If this were your exam question, there are two main biological therapies which you could discuss, anti-psychotic medication or historical biological treatments (ECT and Psychosurgery). For now, let’s just concentrate on anti-psychotic medication.
Anti-psychotics are typically used to treat schizophrenia to correct the excess of the neurotransmitter dopamine, this is believed to be a factor in the disorder. The aim of anti-psychotics is to antagonise (reduce) levels of dopamine in four key dopamine pathways and alleviate some of the symptoms in schizophrenia.
Typical Anti-psychotics aim to do this by binding to D2 receptor sites. This alleviates amplified dopamine levels and reduces the positive symptoms of schizophrenia. However, if dopamine receptor sites were permanently blocked, dopamine levels become too low, which disrupts other behaviours and aggravates negative motor symptoms.
Atypical Anti-psychotics have a much more refined mode of action. They aim to modulate levels of dopamine and serotonin by regulating the actual functioning of dopamine in diverse sensory pathways. For instance, in the Mesolimbic pathway, atypical AP have a ‘hit and run’ action. As this pathway is involved with emotions and sensations of pleasure, by reducing the hyperactivity of dopamine positive symptoms should be reduced. However, if dopamine receptors become completely blocked motor side effects and negative symptoms could occur. Hence these drugs have rapid dissociation which means they block dopamine for a short while and then leave the receptor site available for natural dopamine to have a ‘normal’ effect, with less risk of side effects.
Furthermore, atypical Anti-psychotics also work in the Nigrostriatal dopamine pathway (which helps to control movement). Here Anti-psychotics mode of action affects serotonin. The presence of serotonin in this pathway inhibits dopamine, so atypical Anti-psychotics block/reduce serotonin to indirectly increase natural dopamine. This knock-on effect from antagonising serotonin reduces negative symptoms (e.g. catatonia).
To evaluate, you could use both studies and methodological weaknesses, so for example Borison et al (1996) did a study into the effectiveness of Seroquel (atypical anti-psychotic) in treating positive and negative symptoms of schizophrenia. 109 patients were randomly placed in a treatment or placebo group. Following weekly assessments results showed significant differences between groups, supporting the effectiveness of Seroquel. The reduced positive symptoms didn’t aggravate negative symptoms or create psycho-motor issues. This shows how anti-psychotic treatment does actually work.
However, as schizophrenia is often stated to be a lifelong condition testing after 6 weeks of anti-psychotics appears to be quite superficial. It is documented that side effects can make many patients stop taking medication after a year (50% according to Davison and Neale). This makes the long term effectiveness of Seroquel hard to determine and more longitudinal research is needed.
Furthermore, Elesser did a longitudinal study into the effectiveness of anti-psychotics which found that they couldn’t be used as a cure, despite removing some symptoms. Overall, atypical anti-psychotics only help about 85% of patients and typical Anti-psychotics only 65%. Nevertheless, between 15-35% of patients are not helped.
What’s more, Kopelwicz and Liberman (1998) showed the success of Anti-psychotics can be increased when combined with more traditional psychological therapies. Anti-psychotics may suspend delusionary thoughts and psychotic symptoms, allowing patients to address the more cognitive and family issues related to the disorder, through CBT for example.
Nevertheless, the appropriateness of anti-psychotics is questioned as they can produce many side effects during treatment. This produces an ethical dilemma amongst clinicians. One side effect which can occur is tardive dyskinesia, this affects up to 50% of patients taking Anti-psychotics and is irreversible. It includes symptoms like lip-smacking and tongue thrashing, which can dramatically reduce patient’s quality of life. Many more side effects do reduce the effectiveness of Anti-psychotics, including dystonia and akathisia.
In further evaluation, anti-psychotics can be seen to reduce the patient’s role in their recovery. By simply taking Anti-psychotics, patients have their free will compromised, which could actually aid the therapeutic process. Anti-psychotics tend to restrict patient’s expression of emotional and cognition, have their sensory experience determined and standardised by chemical straight jackets.
Finally, Anti-psychotics can be criticised for only attending to the symptoms of schizophrenia and not tackling the underlying cause of schizophrenia. For instance, something must have instigated dopamine to become elevated (e.g. urban living) and Anti-psychotics do nothing to tackle these issues. Hence, Anti-psychotics are not seen as a complete cure for schizophrenia.