Absconding refers to the departure of patients from hospital wards without permission. The definition of absconding can vary depending on the length of time required for an absence to be considered absconding, and on the method of departure (e.g. leaving a locked ward, leaving the hospital grounds, or failing to return from day leave). Absconding status is influenced by the patient’s admission, whether it be voluntary, involuntary, or legally detained. There are significant implications of absconding for patients, carers and family members.

What is the evidence for absconding?

Moderate to low quality evidence suggests inpatients who abscond are often young men in the first three weeks following admission. Absconding may occur in up to 34% of admissions, and up to 80% of absconders return within 24 hours. A large proportion of absconders indicate intent to leave, and most commonly abscond directly from the ward. There is insufficient evidence regarding interventions for preventing absconding.

August 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.

September 2020

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Acupuncture involves the stimulation of specific acupoints by inserting needles into the skin. Laser acupuncture is essentially the same as needle acupuncture except that laser beams are used instead of needles. Electro-acupuncture uses a pair of needles attached to an electrical device that generates continuous electric pulses that pass from one needle to the other.

What is the evidence for acupuncture for schizophrenia?

Moderate quality evidence suggests general improvement in symptoms of schizophrenia with needle or electro-acupuncture in conjunction with or without, antipsychotic medications compared to antipsychotics alone. Low quality evidence is uncertain of the benefits of laser acupuncture. Review authors state that study quality is very low and all studies were conducted in China, so results may not be applicable to other populations.

September 2020

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Life events that occur during adulthood are defined as particularly significant experiences that result in substantial changes to personal circumstances. These changes may be positive or they may be negative changes and can occur across all aspects of life, including health, education, employment, relationships, bereavement, housing, legal, and financial issues.

What is the evidence for adult life events as risk factors for schizophrenia?

Moderate quality evidence finds a medium-sized increase in recent adverse life events in people with psychosis compared to people without psychosis, measured between 3 months and 3.6 years prior. There was a small association between increased rates of neighbourhood crime and increased rates of psychosis.

Moderate to low quality evidence suggests a small increase in prevalence, and a medium to large increase in incidence of subclinical psychotic symptoms in people reporting prior exposure to stress and trauma. There was a medium-sized increase in perceived stress, but not adverse events, in people at ultra high-risk for psychosis; those with attenuated psychotic symptoms or brief and limited intermittent psychotic symptoms, genetic risk, and functional deterioration.

April 2022

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Differences are observed in the age at onset of psychotic symptoms, which may be influenced by genetic or environmental risk factors, or sex. Understanding the factors that impact on age at the onset of symptoms could lead to better understanding of the risk factors for the disorder and earlier and improved intervention strategies.

What is the evidence for age at onset of schizophrenia?

Moderate to high quality evidence suggests the median age at onset of schizophrenia is around 25 years old. The incidence (i.e., new cases) of schizophrenia is higher in males up until around 40 years of age, then higher in females after around 50 years of age. Substance use, in particular cannabis, is associated with an earlier age at onset of psychosis, with no effect of tobacco use. There was also a small effect of an earlier age at onset in people with a family history of psychosis.

Moderate quality evidence finds small associations between an earlier age at onset and more hospitalisations, more negative, but not positive symptoms, more relapses, poorer overall functioning, and poorer overall clinical outcomes (in males only).

March 2022

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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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Second generation antipsychotics (sometimes referred to as ‘atypical’ antipsychotics) such as amisulpride are a newer class of antipsychotic medication than first generation ‘typical’ antipsychotics. Second generation antipsychotics are effective for the positive symptoms of schizophrenia. 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, whereas positive symptoms include the experiences of perceptual abnormalities (hallucinations) and fixed, false, irrational beliefs (delusions).

Second generation antipsychotics may also cause less extra-pyramidal side effects. These 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 amisulpride?

High quality evidence suggests amisulpride may retain more patients in treatment, and be more effective for global state and negative symptoms than placebo. Moderate quality evidence suggests amisulpride may cause more extrapyramidal symptoms than placebo.

High quality evidence suggests amisulpride may retain more patients in treatment, and be more effective for global state, mental state and negative symptoms, but not positive symptoms, than first generation antipsychotics. Amisulpride may be less likely to cause at least one adverse event or extrapyramidal symptom when compared to first generation antipsychotics.

Moderate quality evidence suggests no differences in any outcome compared to other second generation antipsychotics in general. Moderate to low quality evidence suggests fewer people leaving the study early due to inefficacy with amisulpride compared to ziprasidone. Moderate to high quality evidence suggests amisulpride is associated with less weight gain than risperidone or olanzapine. Moderate quality evidence suggests agitation may be reported more often by patients receiving amisulpride than other second generation antipsychotics, with no difference in cardiac effects or extrapyramidal symptoms between amisulpride and risperidone, olanzapine or ziprasidone.

October 2020

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Amphetamines are potent stimulants that are used to treat attention deficit hyperactivity disorder, narcolepsy, and obesity. Amphetamines may also be related to an increased risk, or worsening, of psychoic symptoms. Amphetamines are not suggested as an adjuctive treatment, but rather as an investigation into their effects on symptoms.

What is the evidence for amphetamines?

Moderate quality evidence suggests single-dose dexamfetamine or methylphenidate increases severity or frequency of positive symptoms, particularly in patients who are not in remission. Compared to placebo, moderate to low quality evidence finds no benefit for cognition.

September 2020

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The amygdala is located deep in the medial temporal lobe, and has reciprocal connections with many regions of the cortex, such as prefrontal and cingulate cortex, as well as sub-cortical regions such as the brainstem and hippocampus. The amygdala is implicated in the processing and memory of emotional responses, particularly emotional learning, as well as mediating the autonomic expression of emotion.

What is the evidence for amygdala alterations?

Moderate to high quality evidence found reduced grey matter volume in the amygdala and the amygdala-hippocampus region of people with schizophrenia compared to controls. There were also reductions in the amygdala of first-episode patients and relatives of people with schizophrenia.

Compared to people with bipolar disorder, moderate to low quality evidence finds a medium-sized effect of reduced amygdala volume in people with schizophrenia.

Moderate quality evidence found people with schizophrenia showed increased activity in the amygdala during executive function tasks, and increased or decreased activity during emotion processing tasks.

October 2020

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