This topic includes both first and second generation antipsychotics.

Antipsychotics are effective for the symptoms of schizophrenia. Positive symptoms include the experiences of perceptual abnormalities (hallucinations) and fixed, false, irrational beliefs (delusions). Negative symptoms include a lack of ordinary mental activities such as emotional expression, social engagement, and motivation. Antipsychotics can also cause side effects. These include extrapyramidal symptoms such as dyskinesias (repetitive, involuntary, and purposeless body or facial movements), Parkinsonism (cogwheel muscle rigidity, pill-rolling tremor and reduced or slowed movements), akathisia (motor restlessness, especially in the legs, and resembling agitation), and dystonias (muscle contractions causing unusual twisting of parts of the body, most often in the neck). These effects are caused by the dopamine receptor antagonist action of antipsychotics. Other side effects may include weight, hormonal and metabolic changes, increased sedation, and ventricular anomalies (QTc prolongation).

What is the evidence for any antipsychotic efficacy compared to placebo?

Overall, moderate to high quality evidence finds a medium-sized effect of greater total symptom improvement with antipsychotics than with placebo. There was less variability in the response to antipsychotics than in the response to placebo, with older studies, those with younger patients, higher dose treatments, and greater mean difference in symptom change being associated with the least variability in response.

For particular antipsychotics, there were symptom improvements with (in descending order of efficacy compared to placebo): clozapine, amisulpride, thiotixene, zotepine, olanzapine, perphenazine, risperidone, thioridazine, zuclopenthixol, paliperidone, sulpiride, haloperidol, loxapine, chlorpromazine, flupentixol, clopenthixol, molindone, quetiapine, aripiprazole, ziprasidone, sertindole, asenapine, lurasidone, cariprazine, iloperidone, and brexpiprazole. There were no significant differences in symptoms between placebo and penfluridol, pimozide, perazine, fluphenazine, trifluoperazine, and levomepromazine.

For social functioning, there were improvements with (in descending order of efficacy compared to placebo) thioridazine, olanzapine, paliperidone, quetiapine, lurasidone, and brexpiprazole. There were no improvements in social functioning between placebo and aripiprazole, sertindole, amisulpride, ziprasidone, flupentixol, or risperidone.

For all-cause discontinuation (in descending order of effects, first being best), there was less discontinuation with clopenthixol, amisulpride, olanzapine, paliperidone, thiotixene, thioridazine, clozapine, loxapine, iloperidone, perphenazine, aripiprazole, risperidone, zuclopenthixol, zotepine, asenapine, quetiapine, lurasidone, brexpiprazole, haloperidol, and ziprasidone. There were no differences between placebo and perazine, levomepromazine, flupentixol, molindone, fluphenazine, chlorpromazine, cariprazine, sulpiride, sertindole, penfluridol, trifluoperazine, and pimozide.

For side effects (in ascending order of harm compared to placebo), there was less use of antiparkinson drugs with clozapine than with placebo, and more use of antiparkinson drugs with paliperidone, ziprasidone, risperidone, lurasidone, zotepine, cariprazine, chlorpromazine, sulpiride, perphenazine, molindone, zuclopenthixol, trifluoperazine, flupentixol, haloperidol, loxapine, penfluridol, fluphenazine, chlorpromazine, thiotixene, and pimozide.

There was more akathisia with aripiprazole, ziprasidone, thioridazine, asenapine, amisulpride, chlorpromazine, thiotixene, risperidone, cariprazine, loxapine, haloperidol, lurasidone, trifluoperazine, sulpiride, molindone, penfluridol, pimozide, fluphenazine, flupentixol, and zuclopenthixol.

There was more weight gain with haloperidol, amisulpride, asenapine, risperidone, paliperidone, clozapine, quetiapine, iloperidone, chlorpromazine, sertindole, olanzapine, and zotepine.

There was less prolactin elevation with aripiprazole, clozapine, and zotepine, and more prolactin elevation with olanzapine, asenapine, lurasidone, sertindole, haloperidol, amisulpride, risperidone, and paliperidone.

There was more sedation with aripiprazole, lurasidone, haloperidol, risperidone, asenapine, loxapine, olanzapine, chlorpromazine, thioridazine, thiotixene, ziprasidone, perazine, clozapine, clopenthixol, quetiapine, sulpiride, zotepine, and zuclopenthixol.

There was more QTc prolongation with quetiapine, olanzapine, risperidone, iloperidone, ziprasidone, amisulpride, and sertindole.

There was more anticholinergic side-effects haloperidol, olanzapine, clozapine, chlorpromazine, zotepine, iloperidone, thioridazine, and quetiapine.

October 2020

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First generation ‘typical’ antipsychotics such as benperidol are an older class of antipsychotic than second generation ‘atypical’ antipsychotics. They are used primarily to treat positive symptoms including the experiences of perceptual abnormalities (hallucinations) and fixed, false, irrational beliefs (delusions). First generation antipsychotics may cause side effects which can differ depending on which antipsychotic is being administered and on individual differences in reaction to the drug. Reactions may include dyskinesias such as repetitive, involuntary, and purposeless body or facial movements, Parkinsonism (cogwheel muscle rigidity, pill-rolling tremor and reduced or slowed movements), akathisia (motor restlessness, especially in the legs, and resembling agitation) and dystonias such as muscle contractions causing unusual twisting of parts of the body, most often in the neck. These effects are caused by the dopamine receptor antagonist action of these drugs.

What is the evidence for benperidol?

Low quality evidence is unable to determine the benefits or harms of benperidol over perphenazine.

October 2020

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First generation ‘typical’ antipsychotics such as bromperidol are an older class of antipsychotic than second generation ‘atypical’ antipsychotics. They are used primarily to treat positive symptoms including the experiences of perceptual abnormalities (hallucinations) and fixed, false, irrational beliefs (delusions). First generation antipsychotics may cause side effects which can differ depending on which antipsychotic is being administered and on individual differences in reaction to the drug. Reactions may include dyskinesias such as repetitive, involuntary, and purposeless body or facial movements, Parkinsonism (cogwheel muscle rigidity, pill-rolling tremor and reduced or slowed movements), akathisia (motor restlessness, especially in the legs, and resembling agitation) and dystonias such as muscle contractions causing unusual twisting of parts of the body, most often in the neck. These effects are caused by the dopamine receptor antagonist action of these drugs.

What is the evidence for bromperidol?

Moderate to low quality evidence suggests depot fluphenazine decanoate and depot haloperidol decanoate may result in less relapses than depot bromperidol decanoate. Moderate to low quality evidence suggests no differences in adverse effects between these medications.

October 2020

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First generation ‘typical’ antipsychotics such as chlorpromazine are an older class of antipsychotic than second generation ‘atypical’ antipsychotics. They are used primarily to treat positive symptoms including the experiences of perceptual abnormalities (hallucinations) and fixed, false, irrational beliefs (delusions). First generation antipsychotics may cause side effects which can differ depending on which antipsychotic is being administered and on individual differences in reaction to the drug. Reactions may include dyskinesias such as repetitive, involuntary, and purposeless body or facial movements, Parkinsonism (cogwheel muscle rigidity, pill-rolling tremor and reduced or slowed movements), akathisia (motor restlessness, especially in the legs, and resembling agitation) and dystonias such as muscle contractions causing unusual twisting of parts of the body, most often in the neck. These effects are caused by the dopamine receptor antagonist action of these drugs.

What is the evidence for chlorpromazine?

Moderate quality evidence finds chlorpromazine reduces rates of relapse and improves symptoms and functioning more than placebo, although chlorpromazine is more sedating, causes more lowering of blood pressure and more weight gain. For chlorpromazine dose, there was greater improvement in global state with high-dose (2gms/day) than low-dose (≤400mg/day) chlorpromazine, but less dystonia and extrapyramidal effects with low-dose chlorpromazine.

Compared to first-generation haloperidol, there was some benefit of chlorpromazine for sedation, but less benefit for any global improvement and study retention. Compared to first-generation piperacetine, there were no differences in global state, mental state or leaving the study early. Compared to first-generation metiapine, there were no differences in clinical improvement, and compared to first-generation penfluridol, there were no differences in leaving the study early. Movement disorders may be more frequent with haloperidol, while chlorpromazine was associated with more hypotension. The need for additional antiparkinsonian medication was less with chlorpromazine than with penfluridol.

Conpared to second-generation clotiapine, moderate to low quality evidence finds no differences in leaving the study early. Lower quality evidence is unable to determine any differences in symptoms or in rates of dyskinesia.

October 2020

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First generation ‘typical’ antipsychotics such as droperidol are an older class of antipsychotic than second generation ‘atypical’ antipsychotics. They are used primarily to treat positive symptoms including the experiences of perceptual abnormalities (hallucinations) and fixed, false, irrational beliefs (delusions). First generation antipsychotics may cause side effects which can differ depending on which antipsychotic is being administered and on individual differences in reaction to the drug. Reactions may include dyskinesias such as repetitive, involuntary, and purposeless body or facial movements, Parkinsonism (cogwheel muscle rigidity, pill-rolling tremor and reduced or slowed movements), akathisia (motor restlessness, especially in the legs, and resembling agitation) and dystonias such as muscle contractions causing unusual twisting of parts of the body, most often in the neck. These effects are caused by the dopamine receptor antagonist action of these drugs.

What is the evidence for droperidol?

Moderate quality evidence shows that droperidol had benefit over haloperidol for less need for an additional injection, with no differences in sedation or need for benzodiazepines.

October 2020

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First-generation ‘typical’ antipsychotics are an older class of antipsychotic than second-generation ‘atypical’ antipsychotics. First-generation antipsychotics are used primarily to treat positive symptoms such as hallucinations and delusions. Second-generation antipsychotics are also effective for the positive symptoms of schizophrenia, and it is sometimes claimed that they are more effective than first-generation antipsychotics in treating the negative symptoms of schizophrenia. Negative symptoms include a lack of ordinary mental activities such as emotional expression, social engagement, thinking and motivation. High potency first-generation antipsychotics usually have high affinity for the dopamine receptor and therefore induce extrapyramidal side effects by the blockade of these dopamine receptors. Extrapyramidal side effects include dyskinesias (repetitive, involuntary, and purposeless body or facial movements), Parkinsonism (cogwheel muscle rigidity, pill-rolling tremor and reduced or slowed movements); akathisia (motor restlessness, especially in the legs, and resembling agitation), and dystonias (muscle contractions causing unusual twisting of parts of the body, most often in the neck). Second-generation antipsychotics generally have a lower affinity for the dopamine receptor and also block serotonin receptors, so may be associated with lower risk of these side effects.

What is the evidence for first versus second-generation antipsychotics?

Efficacy

Moderate to high quality evidence suggests a small effect of improved overall symptoms with second-generation antipsychotics, particularly olanzapine, amilsulpride, and risperidone, compared to first-generation antipsychotics, particularly high-dose haloperidol (>12mg/day), which is not as effective as lower doses. There is a small effect of less all-cause study discontinuation with olanzapine, risperidone, or amisulpride compared to haloperidol in the short-term. Moderate quality evidence suggests only olanzapine may result in less long-term discontinuation due to drug intolerability or inefficiency. Moderate to high quality evidence suggests olanzapine and risperidone may improve cognition more effectively than haloperidol, and moderate quality evidence suggests amisulpride, clozapine and sertindole may improve quality of life more effectively than first-generation antipsychotics in general.

Side effects

Moderate quality evidence suggests a medium-sized effect of less extrapyramidal side effects with second-generation antipsychotics, particularly olanzapine and risperadone, than with haloperidol. Clozapine, olanzapine, and risperidone may also produce fewer extrapyramidal side effects when compared to low-potency first-generation antipsychotics. Moderate quality evidence suggests clozapine, quetiapine, and zotepine may be more sedating, and aripiprazole less sedating, than haloperidol. Compared with low-potency first-generation antipsychotics, only clozapine may be more sedating. Moderate to high quality evidence suggests less use of benzodiazapines, anticholinergeric medications, and beta-blockers with olanzapine than with haloperidol. Moderate quality evidence suggests amisulpride, clozapine, olanzapine, quetiapine, risperidone, sertindole, and zotepine may be associated with more weight gain than haloperidol, with no differences when compared to low-potency first-generation antipsychotics. Moderate quality evidence suggests more cholesterol change with olanzapine than haloperidol, and more tryglyceride change with amisulpride than haloperidol.

October 2020

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Pending enough primary studies, we invite reviews on this topic to be conducted. Alternatively, we will endeavour to conduct our own review to fill this gap in the Library.

October 2020

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First generation ‘typical’ antipsychotics such as fluphenazine are an older class of antipsychotic than second generation ‘atypical’ antipsychotics. They are used primarily to treat positive symptoms including the experiences of perceptual abnormalities (hallucinations) and fixed, false, irrational beliefs (delusions). First generation antipsychotics may cause side effects which can differ depending on which antipsychotic is being administered and on individual differences in reaction to the drug. Reactions may include dyskinesias such as repetitive, involuntary, and purposeless body or facial movements, Parkinsonism (cogwheel muscle rigidity, pill-rolling tremor and reduced or slowed movements), akathisia (motor restlessness, especially in the legs, and resembling agitation) and dystonias such as muscle contractions causing unusual twisting of parts of the body, most often in the neck. These effects are caused by the dopamine receptor antagonist action of these drugs.

What is the evidence for fluphenazine?

Compared to placebo, moderate quality evidence suggests less risk of relapse with oral fluphenazine, however oral fluphenazine may result in drowsiness, akathisia and rigidity. Moderate to high quality evidence suggests no differences in acceptibility or response to treatment between oral fluphenazine and low-potency first generation antipsychotics. Moderate to low quality evidence suggests no differences in relapse rates between fluphenazine decanoate and first or second generation antipsychotics. There is less risk of movement disorders with fluphenazine decanoate than with pimozide or fluphenazine hydrochloride, but more risk of akathisia, dystonia, loss of associated movement, rigor, and tremor with oral fluphenazine than with low-potency first generation antipsychotics. There is greater risk of dizziness, drowsiness, sedation, dry mouth, nausea, and vomiting with low-potency first generation antipsychotics than with oral fluphenazine.

October 2020

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First generation ‘typical’ antipsychotics such as fluspirilene are an older class of antipsychotic than second generation ‘atypical’ antipsychotics. They are used primarily to treat positive symptoms including the experiences of perceptual abnormalities (hallucinations) and fixed, false, irrational beliefs (delusions). First generation antipsychotics may cause side effects which can differ depending on which antipsychotic is being administered and on individual differences in reaction to the drug. Reactions may include dyskinesias such as repetitive, involuntary, and purposeless body or facial movements, Parkinsonism (cogwheel muscle rigidity, pill-rolling tremor and reduced or slowed movements), akathisia (motor restlessness, especially in the legs, and resembling agitation) and dystonias such as muscle contractions causing unusual twisting of parts of the body, most often in the neck. These effects are caused by the dopamine receptor antagonist action of these drugs.

What is the evidence for fluspirilene?

Low quality evidence is unable to determine the benefits or harms of fluspirilene over placebo or other first generation antipsychotics.

October 2020

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First generation ‘typical’ antipsychotics such as haloperidol are an older class of antipsychotic than second generation ‘atypical’ antipsychotics. They are used primarily to treat positive symptoms including the experiences of perceptual abnormalities (hallucinations) and fixed, false, irrational beliefs (delusions). First generation antipsychotics may cause side effects which can differ depending on which antipsychotic is being administered and on individual differences in reaction to the drug. Reactions may include dyskinesias such as repetitive, involuntary, and purposeless body or facial movements, Parkinsonism (cogwheel muscle rigidity, pill-rolling tremor and reduced or slowed movements), akathisia (motor restlessness, especially in the legs, and resembling agitation) and dystonias such as muscle contractions causing unusual twisting of parts of the body, most often in the neck. These effects are caused by the dopamine receptor antagonist action of these drugs.

What is the evidence for haloperidol?

High quality evidence shows haloperidol results in greater clinical improvement and study retention than placebo. Moderate to high quality evidence suggests haloperidol is also more effective for sedation and agitation. However, haloperidol may cause more movement disorders and may increase the risk of one or more other adverse effects than placebo.

High quality evidence shows no differences in clinical improvement between haloperidol and chlorpromazine. Moderate to low quality evidence suggests no differences in clinical response or leaving the study for any reason between haloperidol and low-potency first generation antipsychotics. There may be more movement disorders, but less sedation, dizziness, orthostasis problems and weight gain with haloperidol than with low-potency first generation antipsychotics.

Moderate quality evidence suggests haloperidol is associated with less improvement in mental state and less study retention than olanzapine. Olanzapine also had benefits over haloperidol for sedation, and ziprasidone had benefits over haloperidol for global state. Haloperidol was more effective than risperidone for sedation and aggression, and required fewer injections than aripiprazole. Haloperidol plus promethazine was more effective than haloperidol alone for inducing sleep by 20 minutes. Haloperidol caused more insomnia, dyspepsia, dystonia, and extrapyramidal effects, but less nausea, than aripiprazole. Haloperidol resulted in more risk of dystonia and extrapyramidal effects than olanzapine. Haloperidol resulted in less heartbeat change, but more akathisia than risperidone. Haloperidol resulted in more risk of any adverse event, particularly movement disorders, than ziprasidone.

Moderate to high quality evidence suggests no differences in efficacy between 3 to 7.5mg/day and 15 to 35mg/day haloperidol doses, however, high quality evidence suggests more extrapyramidal side effects with 15 to 35mg/day than 3 to 15mg/day. Moderate to low quality evidence also suggests more extrapyramidal side effects with 7.5 to 15mg/day than 3 to 7.5mg/day.

October 2020

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