizophrenia but also laid the foundation for further research into dopamine's role in mental health and the development of later atypical antipsychotics
RESEARCH FOR TYPICAL ANTI PSYCHOTICS
Research that supports the dopamine hypothesis has shown that drugs such as cocaine, amphetamine, and methamphetamine—which increase dopamine activity—can induce psychosis in people who do not have schizophrenia. This reinforces the idea that excess dopamine is a critical factor in psychotic episodes, and it underscores why drugs like Chlorpromazine are so effective in managing these symptoms.
SIDE EFFECTS ARE DEBILITATING
A major drawback of typical antipsychotics is their high dropout rate. Research shows that the majority of patients who take antipsychotics stop their medication after a short period of time. Lieberman et al., 2005 Questionnaire survey reveals that the reason many patients with schizophrenia discontinue typical antipsychotic treatments is due to the severe side effects, particularly tardive dyskinesia. This is because typical antipsychotics block all types of dopamine activity, (in other parts of the brain as well) and this contributes to harmful side effects.
One of the worse side effects is a neurological condition callesd Tardive dyskinesia. that is characterised by repetitive, involuntary, and purposeless movements such as grimacing, tongue protrusion, lip-smacking, puckering, and rapid eye blinking. This syndrome affects around 20-30% of patients treated with typical antipsychotics (Correll & Schenk, 2008; Jeste et al., 1995). The longer patients are prescribed typical antipsychotics, the greater the likelihood that they will develop tardive dyskinesia, and in many cases, the condition becomes permanent. Some patients have reported that tardive dyskinesia is more distressing than schizophrenia itself (Kane et al., 1988).
As a result of these side effects, patients often stop taking their medications when their symptoms improve, which leads to relapse. This pattern is often referred to as revolving door syndrome, where patients briefly improve, only to relapse and be readmitted to care.
Because of such serious side effects, some clinicians believe it is unwise to prescribe high doses of typical antipsychotics for extended periods. As a result, many patients with schizophrenia are given very small doses of these drugs (Goff et al., 2017). However, this creates a dilemma for clinicians: lowering the dosage increases the chance of relapse, while higher dosages increase the risk of severe and sometimes irreversible side effects (Whitaker, 2010).
DRUG RESISTANCE IN TYPICAL ANTIPSYCHOTICS
A major disadvantage of typical antipsychotics is that approximately 30% of schizophrenics exhibit negative symptoms. Typical antipsychotics do not address these negative symptoms and, in some cases, may even exacerbate them (Kirkpatrick et al., 2006). This failure to treat negative symptoms effectively reveals a limitation not only in the medications themselves but also in the original dopamine hypothesis, which focused on hyperactive dopamine transmission as the sole cause of schizophrenia.
Furthermore, a significant number of patients with schizophrenia do not respond to these drugs, even when they exhibit positive symptoms such as hallucinations and delusions (Leucht et al., 2003). These patients are considered drug-resistant, meaning that despite having symptoms typically associated with excess dopamine activity, they do not experience improvement when treated with typical antipsychotics. This highlights a significant limitation of typical antipsychotics, as they fail to provide relief for a substantial portion of patients who present with positive symptoms.
A01 ATYPICAL ANTIPSYCHOTICS DESCRIPTION
The limitations of typical antipsychotics, particularly their failure to effectively treat negative symptoms and typical drug-resistant positive symptom schizophrenia, as well as their tendency to cause severe side effects such as tardive dyskinesia, led to the development of atypical antipsychotics in the 1990s (Kane et al., 1988). These medications are associated with a 5% risk of tardive dyskinesia, significantly lower than the 20-30% risk posed by typical antipsychotics (Jeste et al., 1995). These newer drugs were designed to alleviate both positive symptoms and negative symptoms which typical antipsychotics often worsened or failed to address (Leucht et al., 2009).
Unlike typical antipsychotics, atypicals target both dopamine and serotonin receptors, accounting for their broader efficacy in treating both positive and negative symptoms.
Among these drugs, Clozapine has been particularly effective in treating treatment-resistant positive schizophrenia, offering relief to patients who do not respond to at least two other typical and atypical antipsychotics (Kane et al., 1988). However, Clozapine carries a significant risk of agranulocytosis, a potentially fatal reduction in white blood cells, which occurs in approximately 1% of patients and requires regular blood monitoring (Kane et al., 1988).
Other widely used atypical antipsychotics include Risperidone (Risperdal), Olanzapine (Zyprexa), Quetiapine (Seroquel), and Ziprasidone (Geodon).
For other patients who are unwilling or unable to take medication regularly, long-acting depot preparations of antipsychotics may be given every two weeks to achieve control.
EVALUATION SPECIFIC TO ATYPICAL ANTIPSYCHOTICS
SIDE EFFECTS OF ATYPICAL ANTIPSYCHOTICS
Atypical antipsychotics are less likely to cause Tardive dyskinesia (5% compared to 20-30%, but there are many new side effects, that may be seen as equally debilitating. For example one of the most common is massive weight gain, which can be as much as a stone (14 pounds) per year and is consistent throughout treatment. This often leads to diabetes in patients.
Other serious side effects include extrapyramidal symptoms, which resemble Parkinson’s disease. These symptoms include tremors, shuffling gait, and drooling. Patients may also experience dystonia, causing muscle rigidity and involuntary movements like chewing or twisting of the body, as well as akathisia, a condition where individuals are unable to stay still and constantly feel the need to move.
Additional effects can include a sense of being in an emotional straightjacket, with sexual dysfunction being a frequent complaint among patients. Though rarer, a serious condition known as neuroleptic malignant syndrome affects around 1% of patients, characterized by severe muscle rigidity, fever, and in extreme cases, coma
RESEARCH STUDIES FOR ATYPICAL DRUGS
Many clinicians view antipsychotic drugs as highly effective because they are relatively cheap to produce, easy to administer and they initially seem to have a positive effect on many sufferers. For example, Kahn et al. (2008) found that antipsychotics are generally effective for at least one year, but that second- generation drugs were no more effective than first-generation ones. This finding was also replicated in a meta–analysis by Crossley Et Al (2010) who suggested that atypical antipsychotics are no more effective, but do have less side effects.
However a large-scale, randomised clinical trial by Lieberman et al. (2005) compared four atypical antipsychotics with one typical antipsychotic. This study involved nearly 1,500 patients across the USA and challenged the belief that atypicals were more effective or produced fewer side effects than typical antipsychotics. The study revealed that:
Atypical drugs were not significantly more effective than typical drugs.
Atypical drugs did not lead to fewer side effects than typical antipsychotics.
Nearly three-quarters of the patients stopped taking their medication before the 18-month study period ended.
Further data from the study showed that:
50% of patients stopped their medication within the first year.
75% discontinued medication by the second year.
Even among patients who continued taking their medication, the relapse rate was high:
40% relapsed in the first year.
15% relapsed in each subsequent year.
These findings suggest that antipsychotic medications, whether typical or atypical, are not particularly effective over the long term, as many patients discontinue treatment due to side effects, disorganised thinking, or the perception that the medication is no longer effective. Additionally, a significant proportion of patients are not symptom-free even while on medication.
A03 EVALUATION OF ANTIPSYCHOTICS: TYPICAL AND ATYPICAL
BEFORE ANTIPSYCHOTICS
Before the introduction of antipsychotic drugs, around 50% of patients admitted to psychiatric hospitals, often referred to as lunatic asylums, stayed there for life. The treatment of these individuals was often brutal or non-existent. Common practices included electric convulsive therapy (ECT), frontal lobotomies, and insulin shock therapy, all of which were invasive and distressing. Living conditions were equally inhumane, with many patients subjected to straitjackets and housed in padded cells. These methods primarily focused on control and containment rather than treatment, and hospital staff were often poorly educated, resorting to harsh methods rather than providing care.
In stark contrast, today, only about 3% of individuals with schizophrenia are in hospitals, and typically only for a few weeks. This dramatic shift reflects significant improvements in the treatment of mental illness, particularly in Western and individualistic societies. However, while antipsychotic drugs played a role in allowing patients to live more independently, it is important to acknowledge that improvements in social awareness and human rights likely would have led to better treatment of individuals with mental health conditions, even without the advent of these drugs.
WHO DO ANTIPSYCHOTIC DRUGS BENEFIT?
For many individuals, antipsychotics have significantly improved their ability to function in daily life, allowing them to maintain jobs, relationships, and a degree of independence. Moreover, as patients become more able to manage their symptoms, there is a positive impact on society as well, as fewer people require long-term institutional care, reducing healthcare costs and enabling some patients to return to work and contribute economically.
However, many patients report feeling emotionally numb or “zombified” while on antipsychotic medication, a feeling that can disconnect them from their emotions, thoughts, and sense of self (Moncrieff, 2009). This emotional blunting, often described as a "pharmacological straitjacket," suggests that the medications may benefit institutions and families more than the patients themselves. For example, caregivers, while well-intentioned, may also push for medication to ease their caregiving burden rather than addressing the patient’s deeper needs for psychological treatment or rehabilitation., This raises ethical concerns, as the drugs may be used as tools of control rather than as a means of supporting the patient's long-term recovery and autonomy. In extreme cases, this can lead to violations of patient rights, with the Human Rights Act ensuring no one is subjected to degrading treatment.
Thomas Szasz and Joanna Moncrieff (Szasz, 1974; Moncrieff, 2009) argue that psychotropic drugs are frequently prescribed to keep patients sedated and compliant, making them easier to handle in institutional settings rather than focusing on their well-being and psychological growth.
In summary, while antipsychotics can certainly improve symptoms and offer patients a chance at a more stable life, there are concerns that their use is sometimes more aligned with institutional convenience and societal expectations than with the best interests of the patient. This raises important questions about the balance between controlling symptoms and promoting long-term recovery and personal autonomy
UP REGULATION IN SCHIZOPHRENIA AND ANTIPSYCHOTIC USE
A major criticism of antipsychotics is the risk of upregulation and its long-term impact. Upregulation is a compensatory process in which the brain increases the number or sensitivity of receptors in response to antagonists, such as antipsychotics, which block neurotransmitter activity. In the case of schizophrenia, typical antipsychotics work by blocking dopamine D2 receptors to reduce the overactivity of dopamine, (Abi-Dargham et al., 2000). However, long-term use of these medications may lead to dopamine receptor upregulation, whereby the brain compensates for the blocked dopamine receptors by increasing dopamine synthesis and receptor density (Seeman, 2009).
This compensatory mechanism can paradoxically lead to worsened psychosis when the medication is discontinued, as the brain’s elevated sensitivity to dopamine exacerbates symptoms of schizophrenia. Moncrieff (2006) describes this phenomenon as "supersensitivity psychosis," where patients who stop taking antipsychotics experience rebound psychosis that is often more severe than the original condition. This occurs because the brain, having adapted to dopamine blockade by upregulating dopamine receptors, suddenly becomes hyper-responsive to dopamine when the drug is removed.
Research conducted on healthy volunteers and schizophrenia patients shows that acute antipsychotic treatment can initially reduce dopamine synthesis, but long-term antipsychotic use leads to an increase in presynaptic dopamine synthesis capacity (Howes & Kapur, 2009). This suggests that while antipsychotics may provide temporary relief, they might worsen the underlying dopamine dysregulation over time, contributing to relapse when patients stop treatment.
Moreover, a study by Seeman (2009) highlights the long-term effects of dopamine receptor upregulation, showing that after prolonged antipsychotic use, the brain compensates by increasing dopamine D2 receptors in certain regions. This upregulation persists for years, and patients may relapse more severely upon drug withdrawal, which is one explanation for the high relapse rates observed after discontinuation of antipsychotic treatment.
In addition, upregulation contributes to the cycle of dependency on antipsychotics. Once the brain has adapted to the presence of these medications, stopping them without tapering can provoke an intense rebound psychosis, making it challenging for patients to discontinue the drugs safely. This cycle raises concerns about the long-term strategy of using dopamine-blocking agents as the primary treatment for schizophrenia.
AKATHISIA, SUICIDE IDEATION, AND VIOLENT BEHAVIOUR
Akathisia is a movement disorder marked by extreme restlessness and an inability to stay still, often caused by antipsychotics, especially typical ones, and some antidepressants like SSRIs (Healy et al., 2006). It leads to severe discomfort, anxiety, and agitation, which can result in suicidal thoughts or even violent behaviour. This inner turmoil is linked to impulsive actions, including self-harm or homicidal tendencies.
Research by Healy (2006) and Whitaker (2010) suggests a possible connection between akathisia and extreme violence, including school shootings. Whitaker (2010) raised concerns about psychiatric drugs triggering violent outbursts, particularly in adolescents. While the link is debated, numerous case reports show a disturbing pattern where individuals, after starting or stopping medication, may become prone to suicide or violence.
Healy (2006) documented several cases where patients experienced suicidal urges or aggressive behaviour shortly after adjusting their medication. Since akathisia symptoms can be mistaken for psychotic agitation, increasing the dose may worsen the problem.
More research is needed to fully understand the connection between akathisia and violent ideation, but current evidence suggests that careful monitoring is essential, particularly for young patients. Whitaker (2010) and other researchers emphasise recognising akathisia early to prevent severe outcomes, such as suicide or violence.
PSYCHOSOCIAL FACTORS AND THE LIMITATIONS OF A PURELY BIOLOGICAL APPROACH
The focus on biological treatments such as antipsychotics overlooks the importance of psychological and environmental factors. Schizophrenia is not entirely genetic, as Gottesman’s twin studies demonstrate. Monozygotic (MZ) twins have a 48% concordance rate for schizophrenia, which is far from 100% (Gottesman, 1991). This indicates that environmental and psychological factors play a significant role in the development of schizophrenia, and as such, treatment should not be entirely biological.
A study by the World Health Organization (WHO) found that patients in developing countries, where antipsychotics are less commonly used, had better long-term recovery outcomes than those in developed countries (Leff, 1992). This suggests that psychosocial factors, such as strong community support and reduced stigma, play a significant role in recovery. Focusing solely on biological treatments like antipsychotics neglects these important contributors to the well-being and recovery of schizophrenia patients.
ETHICAL ISSUES AND DETERMINISM
The use of antipsychotics also raises ethical concerns, particularly around issues of determinism. Biological treatments assume that schizophrenia is entirely the result of brain chemistry, leaving little room for patient autonomy or personal agency.Ross et al. argue that antipsychotic drugs merely reduce the effects of schizophrenia without addressing its underlying cause. In other words, they do not “cure” schizophrenia, rather they dampen symptoms down so that patients can live relatively “normal” lives in the community.This, they argue, diminishes patients' motivation to explore other treatments or to understand the root causes of their illness, leading to an over-reliance on pharmacological interventions. The deterministic view presented by antipsychotic treatments can disempower patients, suggesting they have no control over their condition.
In contrast, psychological therapies, such as Cognitive Behavioural Therapy (CBT), aim to empower patients by helping them challenge distorted thoughts and take control of their symptoms.
ALTERNATIVE TREATMENTS AND HOLISTIC APPROACHES
Psychological treatments such as CBT and family interventions have been shown to reduce relapse rates and improve patient outcomes. CBT helps patients recognise and challenge their distorted thinking patterns, reducing the severity of delusions and hallucinations. Family interventions, particularly those that address expressed emotion, have been shown to reduce relapse rates by creating a more supportive home environment (Davis et al., 1997).
By combining biological and psychological treatments, patients are more likely to achieve long-term stability. This holistic approach acknowledges the complexity of schizophrenia and provides a more personalised treatment plan that addresses not only the biological aspects of the disorder but also the cognitive, social, and environmental factors that influence recovery.
CONCLUSION
Biological treatments, particularly antipsychotic medications, have revolutionised the management of schizophrenia. However, these treatments are not without limitations, including severe side effects, high dropout rates, and their inability to fully address the psychological and social factors contributing to the disorder. A more holistic approach, incorporating both biological and psychological interventions, may offer better long-term outcomes for patients, addressing the full complexity of schizophrenia while empowering patients to take an active role in their recovery.
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