schizophrenia case study female

Module 11: Schizophrenia Spectrum and Other Psychotic Disorders

Case studies: schizophrenia spectrum disorders, learning objectives.

Identify schizophrenia and psychotic disorders in case studies

Case Study: Bryant

Thirty-five-year-old Bryant was admitted to the hospital because of ritualistic behaviors, depression, and distrust. At the time of admission, prominent ritualistic behaviors and depression misled clinicians to diagnose Bryant with obsessive-compulsive disorder (OCD). Shortly after, psychotic symptoms such as disorganized thoughts and delusion of control were noticeable. He told the doctors he has not been receiving any treatment, was not on any substance or medication, and has been experiencing these symptoms for about two weeks. Throughout the course of his treatment, the doctors noticed that he developed a catatonic stupor and a respiratory infection, which was identified by respiratory symptoms, blood tests, and a chest X-ray. To treat the psychotic symptoms, catatonic stupor, and respiratory infection, risperidone, MECT, and ceftriaxone (antibiotic) were administered, and these therapies proved to be dramatically effective. [1]

Case Study: Shanta

Shanta, a 28-year-old female with no prior psychiatric hospitalizations, was sent to the local emergency room after her parents called 911; they were concerned that their daughter had become uncharacteristically irritable and paranoid. The family observed that she had stopped interacting with them and had been spending long periods of time alone in her bedroom. For over a month, she had not attended school at the local community college. Her parents finally made the decision to call the police when she started to threaten them with a knife, and the police took her to the local emergency room for a crisis evaluation.

Following the administration of the medication, she tried to escape from the emergency room, contending that the hospital staff was planning to kill her. She eventually slept and when she awoke, she told the crisis worker that she had been diagnosed with attention-deficit/hyperactive disorder (ADHD) a month ago. At the time of this ADHD diagnosis, she was started on 30 mg of a stimulant to be taken every morning in order to help her focus and become less stressed over the possibility of poor school performance.

After two weeks, the provider increased her dosage to 60 mg every morning and also started her on dextroamphetamine sulfate tablets (10 mg) that she took daily in the afternoon in order to improve her concentration and ability to study. Shanta claimed that she might have taken up to three dextroamphetamine sulfate tablets over the past three days because she was worried about falling asleep and being unable to adequately prepare for an examination.

Prior to the ADHD diagnosis, the patient had no known psychiatric or substance abuse history. The urine toxicology screen taken upon admission to the emergency department was positive only for amphetamines. There was no family history of psychotic or mood disorders, and she didn’t exhibit any depressive, manic, or hypomanic symptoms.

The stimulant medications were discontinued by the hospital upon admission to the emergency department and the patient was treated with an atypical antipsychotic. She tolerated the medications well, started psychotherapy sessions, and was released five days later. On the day of discharge, there were no delusions or hallucinations reported. She was referred to the local mental health center for aftercare follow-up with a psychiatrist. [2]

Another powerful case study example is that of Elyn R. Saks, the associate dean and Orrin B. Evans professor of law, psychology, and psychiatry and the behavioral sciences at the University of Southern California Gould Law School.

Saks began experiencing symptoms of mental illness at eight years old, but she had her first full-blown episode when studying as a Marshall scholar at Oxford University. Another breakdown happened while Saks was a student at Yale Law School, after which she “ended up forcibly restrained and forced to take anti-psychotic medication.” Her scholarly efforts thus include taking a careful look at the destructive impact force and coercion can have on the lives of people with psychiatric illnesses, whether during treatment or perhaps in interactions with police; the Saks Institute, for example, co-hosted a conference examining the urgent problem of how to address excessive use of force in encounters between law enforcement and individuals with mental health challenges.

Saks lives with schizophrenia and has written and spoken about her experiences. She says, “There’s a tremendous need to implode the myths of mental illness, to put a face on it, to show people that a diagnosis does not have to lead to a painful and oblique life.”

In recent years, researchers have begun talking about mental health care in the same way addiction specialists speak of recovery—the lifelong journey of self-treatment and discipline that guides substance abuse programs. The idea remains controversial: managing a severe mental illness is more complicated than simply avoiding certain behaviors. Approaches include “medication (usually), therapy (often), a measure of good luck (always)—and, most of all, the inner strength to manage one’s demons, if not banish them. That strength can come from any number of places…love, forgiveness, faith in God, a lifelong friendship.” Saks says, “We who struggle with these disorders can lead full, happy, productive lives, if we have the right resources.”

You can view the transcript for “A tale of mental illness | Elyn Saks” here (opens in new window) .

Bai, Y., Yang, X., Zeng, Z., & Yang, H. (2018). A case report of schizoaffective disorder with ritualistic behaviors and catatonic stupor: successful treatment by risperidone and modified electroconvulsive therapy. BMC psychiatry , 18(1), 67. https://doi.org/10.1186/s12888-018-1655-5 ↵
Henning A, Kurtom M, Espiridion E D (February 23, 2019) A Case Study of Acute Stimulant-induced Psychosis. Cureus 11(2): e4126. doi:10.7759/cureus.4126 ↵
Modification, adaptation, and original content. Authored by : Wallis Back for Lumen Learning. Provided by : Lumen Learning. License : CC BY: Attribution
A tale of mental illness . Authored by : Elyn Saks. Provided by : TED. Located at : https://www.youtube.com/watch?v=f6CILJA110Y . License : Other . License Terms : Standard YouTube License
A Case Study of Acute Stimulant-induced Psychosis. Authored by : Ashley Henning, Muhannad Kurtom, Eduardo D. Espiridion. Provided by : Cureus. Located at : https://www.cureus.com/articles/17024-a-case-study-of-acute-stimulant-induced-psychosis#article-disclosures-acknowledgements . License : CC BY: Attribution
Elyn Saks. Provided by : Wikipedia. Located at : https://en.wikipedia.org/wiki/Elyn_Saks . License : CC BY-SA: Attribution-ShareAlike
A case report of schizoaffective disorder with ritualistic behaviors and catatonic stupor: successful treatment by risperidone and modified electroconvulsive therapy. Authored by : Yuanhan Bai, Xi Yang, Zhiqiang Zeng, and Haichen Yangcorresponding. Located at : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5851085/ . License : CC BY: Attribution

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Early-Onset Schizophrenia With Predominantly Negative Symptoms: A Case Study of a Drug-Naive Female Patient Treated With Cariprazine

Affiliation.

1 Institute of Genomic Medicine and Rare Disorders, Semmelweis University, Budapest, Hungary.
PMID: 32390838
PMCID: PMC7191004
DOI: 10.3389/fphar.2020.00477

Schizophrenia is a chronic and severe mental disorder characterized by positive, negative, and cognitive symptoms. Negative symptoms are usually present from the prodromal phase; early diagnosis and management of negative symptoms is a major health concern since an insidious onset dominated by negative symptoms is associated with a worse outcome. Antipsychotic medications, which are effective for treating positive symptoms, are generally ineffective for treating negative or cognitive symptoms. We present a 23-year-old woman showing severe symptoms at her first visit to our department. The patient's parents reported that their daughter had experienced several years of psychosocial decline and putative psychiatric symptoms, but no medical attention had been previously sought; as such, the diagnosis of schizophrenia with predominantly negative symptoms was very much delayed. Early onset of schizophrenia, longer duration of untreated psychosis, and severe negative symptoms, which have limited treatment options, suggested a poor prognosis. We initiated monotherapy with cariprazine, a novel antipsychotic that has recently been proven efficacious in treating schizophrenia with predominantly negative symptoms. This report describes a 52-week cariprazine treatment regimen and follows the patient's impressive clinical improvement confirmed by PANSS and CGI scores, and psychological tests.

Keywords: cariprazine; early-onset schizophrenia; negative symptoms; schizophrenia; second-generation antipsychotic.

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Published: 01 May 2020

The clinical course of schizophrenia in women and men—a nation-wide cohort study

Iris E. Sommer 1 ,
Jari Tiihonen 2 , 3 , 4 ,
Anouk van Mourik 1 ,
Antti Tanskanen 2 , 3 &
Heidi Taipale 2 , 3 , 5

npj Schizophrenia volume 6 , Article number: 12 ( 2020 ) Cite this article

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Schizophrenia

Gender differences in schizophrenia have been reported in different aspect of the course of disease and may urge special clinical interventions for female patients. Current literature provides insufficient information to design guidelines for treating women with schizophrenia. We aim to quantify the clinical course of schizophrenia in men and women on premorbid hospitalizations and prescription drugs, age at diagnosis, pharmacological treatment, comorbidity, number of re-hospitalizations, and mortality. Our nationwide cohort study included all patients admitted for the first time to hospital during 2000–2014 for schizophrenia or schizo-affective disorder in Finland. Gender differences were compared with logistic regression, by calculating incidence rates, and mortality was assessed with Cox proportional hazard model. We included 7142 women and 9006 men with schizophrenia/schizo-affective disorder and found that both women (71%) and men (70%) had often been hospitalized for another psychiatric disorder in the 5 years before diagnosis. In women, the last psychiatric hospitalization before schizophrenia/schizo-affective diagnosis was often for mood disorders (62%, OR 2.56, 95% CI 2.28–2.87). Men were diagnosed earlier (mean 34.4 [SD12.6] vs. 38.2 [SD 13.8]) with peak incidence around 22, while incidence in women declining only slowly between age 18 and 65. During ten years follow-up, 69.5% of both genders needed at least one re-hospitalization, with slightly more hospitalizations in women. Women were less often prescribed clozapine or long-acting antipsychotics. Mortality was lower in women (HR = 0.54, 95% CI 0.50–0.60), with fewer suicide and cardiovascular deaths, but more cancer deaths. These results suggest a diagnostic delay for women, which might be shortened by screening women aged 20–65 participating in affective disorder programs. As number of hospitalizations is not lower for women, clinicians should take care not to undertreat women with schizophrenia.

Understanding sex differences in long-term outcomes after a first episode of psychosis

Incidence, prevalence, and global burden of schizophrenia - data, with critical appraisal, from the Global Burden of Disease (GBD) 2019

Large-scale real-world data analysis identifies comorbidity patterns in schizophrenia

Introduction.

Gender differences in schizophrenia affect many domains, including premorbid trajectory, incidence, symptoms, comorbidity, outcome, and mortality 1 , 2 , 3 . The most consistently reported gender difference is the higher age at onset in women 2 , 3 . After diagnosis, the course of disease may also vary between the genders, but literature is less consistent on this aspect 4 , 5 , 6 , 7 , 8 , 9 . Symptoms of schizophrenia may be gender dimorphic too, with approximately half of the studies showing more depressive symptoms in women and more negative symptoms in men, and the other half showing no difference 5 . Women may have the additional benefit of responding better to treatment, yet this benefit appears to dissipate with advancing age 4 . Comorbid substance abuse is higher in men, which applies to cannabis, cocaine, hallucinogens and alcohol, while depression is more common in women 6 , 7 . High prevalence of substance abuse in men with schizophrenia may contribute both to earlier onset and to more severe course in men as compared to women. Mortality has been reported less frequently, with some studies indicating similar rates in men and women 8 , 9 , 10 , but a recent meta-analysis showing higher mortality in men 9 . In sum, gender differences are present in schizophrenia, with most consistent findings for later onset in women and less consistent data on a possibly better course in and lower mortality in women. This raises the question: if schizophrenia expresses itself different in women than in men, should we develop different guidelines for (early) diagnosis and treatment of women? We could envision different expectations about prognosis, specific treatment for comorbidities, and perhaps milder pharmacological treatment. For both men and women with schizophrenia, duration of untreated psychosis (DUP) is an important predictor of outcome 10 . Therefore, early detection is another domain that might benefit from a gendered-approach 5 . As the presentation of schizophrenia in women may be less typical than in men, women run the risk for diagnostic delay, potentially reducing their chances for good outcome. Another potential difference between the genders could be the better response to medication in women, which may result in lower relapse rates. Current literature provides insufficient detailed data on the complete course of schizophrenia in men and women to make clear guideline recommendation for diagnosis and treatment for women. What is needed for such guidelines is longitudinal data from a large group of men and women with schizophrenia to assess early trajectory, age and type of diagnosis, morbidity and comorbidity but also mortality in the same patients. In this study, we aim to describe the clinical course of schizophrenia in both genders, including hospitalizations and psychiatric medication use in the premorbid period, age at diagnosis, pharmacological treatment, comorbidity, number of re-hospitalizations, and mortality in the same persons. We use the Finnish registers, which (together with the Danish registers) hold the most complete and longest follow-up data. As affective symptoms are very common in women, we include patients with either schizophrenia or schizo-affective disorders. Since schizo-affective disorder may represents ‘the more female form of schizophrenia’, restricting inclusion to only schizophrenia would introduce selection bias, especially for the women.

We included 16,148 patients with a schizophrenia-spectrum disorder (SSD). Of these, 7142 were women and 9006 men (ratio 1:1.3). SSD consisted of two diagnoses: schizophrenia and schizo-affective disorder. Schizoaffective disorder was diagnosed for 31.2% ( N = 2231) of women and 17.5% ( N = 1577) of men.

Five years before diagnosis of SSD

Most women (71.2%) and men (70.1%) had been hospitalized for another psychiatric disorder (psychotic and/or other) before the first hospitalization for SSD. 47.8% ( N = 3412) of women had been hospitalized for another psychotic disorder, and this resulted into a median of 56 hospital days (IQR 24–115), while the median number of hospital days for any psychiatric diagnosis (from 70.5% of women, N = 5038) was 81 (IQR 34–178). In men, the median number of hospital days for another psychotic disorder before SSD was 53 (IQR 21–109) for 48.5% of men ( N = 4368), with corresponding median of hospital days due to any psychiatric diagnosis of 65 (IQR 25–146, 69.4% of men, ( N = 6252).

Significant differences occurred in type of diagnoses in the trajectory before SSD, with more frequent mood disorders (with and without mania), anxiety disorders, eating disorders, post-traumatic stress disorder, dissociative disorder, personality disorder, suicide attempts, and self-harm in women (Table 1 ). Men had more often substance disorder and more autism spectrum disorders. The largest gender differences were found for eating disorder (ten times more prevalent for women) and substance abuse, for which women had less than half the risk as men (Table 1 ).

Gender differences in the age of first hospitalization were most pronounced for eating disorders, occurring much earlier in women (mean age in women 21.6, SD 7.9, against 29.4, SD 12.8, in men, p < 0.0001). For women, mood disorder (with and without mania combined) was the most common last diagnosis preceding SSD in 62% (against only 39% in men) (Fig. 1 ). For men, 34% was hospitalized for substance disorder preceding the SSD hospitalization (against only 10% for women).

The vast majority of both women (78%) and men (72%) already used antipsychotic medication before SSD diagnoses. Antidepressants were also used by more than half of women (59%) and men (51%). Benzodiazepine use was high amongst both genders (48% for women and 41% for men), but use of benzodiazepines was started relatively late in the premorbid trajectory. Overall, men started earlier with the use of psychiatric medications than women, but women used them more frequently. The order of medication use in both sexes started with SSRIs, followed by other antidepressant medication and ended with benzodiazepines. Women started earlier with mood stabilization, while men started earlier with antipsychotics. Figure 2 shows the medication use (upper arrows) and previous diagnoses (lower arrows) in the premorbid trajectory for women and men.

Age at diagnosis

Men were on average diagnosed earlier (mean 34.4, SD 12.6, median 31, IQR 24–43) than women (mean 38.2, SD 13.8, median 37, IQR 26–50). In women, but not in men, there appears to be a gap between the last hospitalization for another psychiatric disorder and the first hospitalization for SSD of some 4 years (Fig. 1b ), during which half the women start with benzodiazepines (Fig. 2a ). While men showed a peak around the age of 22, with a distribution skewed to the right, women showed a more plateau-like distribution between the ages of 18 and 65, with slightly higher values between the ages of 18 and 35 and only slowly decreasing incidence (Fig. 3 ).

Last recorded non-psychotic diagnosis for women (right) ( n =2263) and men (left) ( n =2615) before hospitalization for SSD, for those who had at least 1 prior hospitalization.

Prevalence and mean age for ( a ) medication use before first hospitalization for schizophrenia-spectrum diagnosis (SSD) and for ( b ) other psychiatric disorders, by gender (men n = 9006, women n = 7142). SSRI: Serotonin reuptake inhibitors.

Age of first recorded schizophrenia-spectrum diagnosis for men ( n =9006) and women ( n = 7142).

Re-hospitalizations after SSD diagnoses

During the follow-up time of up to 10 years (mean 7.9, SD 2.8 for men and 8.2, SD 2.5 for women), 69.5% of men and women had a psychiatric re-hospitalization. Women had a somewhat higher rate of psychiatric re-hospitalizations (incidence rate per 10 person-years 5.18, 95% CI 5.16–5.20) then men (5.12, CI 5.10–5.13).

Per 10 person-years, women had a incidence rate of hospitalizations for psychotic disorders of 4.13 (CI 4.11–4.15) and for other psychiatric disorders of 5.18 (CI 5.16–5.20). In men, numbers were quite similar for psychotic hospitalizations (4.16 CI 4.15–4.18), with slightly lower for other psychiatric disorders (5.12 CI 5.10–5.13). Mean duration of hospitalizations were similar for both genders.

Figure 2 of the Supplementary material shows comorbid psychiatric hospitalizations after SSD for women and men, with more hospitalizations for substance-use disorders in men, but higher frequency of hospitalizations for all other comorbidities in women. Hospitalization for suicide attempts and self-harm was also significantly more prevalent among women (8.2%) than among men (5.9%).

Pharmacotherapy

Medication use during the first 5 years after the first hospitalization for SSD is displayed in Table 2 , showing that 96.6% of women and 94.4% of men used antipsychotic medication. Men more often used clozapine, olanzapine and long-acting antipsychotics, while women more often used quetiapine and aripiprazole. Odds of using antidepressant and mood stabilizing medication was about 40% higher in women. The use of benzodiazepine and zopiclon/zolpidem was significantly higher in women.

During the follow-up (of up to 17 years), 15.4% ( N = 1387) of men and 10.7% ( N = 765) of women died. Mortality rate per 100 person-years was 1.58 (95% CI 1∙57–1∙59) for men and 1.03 (95% CI 1.02–1.04) for women. The hazard ratio (HR) for women was 0.65 (CI 0.60–0.71) as compared to men. When adjusted for age and comorbidity, mortality was still significantly lower in women: HR = 0.54 (95% CI: 0.50–0.60). Men had higher incidence rate of death by suicide (2.90 suicides per 1000 person-years, 95% CI 2.89–2∙91 vs. 1.60, 95% CI 1.59–1.61 in women), cardiovascular disease (4.14 per 1000-person-years, 95% CI 4.13–4∙16 vs. 2.65, 95% CI 2.64–2.66 in women) and other causes (7.25, 95% CI 9.23–9.27 vs. 4.22, 4.21–4.24 in women), whereas women had higher cancer mortality rate (1.82, 1.81–1.83 in women vs. 1.49, 1.48–1.50 in men).

We investigated the clinical trajectory of SSD in women and men using the Finnish Hospital Discharge Register maintained by the National Institute of Health and Welfare. Data were also retrieved from the National Prescription Register. To our knowledge, this is the largest cohort describing the course of illness of SSD before and after diagnosis in a gender specific way.

Our incidence gender ratio of 1:1.3 is close to the 1:1.4 of Jongsma et al. 11 and the gender difference in incidence rates between 1.28 and 1.56 reported for Quebec 12 . The higher incidence in men may partly reflect higher genetic vulnerability and protective effects of estrogens, but higher premorbid substance abuse showed in men is another important contributing factor 13 , 14 . We found that the vast majority of both women (71%) and men (70%) had been admitted to a psychiatric ward before their first hospitalization for SSD, indicating that most patients were already service users at time of diagnosis. In women, the last hospitalization before the SSD diagnosis was for a mood disorder in 61% (Fig. 1 ). Most patients already used psychiatric medication before SSD diagnosis, with the early premorbid phase dominated by the use of antidepressant medication and the later premorbid phase dominated by the use of antipsychotics and finally the use of benzodiazepine.

Age of diagnosis of SSD was relatively late in both sexes (34 in men and 38 in women), which may partly be due to the fact that treatment for SSD had already started under a different psychotic diagnosis, as was the case in 55% of women and 54% of men. Our finding that mean age of onset is relatively old in both sexes (i.e., above 30 years of age) aligns with Haukka et al. 15 , who showed that in individuals belonging to the susceptible part of the population, the risk of developing schizophrenia increases with age, at least up to the age of 40. Age at onset peaked around the age of 22 in men, but showed a more plateau-like phase in women, starting after the age of 20 and only slightly decreasing over the years with annual incidences still between 1 and 2% up until the age of 65. We did not see a clear second “post-menopausal” peak, as previously described 16 . Our gender difference in age of onset for SSD was 4 years, which is markedly more than the 1 year observed in meta-analysis 17 . We found that in women, but not in men, there was gap of 4 years between the last hospitalization in the premorbid trajectory and the first admission for SSD. Given the fact that 71% of women later diagnosed with SSD were already service users, screening for SSD among service users, especially in programs for affective disorders may help to shorten diagnostic delay in female patients. After diagnosis, comorbidity remained strongly gendered with more substance abuse in men, but other comorbidities, especially mood disorders, being more frequent in women. Suicide attempts and self-harm was also higher in women both before and after SSD diagnosis. Medication use during the first five years after diagnosis differed for antipsychotics: women slightly more often used antipsychotics than men (OR 1.7), with more prescriptions for quetiapine and aripiprazole and fewer for clozapine, olanzapine and long-acting medication. This suggests that women receive on average less effective types of medication than men. We also found a gender difference for other psychiatric medication: more often antidepressants, mood stabilizers, benzodiazepines and other sedatives for women as compared to men. The higher use of sedatives in women is remarkable, as comorbid substance abuse is lower in women. It could be a by-product of the choice for less sedative antipsychotic regimen in women (i.e. clozapine and olanzapine).

During the follow-up time of ten years, 69.5% of both women and men needed at least one psychiatric re-hospitalization, with slightly more hospitalizations for women and similar mean duration. This suggests that relapse rate, one of the reasons for re-hospitalization is similar among men and women. As these data provide no evidence of a milder course in women, caution should be taken not to underestimate female schizophrenia. The choice for less effective antipsychotics in women (i.e., fewer prescriptions for clozapine and long-acting antipsychotics) may underlie this lack in female advantage for re-hospitalizations. Despite women in this sample being some 4 years older, women had about 50% lower relative risk of death. Suicide and cardiovascular deaths were more common in men, while women had more deaths caused by cancer. Our gender difference in mortality aligns with worldwide meta-analytic data 9 . This large gender difference in mortality may partly result from healthier life style in women (lower nicotine and other substance abuse) and partly from lower mortality rate due to suicide in women. Thus, despite lower rates of suicide attempts, death by suicide is considerably higher in men (almost 3 per 1000 person-years in the unrestricted follow-up of up to 17 years after diagnosis). This gender difference probably results from the more aggressive methods for suicide attempts used by men as compared to women.

Although most of our findings align with previous reports, we provide new insights on two main points. One important new finding is that there seems to be a gap between age 34 (last hospitalization before diagnosis of SSD) and age 38 (first hospitalization for SSD) (Fig. 2 ), which is suspect for a diagnostic delay in women. The premorbid trajectory of women is less specific and it may be harder to identify SSD in women at an early stage. For example, in women the last hospitalization before diagnosis of schizophrenia is typically for a mood disorder, which may increase the risk of being misdiagnosed as having psychotic depression. Also, higher rates of self-harm and suicide attempts may increase the risk of being misdiagnosed as borderline personality disorder. In Norway, the average time after first presentation until diagnosis of SSD in women was 2.6 years, which is a full year longer than for men 18 , which is probably the same in other countries. Another Norwegian study showed that DUP correlated to severity of depressive symptoms for women, but not for men 19 . It could indicate that the stress of a long DUP generates depressive symptoms per se, but it is also possible that women are more often misdiagnosed as suffering from (psychotic) depression instead of psychosis and that this in turn leads to a delay in treatment. The female premorbid period might be shortened by screening women participating in other treatment programs, especially those for affective disorder for early symptoms of SSD, for example using the Comprehensive Assessment of At Risk Mental States (CAARMS) 20 . As incidence of SSD remains high in women between age 18 and 65, early recognition programs for women should not focus on young adults, but include the full age range. Our second new finding is that women do not have fewer re-hospitalizations than men, neither for psychosis, nor for other psychiatric disorders, which does not support a milder course in women previously reported 21 , 22 , 23 . In line with our finding, a meta-analysis also found largely similar recovery rates for women (12.9%) and men (12.1%) 24 . These findings repudiate the milder course of illness and issue a warning against undertreatment of women with SSD. Pharmacotherapy should certainly take gender into account, as there are sex differences in pharmacokinetics, liver enzymes and renal elimination, which necessitate dose-adjustment for both oral and injectable antipsychotics. Given the sex difference in CYP enzyme activity and dopamine D2 receptor occupancy, women on average need lower dose for olanzapine and clozapine 25 . However, given their equally high risk for re-hospitalization compared to men, women should not be prescribed less effective antipsychotic options. Thus, treatment with clozapine and long-acting antipsychotics should be considered for women just as much as for men. Finally, women with schizophrenia may have a different course, but not necessarily a lighter course. The findings that women have more frequent comorbid depression, more frequent mania, more self-harm and more suicide attempts, together with the higher use of antidepressants, mood stabilizers and sedatives indicate that the female trajectory of schizophrenia is on average more towards the bipolar spectrum as compared to men. Higher prescriptions of sedative drugs in women may reflect higher levels of distress. Suicide attempts and self-harm, clear signs of high levels of distress were higher in women too. Together with the high prevalence of comorbid depression, suffering may actually be higher in women with SSD as compared to men 26 .

The Finnish registers have clear advantages, most importantly; there is no selection bias, as all patients are automatically registered as such and there is hardly any lost to follow-up. In cohort studies and RCTs, patients with suicidality, aggressive incidents, substance abuse and severe comorbidities are often underrepresented, which is not the case in registry studies, providing real-life data. Also, the sample is larger than in RCTs or cohort studies and follow-up time is long.

The fact that diagnoses are clinician-based makes this cohort comparable to clinical practice, which is a clear advantage. However, this also implies that diagnoses may be made based on the stereotype schizophrenia picture, which men resemble more than women do. In addition, the mere fact that patients were female may also have prolonged diagnostic delay, as previous experiments showed that women with similar symptoms as men more often receive a diagnosis other than schizophrenia 18 . We believe that the Finnish health care system is comparable to that of most other European countries, Australia, Canada and Israel, which makes our findings representative for at least part of the world. Potential disadvantage is that not all information is available. For example, details on symptom severity, cognition and dose of medication are lacking. Another disadvantage is that diagnosis is only recorded in combination with hospital admission. As a psychiatric diagnosis is not always coupled to hospital admission, the small part of SSD patients who never were hospitalized was not included in the data on comorbidity and mortality. Previous studies found that in 18% of SSD patients diagnosis and treatment took place in outpatient setting only 4 , 12 , so we may have presented data on comorbidity and mortality of only some 80% of the true Finnish SSD population. To overcome this problem, we also describe medication use in the period before and after diagnosis, which is registered irrespective of hospital admission. In our data, we found large overlap in comorbidities (i.e., diagnoses coupled to hospitalizations) and medication use (irrespective of hospitalization), which indicates that diagnosis at hospitalization is a reasonable reflection of the total distribution of diagnoses.

In conclusion, gender differences are extensive for comorbidity (both before and after diagnosis), age at diagnosis and mortality, while risk for re-hospitalization and mean number of hospitalizations are not gendered. The suggestion of a diagnostic delay in women urge the use of gendered approaches in early detection programs. The absence of lower re-hospitalization rates in women can be taken as a warning not to undertreat women with SSD. Finally, while the course of schizophrenia is different in women, it is not necessarily lighter than in men.

Study population

The base cohort included all persons hospitalized for a schizophrenia-spectrum disorder (SSD) between 1972 and 2014 in Finland 27 . From the base cohort, all patients newly diagnosed with a schizophrenia-spectrum disorder (SSD), consisting of either schizophrenia or schizo-affective disorder (ICD-10: F20 or F25) with ages between 16–65 years, during 2000–2014 in Finland were included. Persons with SSD were identified from the Hospital Discharge register maintained by the National Institute of Health and Welfare. We restricted analyses to persons diagnosed in their working age (16–65 years). Data for this cohort were also retrieved from the National Prescription register (maintained by Social Insurance Institution, 1995–2017, covering all reimbursed prescription medication dispensings), the National Death Register (dates and causes of death 1972–2017) and the Hospital Discharge Register (1972–2017) which includes all inpatient hospital stays in Finland, recorded for all residents. The year 2000 was chosen to ensure follow-up time of at least five years for medication use before the diagnoses of SSD, since the National Prescription Register starts from year 1995. A longer premorbid period would have been informative, but was not feasible using this database. The research project was approved by the ethics committee of the Finnish National Institute for Health and Welfare. Further permissions were granted by pertinent institutional authorities at the National Institute for Health and Welfare of Finland, the Social Insurance Institution of Finland, and Statistics Finland. As this study uses the Registry data, written informed consent was not needed.

Hospitalizations before and after diagnosis

Psychiatric hospitalizations in patients later diagnosed with SSD were assessed during five years before diagnosis. The number and durations of hospitalizations for SSD and prevalence of other psychiatric diagnoses was also determined up to ten years after the index diagnosis. Psychiatric diagnoses were defined on ICD-10 (and ICD-9) basis (Table 1 in the supplementary material ). Information on diagnoses were collected from Hospital Discharge Register data and these diagnoses are recorded during hospitalization. Therefore, we use psychiatric diagnoses made during hospitalization as a reflection of total diagnoses.

Medication use

Medication use was assessed during five years before and after diagnosis with SSD. Data on medication use were obtained from the Finnish Prescription Registry, which is not coupled to diagnosis. Specifications of medications assessed are provided in Supplementary Table 2 . Medication use was modeled with the PRE2DUP method from purchases into drug use periods as previously described in detail 28 .

Mortality after SSD diagnoses was compared between genders. Persons were censored at the end of study follow-up (December 31, 2017). Causes of death were assessed for broad categories (suicide, cardiovascular disease and cancer).

Figure 1 in Supplementary material provides an overview of study design and outcomes.

Statistical analysis

Descriptive statistics were calculated as means with standard deviations (SD). When the distributions were highly skewed, we also calculated medians with interquartile ranges (IQR) and percentages. Prevalences of comorbidities and medication use were compared between women and men (men as reference) with logistic regression and reported as Odds ratios (ORs) with 95% confidence intervals (CI) and p -values. p -values for continuous variables with skewed distributions (age) were calculated with Wilcoxon rank sum test. We used Bonferroni correction for multiple comparisons. Incidence rates were calculated as the number of events divided by person-years. Mortality was assessed with Cox proportional hazard model, with death as an outcome and by censoring to end of follow-up time, and expressed as HRs with 95% CIs.

Reporting summary

Further information on research design is available in the Nature Research Reporting Summary linked to this article.

Data availability

All data generated or analysed during this study are included in this published article (and its supplementary information files ).

Code availability

Codes used are provided in the supplementary information files .

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Acknowledgements

The work of IS is funded by ZonMW, Medical Research Council of the Netherlands, HT is funded by Academy of Finland (grants 315969 and 320107).

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I.S. wrote first version of manuscript and revised using critique from other authors, J.T. provided essential edits and critical comments, A.M. wrote first version of tables and figures and edited final version, A.T. provided data on pharmacological research questions and provided edits to each version, H.T. performed all statistics and helped design plan and edited all versions.

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Sommer, I.E., Tiihonen, J., van Mourik, A. et al. The clinical course of schizophrenia in women and men—a nation-wide cohort study. npj Schizophr 6 , 12 (2020). https://doi.org/10.1038/s41537-020-0102-z

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Our Most Troubling Madness: Case Studies in Schizophrenia Across Cultures

Etheldreda Nakimuli-Mpungu , M.Med.(Psych), Ph.D.

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For the past four decades, most researchers have observed that persons living with schizophrenia in developing countries have better outcomes than their Western counterparts ( 1 , 2 ). This paradox has been attributed to sociocultural differences between the two regions, but the nature of these sociocultural factors has been elusive. For those who are intrigued by this paradox, the volume Our Most Troubling Madness: Case Studies in Schizophrenia Across Cultures , edited by T.M. Luhrmann and Jocelyn Marrow, with contributions from several young anthropologists, is a must read.

This book, in one of the editor’s own words, “examines the way this terrible illness is shaped by its social context: how life is lived with this illness in different settings, and what it is about those settings that alters the course of the illness, its outcome, and even the structure of its symptoms” (p. 2). The book is organized into three sections. The first section starts with a thought-provoking foreword and an introduction to the rest of the book. The second section consists of 12 case studies, which are presented in a detailed and articulate manner, spanning four continents. Each case study illustrates in detail a particular sociocultural context that affects the healing process for schizophrenia. Readers can select which case studies to read based on their interest.

In summary, the case studies confirm the above-mentioned paradox. In developed countries, individuals are quickly labeled as schizophrenic and identify themselves in their day-to-day lives as, “I am schizophrenic.” This diagnosis, which is regarded as a death sentence by Western societies, is a prerequisite for obtaining health care and social services. Therefore, for affected individuals, the diagnosis becomes a part of their identity, which makes them feel less human for the rest of their lives. Worse still, the nature of the health care system does not allow family members to be actively involved in the care of those living with schizophrenia.

In contrast, the several case studies described from developing countries illustrate that although psychiatrists may indicate in patient records that one meets criteria for schizophrenia, psychiatrists may not reveal this diagnosis to the patient and family members and do not share facts about prognosis. As a result, affected individuals and their family members remain hopeful that they will improve, and family members are motivated to actively participate in the care of affected individuals. Moreover, in the developing world, society requires affected individuals only to be able to fulfill their gender and social roles in their households to be regarded as productive members of society, as opposed to the developed world where one is expected to hold a salaried job to be considered a productive member of society.

In the third and last section of the book, the editors conclude that the different social challenges experienced across different settings all have one thing in common, “the experience of social defeat” (p. 197), which they hypothesize to have effects on the body and brain that increase the risk of psychosis. The editors note that opportunities for social defeat are more abundant in developed than in developing countries, and they provide practical suggestions to improve outcomes of schizophrenia in the Western world.

Although this book falls short on details about the early social environment (e.g., perinatal, childhood, and adolescence) for the majority of cases described, it provides a great starting point where one can find the lived “social experience of schizophrenia” (p. 3). Furthermore, the book illustrates how the case studies from developing countries lend support to some of the novel approaches being used to manage schizophrenia in the United States ( 3 , 4 ). For this reason, I believe this book is suitable not only for the general public but also for scientists, clinicians, and policy makers, especially those in the field of global mental health.

The author reports no financial relationships with commercial interests.

1 Holla B, Thirthalli J : Course and outcome of schizophrenia in Asian countries: review of research in the past three decades . Asian J Psychiatr 2015 ; 14:3–12 Crossref , Medline , Google Scholar

2 Kulhara P, Shah R, Grover S : Is the course and outcome of schizophrenia better in the ‘developing’ world? Asian J Psychiatr 2009 ; 2:55–62 Crossref , Medline , Google Scholar

3 Aubry T, Tsemberis S, Adair CE, et al. : One-year outcomes of a randomized controlled trial of Housing First with ACT in five Canadian cities . Psychiatr Serv 2015 ; 66:463–469 Link , Google Scholar

4 Alanen YO : Towards a more humanistic psychiatry: development of need‐adapted treatment of schizophrenia group psychoses . Psychosis 2009 ; 1:156–166 Crossref , Google Scholar

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Schizophrenia
Case Studies
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Social Defeat
Serious Psychotic Disorder
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Early-Onset Schizophrenia With Predominantly Negative Symptoms: A Case Study of a Drug-Naive Female Patient Treated With Cariprazine

Associated data.

All datasets generated for this study are included in the article/supplementary material.

Schizophrenia is a chronic and severe mental disorder characterized by positive, negative, and cognitive symptoms. Negative symptoms are usually present from the prodromal phase; early diagnosis and management of negative symptoms is a major health concern since an insidious onset dominated by negative symptoms is associated with a worse outcome. Antipsychotic medications, which are effective for treating positive symptoms, are generally ineffective for treating negative or cognitive symptoms. We present a 23-year-old woman showing severe symptoms at her first visit to our department. The patient’s parents reported that their daughter had experienced several years of psychosocial decline and putative psychiatric symptoms, but no medical attention had been previously sought; as such, the diagnosis of schizophrenia with predominantly negative symptoms was very much delayed. Early onset of schizophrenia, longer duration of untreated psychosis, and severe negative symptoms, which have limited treatment options, suggested a poor prognosis. We initiated monotherapy with cariprazine, a novel antipsychotic that has recently been proven efficacious in treating schizophrenia with predominantly negative symptoms. This report describes a 52-week cariprazine treatment regimen and follows the patient’s impressive clinical improvement confirmed by PANSS and CGI scores, and psychological tests.

Schizophrenia is a severe, chronic, and heterogeneous mental disorder that often has debilitating long-term outcomes. Its lifetime prevalence rate is estimated to be approximately 1% worldwide in the adult population ( Lehman et al., 2010 ). Onset generally occurs in late adolescence or early adulthood, with an average age of 18 years for men and 25 years for women. 1 The term early-onset schizophrenia (EOS) is used to refer to patients who are diagnosed with the disorder before this age. EOS is a severe, frequently disabling, and chronic condition with a prevalence approaching 0.5% in those younger than 18 years ( Hafner and Van der Heiden, 1997 ).

Schizophrenia is accompanied by a distortion of personality that affects fundamental mental and social functions, making everyday life extremely difficult for patients. Clinical symptoms are often classified in three main domains: positive symptoms, such as hallucinations, delusions, suspiciousness/persecution; negative symptoms, such as emotional withdrawal, blunted affect, and passive social withdrawal; and cognitive symptoms, such as impaired perception, learning, thinking, and memorizing. EOS may be accompanied by greater symptom severity, premorbid developmental impairment, ‘soft’ neurological signs (eg, clumsiness, motor incoordination), and a higher rate of substance abuse ( Hsiao and McClellan, 2008 ; Clemmensen et al., 2012 ; Immonen et al., 2017 ). Accordingly, diagnosis of EOS is often difficult and frequently delayed since onset is more commonly insidious than acute, which makes it difficult to differentiate EOS from underlying cognitive deficits, premorbid functional impairment, or other abnormalities ( Russell, 1994 ; Bartlet, 2014 ). Given this common delay in recognition of the disorder, the duration of untreated psychosis is often very long, further contributing to a poor outcome ( Penttila et al., 2014 ).

Although various hypotheses have been developed, the etiopathogenesis of schizophrenia and EOS is not fully understood ( McGuffin, 2004 ; Klosterkotter et al., 2011 ). 2 Among the rising and falling neurochemical theories, the dopamine hypothesis has remained a primary hypothesis guiding the treatment of schizophrenia. There are four dopaminergic pathways in the human brain: the mesolimbic, the mesocortical, the tuberoinfundibular, and the nigrostriatal. Positive symptoms of schizophrenia are associated with the hyperdopaminergic state of D 2 receptors in the mesolimbic area, while negative and cognitive symptoms are believed to be related to the hypodopaminergic dysregulation of the prefrontal cortex ( Stahl, 2003 ).

Negative symptoms of schizophrenia, which affect up to 60% of patients with schizophrenia ( Rabinowitz et al., 2013 ), form a complex clinical constellation of symptoms that challenge both diagnosis and treatment. By definition, negative symptoms mean the absence of normal functions. Negative symptoms are classified by their etiology as primary negative symptoms, which are core features of the disease itself, and secondary negative symptoms, which are consequences of positive symptoms, antipsychotic treatment, depression or extrapyramidal side effects. Five constructs have been accepted by general consensus as key aspects of negative symptoms: blunted affect, alogia, anhedonia, asociality, and avolition ( Marder and Galderisi, 2017 ). Patients with predominant negative symptoms lose their motivation, cannot function at school or work, and their interpersonal relationships severely decay. Due to impaired daily functioning and social amotivation, they may need constant care.

Although early intervention is associated with improvement in negative symptoms ( Boonstra et al., 2012 ), this may be challenging since negative symptoms develop slowly and may be difficult to detect or differentiate from other clinical features ( Kirkpatrick et al., 2001 ; Galderisi et al., 2018 ). Moreover, a more insidious onset predicts poorer outcome and more severe negative symptoms ( Kao and Liu, 2010 ; Immonen et al., 2017 ; Murru and Carpiniello, 2018 ). Diagnosis of patients with predominantly negative symptoms (lacking manifest psychotic signs) is often delayed, resulting in a longer duration of untreated psychosis. The length of untreated psychosis is closely related to poorer functional outcome ( Perkins et al., 2005 ).

Negative symptoms have traditionally had minimal response to antipsychotic treatment. First-generation antipsychotics are effective in treating positive symptoms, but negative symptom improvement is only evident when symptoms are secondary to positive symptoms. It was initially hoped that second-generation antipsychotics would target both positive and negative symptoms, but efficacy data have been disappointing. This was a large meta-analysis where only four second-generation drugs (amisulpride, risperidone, olanzapine, and clozapine) resulted to be more efficacious than first-generation antipsychotics in the overall change of symptoms, including positive and negative symptoms. The other examined second-generation antipsychotics were only as efficacious as first-generation antipsychotic agents ( Leucht et al., 2009 ). These studies were mainly conducted in patients with general symptoms of schizophrenia, therefore a secondary effect on negative symptoms could not be ruled out. Therefore negative symptom improvement cannot be considered a core component of atypicality ( Veerman et al., 2017 ). Previous studies have demonstrated that no drug had a beneficial effect on negative symptoms when compared to another drug ( Arango et al., 2013 ; Millan et al., 2014 ; Fusar-Poli et al., 2015 ), meaning that head to head comparisons of different agents among each other did not result in superiority of one drug to another. The latest comparison ( Krause et al., 2018 ) evaluated all studies that have been performed in the negative symptom population so far, and has found that amisulpride claimed superiority only to placebo, olanzapine was superior to haloperidol, but only in a small trial (n = 35), and cariprazine outperformed risperidone in a large well-controlled trial.

Hence cariprazine emerged as an agent of particular interest in regard to negative symptoms. Cariprazine is a dopamine D 3 /D 2 receptor partial agonist and serotonin 5-HT 1A receptor partial agonist. It has been hypothesized that cariprazine is the only antipsychotic that can block D 3 receptors in the living brain, thereby exhibiting functions that are related to D 3 blockade (e.g., improvement of negative symptoms) ( Stahl, 2016 ). In that large clinical trial including 460 patients with predominant negative symptoms and stable positive symptoms of schizophrenia, cariprazine was significantly more effective than risperidone in improving negative symptoms and patient functioning ( Nemeth et al., 2017 ).

Case Description

The 23-year-old female patient visited the Institute of Rare Diseases at our university with her parents. They had suspected for a long time that something was wrong with their daughter, but this was the first time they had asked for medical help. The patient was quiet and restrained since she did not speak much, her parents told us her story instead. Initially, the patient had done very well in a bilingual secondary school and was socially active with friends and peers. At the age of 15 years, her academic performance started to deteriorate, with her first problems associated with difficulty learning languages and memorizing. Her school grades dropped, and her personality started to gradually change. She became increasingly irritated, and was verbally and physically hostile toward her classmates, resorting to hitting and kicking at times. She was required to repeat a school year and subsequently dropped out of school at the age of 18 because she was unable to complete her studies. During these years, her social activity greatly diminished. She lived at home with her parents, did not go out with friends, or participate in relationships. Most of the time she was silent and unsociable, but occasionally she had fits of laughter without reason. Once the patient told her mother that she could hear the thoughts of others and was probably hearing voices as well. Slowly, her impulse-control problems faded; however, restlessness of the legs was quite often present.

Our patient’s medical history was generally unremarkable. She lacked neurological or psychiatric signs. She had a tonsillectomy and adenotomy at age 7 years. Epilepsy was identified in the patient’s family history (father’s uncle). On physical examination, there were no signs of internal or neurological disease; body mass index was 21.5 (normal weight).

During the first psychiatric interview and examination, we found that our patient was alert and vigilant, but had trouble relating due to decreased integrity of consciousness. Her attention could be aroused or partially directed, and she had difficulty keeping a target idea. Autopsychic and allopsychic orientations were preserved. Longer thinking latencies and slowed movement responses were observed, sometimes with even cataleptic impressions. Cognitive functions, such as thinking, memory, and concept formation, were severely impaired, and we were unable to carry out some of our neurocognitive tests -such as the Addenbrooke’s Cognitive Examination ( Hsieh et al., 2013 ), the Toulouse-Pieron attention test (Kanizsa G1951), Bells test ( Gauthier et al., 1989 ) and the Trail Making Test- because of the patient’s denial of symptoms and refusal to cooperate.

She often looked aside and laughed frequently, suggesting the presence of perceptual disturbances, but she denied her symptoms when asked. In contrast to the periodic inappropriate laughing, apathy and anhedonia were markedly present. During the examination, the patient could not recall anything she would do or even think of with pleasure. According to the heteroanamnesis, she lost her interest in activities she used to like, did not go out with friends anymore, and showed no signs of joy or intimacy towards her family members either.

Along with the affective hyporesponsiveness, amotivation and a general psychomotor slowing were observed. Hypobulia, void perspectives, and lack of motivation were explored. Parental statements indicated that the patient’s social activity had continued to diminish, and her appearance and personal physical hygiene had deteriorated. When we initiated a conversation, the patient was negativistic and agitated. Her critical thinking ability was reduced, which led to inappropriate behavior (she, e.g., unexpectedly stood up and left the room while the examination was still ongoing). Considering her status, she was admitted to the clinic after her first visit.

After several differential diagnostic tests were performed (e.g., routine diagnostic laboratory parameters, immune serological analyses, electroencephalogram, magnetic resonance imaging, genetic testing), all the possible common and rare disorders, such as Huntington’s disease, Niemann Pick C disease, mitochondrial disorders, and autoimmune diseases, were ruled out.

At first contact, to differentiate the symptoms and severity of putative schizophrenia, we mapped the positive, negative, and general symptoms, as well as a clinical impression, using the Positive and Negative Syndrome Scale (PANSS), the Scale for Assessment of Negative Symptoms, and the Clinical Global Impressions-Severity (CGI-S) ( Groth-Marnat, 2009 ).

The patient had a very high PANSS total score, which corresponded to being considered “severely ill” or “among the most severely ill’ on the CGI-S ( Leucht et al., 2005 ). The PANSS score was derived dominantly from the negative items of the scale. Overall, her negative symptoms fulfilled criteria for predominantly negative symptoms, meaning that positive symptomatology was reduced, while negative symptoms were more explicit and dominated the clinical picture ( Riedel et al., 2005 ; Olie et al., 2006 ; Mucci et al., 2017 ). Baseline rating scale sores are presented in Table 1 .

Summary of symptom scale scores at the time of admission to the hospital.

	Score at first contact/admission to hospital	Maximum score possible
PANSS Total Score	150	210
PANSS Positive Subscale Score	26	49
PANSS Negative Subscale Score	45	49
PANSS General Psychopathology Subscale Score	79	112
PANSS-FSPS	20	42
PANSS-FSNS	46	49
CGI-S	6	7

PANSS, Positive and Negative Syndrome Scale; PANSS-FSNS, Positive and Negative Syndrome Scale factor score for negative symptoms; PANSS-FSPS, Positive and Negative Syndrome Scale factor score for positive symptoms; CGI-S, Clinical Global Impressions-Severity Scale.

The diagnosis of EOS with predominantly negative symptoms was given and treatment with the antipsychotic agent cariprazine was initiated. The patient was hospitalized for 2 weeks following her arrival at the clinic. Cariprazine was started at the dose of 1.5 mg/day and titrated up to 4.5 mg/day over a 2-week period: the patient received 1.5 mg/day for the first 3 days, 3 mg/day from day 4 to day 12, and eventually 4.5 mg/day from day 13 onward. During these 2 weeks, which were spent in hospital, the patient’s explicit negative symptoms such as poverty of speech, psychomotor retardation, poor eye contact, and affective nonresponsiveness improved; however, delusions and hallucinatory perceptions did not fade significantly.

Two weeks after discharge, we saw the patient for her first outpatient visit. Significant clinical improvement was observed. The patient calmly cooperated during the examination, with no signs of agitation. She was oriented to time, place, and self, attention could be drawn and directed, and she was able to keep a target idea and change the subject. Although according to the family, perceptual disturbances were still present, laughing with no reason and looking aside were much less frequent, and restlessness of the legs had stopped; these symptoms were not observed during the examination. Psychomotoric negativism had improved greatly, the patient was more communicative, and she paid more attention to the activities of family members. The pace of speech was close to normal: the thinking latencies and slowed movement responses as observed at admission were not seen anymore. The patient had adequate reaction time to questions asked and could focus in the interview. Mild obstipation and somnolence in the evening were her main complaints. Apart from some tick-like eye closures, there was no pathological finding during physical and neurological examination. At this point, cariprazine was reduced to 3 mg per day.

At her second outpatient visit, which occurred 8 weeks after treatment initiation, further improvement was observed. According to her mother, the patient was more active and open at home. Neurological examination found that the alternating movements of her fingers were slightly slowed. Cariprazine 3 mg/day was continued with concomitant anticholinergic medication.

At the third outpatient visit, which occurred 16 weeks after the first contact, the patient’s overall symptoms, including cognitive functions, such as memory and abstract thinking, as well as functions in activities of daily living, had improved remarkably. She had started to participate in the family’s daily life, even taking responsibility for some household duties; further, she went to the hairdresser for the first time in years, a step forward from her previous state of self-neglect. She was probably still having auditory hallucinations, which she considered natural, and some extrapyramidal symptom (EPS)-like ruminating movements, like to-and-fro swinging of her trunk, were observed. She did not look aside any more and tics were no longer present. Compared with previous visits overall, she was very relaxed, retained eye contact, cooperated, and communicated adequately during the interview. She started to develop insight into her condition, and she told us that her “thoughts were not healthy.” At the last two visits, the synkinesis of the arms was reduced.

After 16 weeks of treatment, the patient’s PANSS Negative Subscale Score and PANSS factor score for negative symptoms (PANSS-FSNS) score were reduced by 44.44% and 41.31%, respectively. Recent studies have demonstrated that linking the percentage improvement of PANSS with CGI-S and -Improvement (CGI-I) scores shows that a 25–50% reduction of PANSS scores corresponds to clinically meaningful change ( Correll et al., 2011 ; Fusar-Poli et al., 2015 ). In acutely ill patients with predominantly positive symptoms who are more likely to respond well to treatment, the 50% cutoff would be a more clinically meaningful criterion; however, since even slight improvement might represent a clinically significant effect in a patient with atypical schizophrenia, the use of 25% cutoff is justified ( Correll et al., 2011 ; Fusar-Poli et al., 2015 ).

In this regard, the 44.44% (change from baseline: −20) and 41.31% (change from baseline: −19) improvement demonstrated on PANSS Negative Symptom subscale and PANSS-FSNS, respectively, are considered a clearly clinically relevant change. Beyond the impaired synkinesis and alternating movement of the arms and fingers, there were no other treatment-related physical dysfunctions. Change from baseline on the PANSS and CGI scales are shown over the course of treatment in Table 2 .

Summary of symptom scale scores at weeks 16, 32, and 52.

	Score at admission	Score at 16 weeks of treatment	Percent change from baseline (change from baseline)	Score at 32 weeks of treatment	Percent change from baseline (change from baseline)	Score at 52 weeks of treatment	Percent change from baseline (change from baseline)
PANSS Total Score	150	92	38.66% (−58)	37	75.33% (−113)	37	75.33% (−113)
PANSS- PSS	26	14	46.15% (−12)	9	65.38% (−17)	9	65.38% (−17)
PANSS- NSS	45	25	44.44% (−20)	15	66.67% (−30)	15	66.67% (−30)
PANSS-FSPS	20	9	55.00% (−11)	6	70.00% (−14)	6	70.00% (−14)
PANSS-FSNS	46	27	41.31% (−19)	14	69.56% (−32)	14	69.56% (−32)
CGI-S	6	4	NA	2	NA	2	NA
CGI-I	NA	2	NA	1	NA	1	NA

PANSS, Positive and Negative Syndrome Scale; PANSS-PSS, PANSS Positive Subscale Score; PANSS-NSS, PANSS Negative Subscale Score; PANSS-FSNS, Positive and Negative Syndrome Scale factor score for negative symptoms; PANSS-FSPS, Positive and Negative Syndrome Scale factor score for positive symptoms; CGI-S, Clinical Global Impressions-Severity Scale; CGI-I, Clinical Global Impressions-Improvement Scale. NA indicates not applicable.

Since our patient’s symptoms demonstrated strong improvement and tolerability was favorable, cariprazine therapy was continued. Improvement in both negative and positive symptoms was maintained over the course of treatment. At her later visits (32 and 52 weeks), PANSS total score was reduced to a level that was close to the minimum, and the decrease in negative symptom scores was considerable (PANSS-NSS=66.67% and PANS-FSNS=70.00% at both time points). The patient’s progress was also reflected in clinical and functional measurements, with the CGI-S score reduced to 2 (borderline mentally ill) and a CGI-I score of 1 (very much improved) indicating notable improvement.

Cariprazine has demonstrated broad spectrum efficacy in the treatment of positive and negative symptoms of schizophrenia. In a field where no treatment is available for difficult-to-treat negative symptoms, this case is unique and may have important implications for schizophrenia treatment. Despite experiencing approximately 8 years of untreated symptoms and functional impairment associated with predominantly negative symptom EOS, our 23-year-old female patient showed considerable symptomatic and functional improvement after several weeks of treatment with cariprazine. Given that the duration of untreated negative symptoms is associated with worse functional outcomes ( Boonstra et al., 2012 ), the remarkable improvement seen in this case shows how valuable cariprazine could be for patients with similar symptom presentations. Although it is not possible to generalize the observations and findings of this single case, it has the novelty of detecting a potential effect of cariprazine in a drug-naïve patient with marked negative symptoms of early-onset schizophrenia. To our knowledge, no cariprazine-related data has been published in this type of patients. A single case study is obviously far from being predictive for the efficacy of a drug, however, the results seen with this case are promising. With a dose recommended for patients with negative symptoms, our patient’s clinical condition, including positive, negative, and cognitive symptoms, as well as social functioning have improved notably, with the effect maintained for over 12 months. Generally, cariprazine has been well tolerated, with mild EPS observed after 8 weeks, but no metabolic, cardiac, or other side effects.

This case report suggests that the management of patients with EOS and prominent negative symptoms is achievable in everyday practice with cariprazine. More real-world clinical experience is needed to support this finding.

Data Availability Statement

Ethics statement.

Written informed consent was obtained from the individual(s), and minor(s)’ legal guardian/next of kin, for the publication of any potentially identifiable images or data included in this article.

Author Contributions

All authors listed have made substantial, direct, and intellectual contribution to the work and approved it for publication.

This work was supported from Research and Technology Innovation Fund by the Hungarian National Brain Research Program (KTIA_NAP_ 2017-1.2.1-NKP-2017-00002). Editorial support for this case report was supported by funding from Gedeon Richter. The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this article or the decision to submit it for publication.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be constructed as a potential conflict of interest.

Acknowledgments

We are thankful to the patient and her family for giving us the opportunity to share her story in the form of a publication. Also, we acknowledge editorial assistance was provided by Carol Brown, MS, ELS, of Prescott Medical Communications Group, Chicago, Illinois, USA, a contractor of Gedeon Richter plc.

1 http://www.schizophrenia.com/szfacts.htm

2 https://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml

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Schizophrenia case studies: putting theory into practice

This article considers how patients with schizophrenia should be managed when their condition or treatment changes.

DR P. MARAZZI/SCIENCE PHOTO LIBRARY

Treatments for schizophrenia are typically recommended by a mental health specialist; however, it is important that pharmacists recognise their role in the management and monitoring of this condition. In ‘ Schizophrenia: recognition and management ’, advice was provided that would help with identifying symptoms of the condition, and determining and monitoring treatment. In this article, hospital and community pharmacy-based case studies provide further context for the management of patients with schizophrenia who have concurrent conditions or factors that could impact their treatment.

Case study 1: A man who suddenly stops smoking

A man aged 35 years* has been admitted to a ward following a serious injury. He has been taking olanzapine 20mg at night for the past three years to treat his schizophrenia, without any problems, and does not take any other medicines. He smokes 25–30 cigarettes per day, but, because of his injury, he is unable to go outside and has opted to be started on nicotine replacement therapy (NRT) in the form of a patch.

When speaking to him about his medicines, he appears very drowsy and is barely able to speak. After checking his notes, it is found that the nurses are withholding his morphine because he appears over-sedated. The doctor asks the pharmacist if any of the patient’s prescribed therapies could be causing these symptoms.

What could be the cause?

Smoking is known to increase the metabolism of several antipsychotics, including olanzapine, haloperidol and clozapine. This increase is linked to a chemical found in cigarettes, but not nicotine itself. Tobacco smoke contains aromatic hydrocarbons that are inducers of CYP1A2, which are involved in the metabolism of several medicines [1] , [2] , [3] . Therefore, smoking cessation and starting NRT leads to a reduction in clearance of the patient’s olanzapine, leading to increased plasma levels of the antipsychotic olanzapine and potentially more adverse effects — sedation in this case.

Patients who want to stop, or who inadvertently stop, smoking while taking antipsychotics should be monitored for signs of increased adverse effects (e.g. extrapyramidal side effects, weight gain or confusion). Patients who take clozapine and who wish to stop smoking should be referred to their mental health team for review as clozapine levels can increase significantly when smoking is stopped [3] , [4] .

For this patient, olanzapine is reduced to 15mg at night; consequently, he seems much brighter and more responsive. After a period on the ward, he has successfully been treated for his injury and is ready to go home. The doctor has asked for him to be supplied with olanzapine 15mg for discharge along with his NRT.

What should be considered prior to discharge?

It is important to discuss with the patient why his dose was changed during his stay in hospital and to ask whether he intends to start smoking again or to continue with his NRT. Explain to him that if he wants to begin, or is at risk of, smoking again, his olanzapine levels may be impacted and he may be at risk of becoming unwell. It is necessary to warn him of the risk to his current therapy and to speak to his pharmacist or mental health team if he does decide to start smoking again. In addition, this should be used as an opportunity to reinforce the general risks of smoking to the patient and to encourage him to remain smoke-free.

It is also important to speak to the patient’s community team (e.g. doctors, nurses), who specialise in caring for patients with mental health disorders, about why the olanzapine dose was reduced during his stay, so that they can then monitor him in case he does begin smoking again.

Case 2: A woman with constipation

A woman aged 40 years* presents at the pharmacy. The pharmacist recognises her as she often comes in to collect medicine for her family. They are aware that she has a history of schizophrenia and that she was started on clozapine three months ago. She receives this from her mental health team on a weekly basis.

She has visited the pharmacy to discuss constipation that she is experiencing. She has noticed that since she was started on clozapine, her bowel movements have become less frequent. She is concerned as she is currently only able to go to the toilet about once per week. She explains that she feels uncomfortable and sick, and although she has been trying to change her diet to include more fibre, it does not seem to be helping. The patient asks for advice on a suitable laxative.

What needs to be considered?

Constipation is a very common side effect of clozapine . However, it has the potential to become serious and, in rare cases, even fatal [5] , [6] , [7] , [8] . While minor constipation can be managed using over-the-counter medicines (e.g. stimulant laxatives, such as senna, are normally recommended first-line with stool softeners, such as docusate, or osmotic laxatives, such as lactulose, as an alternative choice), severe constipation should be checked by a doctor to ensure there is no serious bowel obstruction as this can lead to paralytic ileus, which can be fatal [9] . Symptoms indicative of severe constipation include: no improvement or bowel movement following laxative use, fever, stomach pain, vomiting, loss of appetite and/or diarrhoea, which can be a sign of faecal impaction overflow.

As the patient has been experiencing this for some time and is only opening her bowels once per week, as well as having other symptoms (i.e. feeling uncomfortable and sick), she should be advised to see her GP as soon as possible.

The patient returns to the pharmacy again a few weeks later to collect a prescription for a member of their family and thanks the pharmacist for their advice. The patient was prescribed a laxative that has led to resolution of symptoms and she explains that she is feeling much better. Although she has a repeat prescription for lactulose 15ml twice per day, she says she is not sure whether she needs to continue to take it as she feels better.

What advice should be provided?

As she has already had an episode of constipation, despite dietary changes, it would be best for the patient to continue with the lactulose at the same dose (i.e. 15ml twice daily), to prevent the problem occurring again. Explain to the patient that as constipation is a common side effect of clozapine, it is reasonable for her to take laxatives before she gets constipation to prevent complications.

Pharmacists should encourage any patient who has previously had constipation to continue taking prescribed laxatives and explain why this is important. Pharmacists should also continue to ask patients about their bowel habits to help pick up any constipation that may be returning. Where pharmacists identify patients who have had problems with constipation prior to starting clozapine, they can recommend the use of a prophylactic laxative such as lactulose.

Case 3: A mother is concerned for her son who is talking to someone who is not there

A woman has been visiting the pharmacy for the past 3 months to collect a prescription for her son, aged 17 years*. In the past, the patient has collected his own medicine. Today the patient has presented with his mother; he looks dishevelled, preoccupied and does not speak to anyone in the pharmacy.

His mother beckons you to the side and expresses her concern for her son, explaining that she often hears him talking to someone who is not there. She adds that he is spending a lot of time in his room by himself and has accused her of tampering with his things. She is not sure what she should do and asks for advice.

What action can the pharmacist take?

It is important to reassure the mother that there is help available to review her son and identify if there are any problems that he is experiencing, but explain it is difficult to say at this point what he may be experiencing. Schizophrenia is a psychotic illness which has several symptoms that are classified as positive (e.g. hallucinations and delusions), negative (e.g. social withdrawal, self-neglect) and cognitive (e.g. poor memory and attention).

Many patients who go on to be diagnosed with schizophrenia will experience a prodromal period before schizophrenia is diagnosed. This may be a period where negative symptoms dominate and patients may become isolated and withdrawn. These symptoms can be confused with depression, particularly in younger people, though depression and anxiety disorders themselves may be prominent and treatment for these may also be needed. In this case, the patient’s mother is describing potential psychotic symptoms and it would be best for her son to be assessed. She should be encouraged to take her son to the GP for an assessment; however, if she is unable to do so, she can talk to the GP herself. It is usually the role of the doctor to refer patients for an assessment and to ensure that any other medical problems are assessed.

Three months later, the patient comes into the pharmacy and seems to be much more like his usual self, having been started on an antipsychotic. He collects his prescription for risperidone and mentions that he is very worried about his weight, which has increased since he started taking the newly prescribed tablets. Although he does not keep track of his weight, he has noticed a physical change and that some of his clothes no longer fit him.

What advice can the pharmacist provide?

Weight gain is common with many antipsychotics [10] . Risperidone is usually associated with a moderate chance of weight gain, which can occur early on in treatment [6] , [11] , [12] . As such, the National Institute for Health and Care Excellence recommends weekly monitoring of weight initially [13] . As well as weight gain, risperidone can be associated with an increased risk of diabetes and dyslipidaemia, which must also be monitored [6] , [11] , [12] . For example, the lipid profile and glucose should be assessed at 12 weeks, 6 months and then annually [12] .

The pharmacist should encourage the patient to attend any appointments for monitoring, which may be provided by his GP or mental health team, and to speak to his mental health team about his weight gain. If he agrees, the pharmacist could inform the patient’s mental health team of his weight gain and concerns on his behalf. It is important to tackle weight gain early on in treatment, as weight loss can be difficult to achieve, even if the medicine is changed.

The pharmacist should provide the patient with advice on healthy eating (e.g. eating a balanced diet with at least five fruit and vegetables per day) and exercising regularly (e.g. doing at least 150 minutes of moderate-intensity activity or 75 minutes of vigorous-intensity activity per week), and direct him to locally available services. The pharmacist can record the adverse effect on the patient’s medical record, which will help flag this in the future and thus help other pharmacists to intervene should he be prescribed risperidone again.

*All case studies are fictional.

Useful resources

Mind — Schizophrenia
Rethink Mental Illness — Schizophrenia
Mental Health Foundation — Schizophrenia
Royal College of Psychiatrists — Schizophrenia
NICE guidance [CG178] — Psychosis and schizophrenia in adults: prevention and management
NICE guidance [CG155] — Psychosis and schizophrenia in children and young people: recognition and management
British Association for Psychopharmacology — Evidence-based guidelines for the pharmacological treatment of schizophrenia: updated recommendations from the British Association for Psychopharmacology

About the author

Nicola Greenhalgh is lead pharmacist, Mental Health Services, North East London NHS Foundation Trust

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Case Study Illustrates How Schizophrenia Can Often Be Overdiagnosed

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Study author Russell Margolis, director of the Johns Hopkins Schizophrenia Center, answers questions on misdiagnosis of the condition and reiterates the importance of thorough examination.

It’s not uncommon for an adolescent or young adult who reports hearing voices or seeing things to be diagnosed with schizophrenia, but using these reports alone can contribute to the disease being overdiagnosed, says Russell Margolis , clinical director of the Johns Hopkins Schizophrenia Center.

Many clinicians consider hallucinations as the sine qua non, or essential condition, of schizophrenia, he says. But even a true hallucination might be part of any number of disorders — or even within the range of normal. To diagnose a patient properly, he says, “There’s no substitute for taking time with patients and others who know them well. Trying to [diagnose] this in a compressed, shortcut kind of way leads to error.”

A case study he shared recently in the Journal of Psychiatric Practice illustrates the problem. Margolis, along with colleagues Krista Baker, schizophrenia supervisor at Johns Hopkins Bayview Medical Center, visiting resident Bianca Camerini, and Brazilian psychiatrist Ary Gadelha, described a 16-year-old girl who was referred to the Early Psychosis Intervention Clinic at Johns Hopkins Bayview for a second opinion concerning the diagnosis and treatment of suspected schizophrenia.

The patient made friends easily but had some academic difficulties. Returning to school in eighth grade after a period of home schooling, she was bullied, sexually groped and received texted death threats. She then began to complain of visions of a boy who harassed her, as well as three tall demons. The visions waxed and waned in relation to stress at school. The Johns Hopkins consultants determined that this girl did not have schizophrenia (or any other psychotic disorder), but that she had anxiety. They recommended psychotherapy and viewing herself as a healthy, competent person, instead of a sick one. A year later, the girl reported doing well: She was off medications and no longer complained of these visions.

Margolis answers Hopkins Brain Wise ’s questions.

Q: How are anxiety disorders mistaken for schizophrenia?

A: Patients often say they have hallucinations, but that doesn’t always mean they’re experiencing a true hallucination. What they may mean is that they have very vivid, distressing thoughts — in part because hallucinations have become a common way of talking about distress, and partly because they may have no other vocabulary with which to describe their experience.

Then, even if it is a true hallucination, there are features of the way psychiatry has come to be practiced that cause difficulties. Electronic medical records are often designed with questionnaires that have yes or no answers. Sometimes, whether the patient has hallucinations is murky, or possible — not yes or no. Also, one can’t make a diagnosis based just on a hallucination; the diagnosis of disorders like schizophrenia is based on a constellation of symptoms.

Q: How often are patients in this age range misdiagnosed?

A: There’s no true way to know the numbers. Among a very select group of people in our consultation clinic where questions have been raised, about half who were referred to us and said to have schizophrenia or a related disorder did not. That is not generalizable.

Q: Why does that happen?

A: There is a lack of attention to the context of symptoms and other details, and there’s also a tendency to take patients literally. If a patient complains about x, there’s sometimes a pressure to directly address x. In fact, that’s not appropriate medicine. It is very important to pay attention to a patient’s stated concerns, but to place these concerns in the bigger picture. Clinicians can go too far in accepting at face value something that needs more exploration.

Q: What lessons do you hope to impart by publishing this case?

A: I want it to be understood that the diagnosis of schizophrenia has to be made with care. Clinicians need to take the necessary time and obtain the necessary information so that they’re not led astray. Eventually, we would like to have more objective measures for defining our disorders so that we do not need to rely totally on a clinical evaluation.

Learn more about Russell Margolis’ research regarding the challenges of diagnosing schizophrenia .

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Case Reports in Schizophrenia and Psychotic Disorders: 2023

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Understanding Schizophrenia: A Case Study

Schizophrenia is characterized mainly, by the gross distortion of reality, withdrawal from social interaction, disorganization and fragmentation of perception, thoughts and emotions. Insight is an important concept in clinical psychiatry, a lack of insight is particularly common in schizophrenia patient. Previous studies reported that between 50-80% of patients with schizophrenia do not believe, they have a disorder. By the help of psychological assessment, we can come to know an individual's problems especially in cases, where patient is hesitant or has less insight into illness. Assessment is also important for the psychological management of the illness. Knowing the strengths and weaknesses of that particular individual with psychological analysis tools can help to make better plan for the treatment. The present study was designed to assess the cognitive functioning, to elicit severity of psychopathology, understanding diagnostic indicators, personality traits that make the individual vulnerable to the disorder and interpersonal relationship in order to plan effective management. Schizophrenia is a chronic disorder, characterized mainly by the gross distortion of reality, withdrawal from social interaction, and disorganization and fragmentation of perception, thought and emotion. Approximately, 1% world population suffering with the problem of Schizophrenia. Both male and female are almost equally affected with slight male predominance. Schizophrenia is socioeconomic burden with suicidal rate of 10% and expense of 0.02-1.65% of GDP spent on treatment. Other co-morbid factors associated with Schizophrenia are diabetes, Obesity, HIV infection many metabolic disorders etc. Clinically, schizophrenia is a syndrome of variables symptoms, but profoundly disruptive, psychopathology that involves cognition, emotion, perception, and other aspects of behavior. The expression of these manifestations varies across patients and over the time, but the effect of the illness is always severe and is usually long-lasting. Patients with schizophrenia usually get relapse after treatment. The most common cause for the relapse is non-adherent with the medication. The relapse rate of schizophrenia increases later time on from 53.7% at 2 years to

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The Woman Behind Freud’s First Case Study

The case of anna o. showed that psychoanalysis worked. did freud tamper with it.

There is perhaps no one more devoted to the cause than a convert, and there is no one more violent toward it than a person who has lost their faith. The faithful turned faithless take up the act of crusade, but in reverse: new atheists confronting the world with secular eyes, children who learn that their parents aren’t omnipotent. They have suffered the loss of an organizing principle, the very thing they built their life around. Now, they may seek revenge on the object that caused an earlier delusion. The commitment doesn’t end—it just takes on new guises.

Beyond the reactions of former lovers and former zealots, we see this in the history of psychoanalysis, perhaps because the practice attracts and demands those same qualities of immersion and devotion. Many have justly loved psychoanalysis, and many have justly despaired of it. This includes the very founders of rational emotive behavioral therapy and cognitive behavioral therapy, who brought about a sea change in mental health care, and the critics Frederick Crews, Jeffrey Masson, and Philip Rieff, who turned against Freud even after he had been unthroned as king of the twentieth century. This hatred can feel quasi-personal, aimed at the originator, their father figure, Sigmund Freud.

This loss of faith looms over Gabriel Brownstein’s book, The Secret Mind of Bertha Pappenheim: The Woman Who Invented Freud’s Talking Cure . On its face, the book is a study of the first analytic patient (although she didn’t exactly receive psychoanalytic treatment), Bertha Pappenheim. Pappenheim, who was treated by Freud’s mentor Josef Breuer in Vienna, was the subject of one of Breuer’s case studies and was much discussed by Freud throughout his own career. The book’s stated aim is to offer a full portrait of someone flattened and circulated as a specimen. For Pappenheim is best known by another name—Anna O.—and is best known not as her full person, who left a legacy of feminist and activist patronage, but as the world’s most famous hysteric.

But quietly, this is also a book about the birth and death of psychoanalysis—which is to say that the narrative of Freud’s ascendance and betrayal is the engine that drives the book. Brownstein argues, sometimes contradictorily, that Freud’s brilliance and his drive to make his way as a medical doctor propelled him to tamper with Bertha’s story.

Given that Pappenheim’s stunning cure is the origin story of psychoanalysis, Brownstein seeks to denigrate the whole endeavor on these grounds. If the Anna O. case was a fraud, so, too, would the cure be that she discovered.

Hysteria, much like psychoanalysis, has a storied past, one with a powerful crescendo followed by a caesura. Though the term “hysteric” is now assumed in common speech to be either a pejorative epithet, synonymous with performative hyper-emotionality ( he was hysterical ), or a historical diagnosis made up by misogynistic doctors (like, some argue, Breuer and Freud), the condition was once quite common. For the uninitiated, hysteria is an illness where the body speaks, where neurotic symptoms appear in and on it. It was treated by an array of cures, from gynecological massage (prescribed orgasm), hypnotism, rest, and drugging, to change of scenery, and, yes, for a very few patients, starting in the late nineteenth century, Breuer and Freud’s cathartic method. This eventually became psychoanalysis. This was, it must be said, a treatment that seems preferable to the other options.

Bertha Pappenheim was in many ways a typical hysterical patient, and an extraordinary woman. When she went to see Breuer in 1880, she presented with the typical hysterical complaints: partial paralysis, disturbances of appetite and language, pain. She couldn’t recall her native German and only spoke in English. She wouldn’t drink water. She had fallen ill while nursing her father, and her condition deteriorated upon his death. She was treated both in her home and in an asylum, often with high doses of drugs. What marks her case as special is that Pappenheim was the first person on Earth to be treated by the cathartic method, in large part because she invented it. Anytime you hear someone say “talking cure,” they’re using the very term Pappenheim ascribed to the yearslong experiment she undertook, morning and night, with her doctor. As she chattered on, as she engaged in the “chimney sweeping” of her mind—so the story goes—she felt better.

Freud and Breuer went on to co-write the groundbreaking Studies on Hysteria , published in 1895. The two doctors, one senior and one junior, open the book with a co-written introduction and end it with a pair of stand-alone essays (Freud’s undermining Breuer’s) in which the nascent theories of repression, defense, catharsis, and abreaction first appear. Each supplied case material of hysteric women treated by this nascent cathartic method. Freud wrote up four cases, and Breuer only contributed the case of Pappenheim, now disguised and named “Anna O.” The two detailed the symptoms of their patients and how each was aided, if not outright cured, by this new talking protocol.

In Breuer’s write-up of Anna O., which only runs about 25 pages, he elaborates on the case study, telling his readers how ill Anna was, when, and why. He then goes on to describe his therapeutic practice of sitting with her at night, and how, while Anna O. was under hypnosis, the two came to “develop a therapeutic technique” of linking each of her symptoms to the moment it appeared. The water she will not drink, for instance, is linked to a moment she saw her English ladies’ companion let a little dog drink from her glass. After the connection is revealed under hypnosis, Breuer tells us, Anna O. drinks water once more. The process repeated until there were no symptoms left, and Anna O.’s mental state presumably returned to normal.

The problem is—and basically all historians of psychoanalysis agree on this point—that even though Breuer and Freud reported a miracle cure, Anna O. didn’t get better. In fact, she got worse and was put in a sanatorium. The question is why. Brownstein, following the anti-Freud tradition, attributes this failure to the treatment. Freud, of course, attributed this failure to the person who offered the treatment—Breuer—not because he couldn’t cure her, but because he didn’t finish doing so.

Like all origin myths, the case has been subject to endless interpretation and reinterpretation. Even the original case study is retrospective: Breuer didn’t write up the Anna O. case at the time of treatment. He did so at Freud’s urging, so that the two might document this new technique of psychotherapy. Anna O. thus became the first patient of psychoanalysis only after the fact, and even though her treatment has just about nothing in common with psychoanalysis today, she is celebrated as such. Freud then revised the case multiple times across his life (in private letters, then in publications in 1910 and 1914), often to diminish Breuer’s role in the origin of psychoanalysis. This is in part due to what Freud thought of privately as Breuer’s failure: When Anna O. showed Breuer she had transferred onto him—by fantasizing about having his baby—Breuer ran away. Breuer could have invented psychoanalysis had he stayed in the room—but he didn’t dare. And thus Anna remained ill, but, in Freud’s understanding, psychoanalysis was not at fault.

Once Freud died, others revised the case in their own ways. Stacks of books can be called up in any research library by those who either defend or revile Freud—and nearly all of them, at one point, turn to Anna O. These studies often seek to collate and correlate Breuer’s flattened write-up of the case with historical reality, trying to reconstruct both Anna O.’s illness and her medical treatment. Some are feminist rereadings of the case, arguing that Anna O. was sick with patriarchy; others center squarely on Freud’s obsession with the case, excavating his letters about Anna O. to various ends.

What’s plain as day: Pappenheim has become the Rorschach test for the field. What we see in her case tends to be run through our feelings about psychoanalysis. The great historian of psychoanalysis John Forrester has argued that the baby that Anna O. spoke of wanting to have with Breuer was psychoanalysis—something she conceived with Breuer, even though he wouldn’t stick around and take responsibility for it. Anti-Freudian Mikkel Borch-Jacobsen sees Anna O.’s case as entirely fabricated, a young woman taken in by her handsome doctor and given huge quantities of drugs; if she invented psychoanalysis, she was the first to be duped by it. As the late Peter Gay observed, “There are contradictions and obscurities in successive versions of the case, but this much is more or less beyond dispute: In 1880, when Anna O. fell ill, she was twenty-one.”

But because very little besides Breuer’s documents is known of her life at the time of treatment, we project what we want onto her, and we can, for her history is a mere fragment. That we continue to do so makes exquisite sense: Psychoanalysis teaches us we must go back to our origins to go forward. And the treatment of Anna O. by Breuer is one way—a decent way—to conceptualize the start of Freud’s theory of mind.

Brownstein’s main critique of Freud’s use of Anna O. is this: that he took her case for his own material ends (though, by the same token, we might ask after Brownstein’s book advance). Freud was a broke young doctor; he needed to get married, and, to do so, he needed to press Breuer into writing Studies on Hysteria so that he could practice this new treatment with a kind of paternal authorization, styling himself as a doctor of “the cathartic method of J. Breuer.”

Brownstein agrees with anti-Freudians like Borch-Jacobsen and Crews that Anna O.’s treatment was a dismal failure. And even though that would make the lie—that Anna O. was cured—Breuer’s, Brownstein argues it was Freud who metaphorically had a gun to his mentor’s head and forced him to write it. More softly, Brownstein argues that Anna O. obscures Bertha Pappenheim, whom Brownstein now promises to deliver to us. Here’s the problem: Brownstein wants to make Freud the (very) bad guy of a story that had little to do with him, even if he had a great deal to do with the case becoming a story. So much so that Brownstein treats the possibility of Freud seeing Bertha Pappenheim at a party years after the treatment as corroborating evidence for some kind of misdeed.

Brownstein thus rewrites up the notorious case, with his chatty, negative asides and interpretations taking center stage. His first close reading from the book is, appropriately, from the first page. He argues that, though Studies purports to be “about the sex lives and sex drives of young bourgeois women,” it “begins by announcing that, for the purposes of propriety, any discussion of their actual intimate lives will be avoided.” Brownstein argues that this is a cover—that Breuer and Freud are maliciously withholding evidence for their theory because there isn’t any and because the doctors wanted to appear respectable. But if we read the first page of Studies , here’s what Breuer and Freud actually wrote: “It would be a grave breach of confidence to publish material of this kind, with the risk of patients being recognized and their acquaintances becoming informed of facts which were confided only to the physician.” There is a deep truth to what Freud and Breuer argue: They were working in a small coterie of largely wealthy Viennese Jewish patients. Everyone knew one another (hence, the great possibility of Freud running into Pappenheim). If you circulated reports of the ills of a young woman’s “marriage bed” or lack thereof, it would have meant no father would refer his daughter to Breuer or Freud, let alone the greater ethical considerations Brownstein says are gestured to half-heartedly.

Elsewhere, Brownstein accuses Freud of having a faulty memory and disguising the patient (despite the authors’ own opening warning to the reader not to go looking for biographical information of Pappenheim). To cover over the lack of details about her, Brownstein freely narrativizes the case, turning it into a historical fiction. At other times, Brownstein seems furious that Freud tends to write beautifully—Brownstein takes this as a sign of fudging the facts—while he then turns to close reading it like a literary critic.

By the end, we know from Brownstein that we’re supposed to find Breuer largely unobjectionable, but in the grips of a young Freud. The cardinal sin for Brownstein, though, is that Anna O. wasn’t made better. (Brownstein believes that she was in fact suffering from a functional neurological disorder, a contemporary diagnosis that overlaps with hysteria.) She was transported back to the asylum, so ill that Breuer reportedly told Freud his beloved patient might be better off dead, so that she might be free of suffering. Yet we might pause and say something did indeed happen in that treatment: Pappenheim was ultimately able to recover enough. By 1889, at 29 years of age, she was able not only to get out of bed, to talk, but to work in a soup kitchen. From this year on, she published—first anonymously and then pseudonymously, under the name Paul Berthold. Soon, Pappenheim was finally known not as Anna O., not as Berthold, but as herself. She also became famous as herself, a powerful, feminist leader, founding the Jewish Women’s Association and centralizing Jewish women’s organizing toward both employment and charity.

Why a book about Bertha Pappenheim now? One answer: With its claim that it will deliver readers Pappenheim in full, Brownstein’s book sits on that ever-expanding shelf of nonfiction books that seek to tell the stories of women who have been relegated to the margins of history, returning them to their larger, unobfuscated import. The book, too, in trying to bring Pappenheim’s story up to the present by rediagnosing her with functional neurological disorder, joins the book market for explorations of contested illness. Yet this book isn’t exactly proper to either of these subgenres. Instead, we might make sense of it as a work of backlash: Just as a range of analysts and writers have turned once more to Freud (as The New York Times proclaimed in an article not quite aptly titled “Not Your Daddy’s Freud”), so have others returned to maligning him. Brownstein has offered us, perhaps, the first book of the Freud Wars 2.0.

Brownstein, in fact, inherits the role of Freud skeptic from an earlier generation. His father, Dr. Shale Brownstein, was a prominent New York psychiatrist and psychoanalyst with a Rolodex of famous patients. Sometime in the 1980s, Dr. Brownstein became disillusioned with psychoanalysis and became an anti-Freudian—though we are never quite told why. One night, when Brownstein went to visit his father, he found him in his underwear, speaking wildly. The subject: Bertha Pappenheim. His father held a thick envelope filled with scientific and historic papers, newspaper clippings, reviews of books, and his own essay on the subject.

His father gave him the manila envelope. The younger Brownstein went home to Brooklyn, and the next day his father was dead. As if in a novel, Brownstein then becomes fixated on the envelope and its contents only to discover he has misplaced it. His own book is as much an attempt to decipher his father’s theory about Bertha Pappenheim as to understand his father’s turn against Freud. Brownstein makes clear that his father was a devoted doctor, and treated luminaries in downtown New York, including Peter Hujar and Richard Serra. Dr. Brownstein tended to babies with HIV in the 1980s who languished otherwise in their cots, when others wouldn’t dare go near. Dr. Brownstein gave everything to psychoanalysis, but then something changed. We don’t quite know what, but his father became so disillusioned that he burned all 24 volumes of Freud’s Standard Edition .

Was it the homophobia of mainstream psychoanalysis that rightfully made him repudiate his training? Was it indeed the legacy of Anna O.? I wish we knew what Brownstein felt as he wrestled with Freud via his father. As author and son, Brownstein is overwhelmed by the research subject he must now try to understand and, more importantly, terribly overwhelmed by the pain of being alive when life is most brutal. Shortly after his father’s death, his wife is diagnosed with terminal pancreatic cancer, and when the global pandemic arrives, Brownstein must weather it without them.

While Brownstein seemingly hates Freud, he, like many others, can’t escape him. Early in the book, he disparages two Freudian terms: “secondary gain,” which can be described as the unconscious advantage patients acquire through their illness (stereotyped here as attention), and “ la belle indifférence ,” a calm character in the face of crisis. But toward the book’s close, Brownstein suddenly tips his hand: He comes to a form of self-understanding through these concepts. In not getting treated for a heart problem, he says he has a case of la belle indifférence . In writing the book, he self-analyzes, he can be understood as having a case of secondary gain—after all, Brownstein was quite literally paid for producing it.

But Brownstein uses these concepts defensively—to show his reader he is in on the joke. The book itself, more movingly, is a testament to yet another set of Freudian concepts: the return of the repressed, as evidenced by his return to the use of Freud; working through (here, loss of his father, his wife); and, indeed, sublimation. Writing the book then might be an act of Freudian sublimation; it is also an act of devotion. This article has been updated.

Hannah Zeavin is an assistant professor of history at UC Berkeley. She is the author of The Distance Cure: A History of Teletherapy .

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ABDOMEN/ABDOMINAL body cavity below diaphragm that contains stomach, intestines, liver and other organs ABSORB take up fluids, take in ACIDOSIS condition when blood contains more acid than normal ACUITY clearness, keenness, esp. of vision and airways ACUTE new, recent, sudden, urgent ADENOPATHY swollen lymph nodes (glands) ADJUVANT helpful, assisting, aiding, supportive ADJUVANT TREATMENT added treatment (usually to a standard treatment) ANTIBIOTIC drug that kills bacteria and other germs ANTIMICROBIAL drug that kills bacteria and other germs ANTIRETROVIRAL drug that works against the growth of certain viruses ADVERSE EFFECT side effect, bad reaction, unwanted response ALLERGIC REACTION rash, hives, swelling, trouble breathing AMBULATE/AMBULATION/AMBULATORY walk, able to walk ANAPHYLAXIS serious, potentially life-threatening allergic reaction ANEMIA decreased red blood cells; low red cell blood count ANESTHETIC a drug or agent used to decrease the feeling of pain, or eliminate the feeling of pain by putting you to sleep ANGINA pain resulting from not enough blood flowing to the heart ANGINA PECTORIS pain resulting from not enough blood flowing to the heart ANOREXIA disorder in which person will not eat; lack of appetite ANTECUBITAL related to the inner side of the forearm ANTIBODY protein made in the body in response to foreign substance ANTICONVULSANT drug used to prevent seizures ANTILIPEMIC a drug that lowers fat levels in the blood ANTITUSSIVE a drug used to relieve coughing ARRHYTHMIA abnormal heartbeat; any change from the normal heartbeat ASPIRATION fluid entering the lungs, such as after vomiting ASSAY lab test ASSESS to learn about, measure, evaluate, look at ASTHMA lung disease associated with tightening of air passages, making breathing difficult ASYMPTOMATIC without symptoms AXILLA armpit

BENIGN not malignant, without serious consequences BID twice a day BINDING/BOUND carried by, to make stick together, transported BIOAVAILABILITY the extent to which a drug or other substance becomes available to the body BLOOD PROFILE series of blood tests BOLUS a large amount given all at once BONE MASS the amount of calcium and other minerals in a given amount of bone BRADYARRHYTHMIAS slow, irregular heartbeats BRADYCARDIA slow heartbeat BRONCHOSPASM breathing distress caused by narrowing of the airways

CARCINOGENIC cancer-causing CARCINOMA type of cancer CARDIAC related to the heart CARDIOVERSION return to normal heartbeat by electric shock CATHETER a tube for withdrawing or giving fluids CATHETER a tube placed near the spinal cord and used for anesthesia (indwelling epidural) during surgery CENTRAL NERVOUS SYSTEM (CNS) brain and spinal cord CEREBRAL TRAUMA damage to the brain CESSATION stopping CHD coronary heart disease CHEMOTHERAPY treatment of disease, usually cancer, by chemical agents CHRONIC continuing for a long time, ongoing CLINICAL pertaining to medical care CLINICAL TRIAL an experiment involving human subjects COMA unconscious state COMPLETE RESPONSE total disappearance of disease CONGENITAL present before birth CONJUNCTIVITIS redness and irritation of the thin membrane that covers the eye CONSOLIDATION PHASE treatment phase intended to make a remission permanent (follows induction phase) CONTROLLED TRIAL research study in which the experimental treatment or procedure is compared to a standard (control) treatment or procedure COOPERATIVE GROUP association of multiple institutions to perform clinical trials CORONARY related to the blood vessels that supply the heart, or to the heart itself CT SCAN (CAT) computerized series of x-rays (computerized tomography) CULTURE test for infection, or for organisms that could cause infection CUMULATIVE added together from the beginning CUTANEOUS relating to the skin CVA stroke (cerebrovascular accident)

DERMATOLOGIC pertaining to the skin DIASTOLIC lower number in a blood pressure reading DISTAL toward the end, away from the center of the body DIURETIC "water pill" or drug that causes increase in urination DOPPLER device using sound waves to diagnose or test DOUBLE BLIND study in which neither investigators nor subjects know what drug or treatment the subject is receiving DYSFUNCTION state of improper function DYSPLASIA abnormal cells

ECHOCARDIOGRAM sound wave test of the heart EDEMA excess fluid collecting in tissue EEG electric brain wave tracing (electroencephalogram) EFFICACY effectiveness ELECTROCARDIOGRAM electrical tracing of the heartbeat (ECG or EKG) ELECTROLYTE IMBALANCE an imbalance of minerals in the blood EMESIS vomiting EMPIRIC based on experience ENDOSCOPIC EXAMINATION viewing an internal part of the body with a lighted tube ENTERAL by way of the intestines EPIDURAL outside the spinal cord ERADICATE get rid of (such as disease) Page 2 of 7 EVALUATED, ASSESSED examined for a medical condition EXPEDITED REVIEW rapid review of a protocol by the IRB Chair without full committee approval, permitted with certain low-risk research studies EXTERNAL outside the body EXTRAVASATE to leak outside of a planned area, such as out of a blood vessel

FDA U.S. Food and Drug Administration, the branch of federal government that approves new drugs FIBROUS having many fibers, such as scar tissue FIBRILLATION irregular beat of the heart or other muscle

GENERAL ANESTHESIA pain prevention by giving drugs to cause loss of consciousness, as during surgery GESTATIONAL pertaining to pregnancy

HEMATOCRIT amount of red blood cells in the blood HEMATOMA a bruise, a black and blue mark HEMODYNAMIC MEASURING blood flow HEMOLYSIS breakdown in red blood cells HEPARIN LOCK needle placed in the arm with blood thinner to keep the blood from clotting HEPATOMA cancer or tumor of the liver HERITABLE DISEASE can be transmitted to one’s offspring, resulting in damage to future children HISTOPATHOLOGIC pertaining to the disease status of body tissues or cells HOLTER MONITOR a portable machine for recording heart beats HYPERCALCEMIA high blood calcium level HYPERKALEMIA high blood potassium level HYPERNATREMIA high blood sodium level HYPERTENSION high blood pressure HYPOCALCEMIA low blood calcium level HYPOKALEMIA low blood potassium level HYPONATREMIA low blood sodium level HYPOTENSION low blood pressure HYPOXEMIA a decrease of oxygen in the blood HYPOXIA a decrease of oxygen reaching body tissues HYSTERECTOMY surgical removal of the uterus, ovaries (female sex glands), or both uterus and ovaries

IATROGENIC caused by a physician or by treatment IDE investigational device exemption, the license to test an unapproved new medical device IDIOPATHIC of unknown cause IMMUNITY defense against, protection from IMMUNOGLOBIN a protein that makes antibodies IMMUNOSUPPRESSIVE drug which works against the body's immune (protective) response, often used in transplantation and diseases caused by immune system malfunction IMMUNOTHERAPY giving of drugs to help the body's immune (protective) system; usually used to destroy cancer cells IMPAIRED FUNCTION abnormal function IMPLANTED placed in the body IND investigational new drug, the license to test an unapproved new drug INDUCTION PHASE beginning phase or stage of a treatment INDURATION hardening INDWELLING remaining in a given location, such as a catheter INFARCT death of tissue due to lack of blood supply INFECTIOUS DISEASE transmitted from one person to the next INFLAMMATION swelling that is generally painful, red, and warm INFUSION slow injection of a substance into the body, usually into the blood by means of a catheter INGESTION eating; taking by mouth INTERFERON drug which acts against viruses; antiviral agent INTERMITTENT occurring (regularly or irregularly) between two time points; repeatedly stopping, then starting again INTERNAL within the body INTERIOR inside of the body INTRAMUSCULAR into the muscle; within the muscle INTRAPERITONEAL into the abdominal cavity INTRATHECAL into the spinal fluid INTRAVENOUS (IV) through the vein INTRAVESICAL in the bladder INTUBATE the placement of a tube into the airway INVASIVE PROCEDURE puncturing, opening, or cutting the skin INVESTIGATIONAL NEW DRUG (IND) a new drug that has not been approved by the FDA INVESTIGATIONAL METHOD a treatment method which has not been proven to be beneficial or has not been accepted as standard care ISCHEMIA decreased oxygen in a tissue (usually because of decreased blood flow)

LAPAROTOMY surgical procedure in which an incision is made in the abdominal wall to enable a doctor to look at the organs inside LESION wound or injury; a diseased patch of skin LETHARGY sleepiness, tiredness LEUKOPENIA low white blood cell count LIPID fat LIPID CONTENT fat content in the blood LIPID PROFILE (PANEL) fat and cholesterol levels in the blood LOCAL ANESTHESIA creation of insensitivity to pain in a small, local area of the body, usually by injection of numbing drugs LOCALIZED restricted to one area, limited to one area LUMEN the cavity of an organ or tube (e.g., blood vessel) LYMPHANGIOGRAPHY an x-ray of the lymph nodes or tissues after injecting dye into lymph vessels (e.g., in feet) LYMPHOCYTE a type of white blood cell important in immunity (protection) against infection LYMPHOMA a cancer of the lymph nodes (or tissues)

MALAISE a vague feeling of bodily discomfort, feeling badly MALFUNCTION condition in which something is not functioning properly MALIGNANCY cancer or other progressively enlarging and spreading tumor, usually fatal if not successfully treated MEDULLABLASTOMA a type of brain tumor MEGALOBLASTOSIS change in red blood cells METABOLIZE process of breaking down substances in the cells to obtain energy METASTASIS spread of cancer cells from one part of the body to another METRONIDAZOLE drug used to treat infections caused by parasites (invading organisms that take up living in the body) or other causes of anaerobic infection (not requiring oxygen to survive) MI myocardial infarction, heart attack MINIMAL slight MINIMIZE reduce as much as possible Page 4 of 7 MONITOR check on; keep track of; watch carefully MOBILITY ease of movement MORBIDITY undesired result or complication MORTALITY death MOTILITY the ability to move MRI magnetic resonance imaging, diagnostic pictures of the inside of the body, created using magnetic rather than x-ray energy MUCOSA, MUCOUS MEMBRANE moist lining of digestive, respiratory, reproductive, and urinary tracts MYALGIA muscle aches MYOCARDIAL pertaining to the heart muscle MYOCARDIAL INFARCTION heart attack

NASOGASTRIC TUBE placed in the nose, reaching to the stomach NCI the National Cancer Institute NECROSIS death of tissue NEOPLASIA/NEOPLASM tumor, may be benign or malignant NEUROBLASTOMA a cancer of nerve tissue NEUROLOGICAL pertaining to the nervous system NEUTROPENIA decrease in the main part of the white blood cells NIH the National Institutes of Health NONINVASIVE not breaking, cutting, or entering the skin NOSOCOMIAL acquired in the hospital

OCCLUSION closing; blockage; obstruction ONCOLOGY the study of tumors or cancer OPHTHALMIC pertaining to the eye OPTIMAL best, most favorable or desirable ORAL ADMINISTRATION by mouth ORTHOPEDIC pertaining to the bones OSTEOPETROSIS rare bone disorder characterized by dense bone OSTEOPOROSIS softening of the bones OVARIES female sex glands

PARENTERAL given by injection PATENCY condition of being open PATHOGENESIS development of a disease or unhealthy condition PERCUTANEOUS through the skin PERIPHERAL not central PER OS (PO) by mouth PHARMACOKINETICS the study of the way the body absorbs, distributes, and gets rid of a drug PHASE I first phase of study of a new drug in humans to determine action, safety, and proper dosing PHASE II second phase of study of a new drug in humans, intended to gather information about safety and effectiveness of the drug for certain uses PHASE III large-scale studies to confirm and expand information on safety and effectiveness of new drug for certain uses, and to study common side effects PHASE IV studies done after the drug is approved by the FDA, especially to compare it to standard care or to try it for new uses PHLEBITIS irritation or inflammation of the vein PLACEBO an inactive substance; a pill/liquid that contains no medicine PLACEBO EFFECT improvement seen with giving subjects a placebo, though it contains no active drug/treatment PLATELETS small particles in the blood that help with clotting POTENTIAL possible POTENTIATE increase or multiply the effect of a drug or toxin (poison) by giving another drug or toxin at the same time (sometimes an unintentional result) POTENTIATOR an agent that helps another agent work better PRENATAL before birth PROPHYLAXIS a drug given to prevent disease or infection PER OS (PO) by mouth PRN as needed PROGNOSIS outlook, probable outcomes PRONE lying on the stomach PROSPECTIVE STUDY following patients forward in time PROSTHESIS artificial part, most often limbs, such as arms or legs PROTOCOL plan of study PROXIMAL closer to the center of the body, away from the end PULMONARY pertaining to the lungs

QD every day; daily QID four times a day

RADIATION THERAPY x-ray or cobalt treatment RANDOM by chance (like the flip of a coin) RANDOMIZATION chance selection RBC red blood cell RECOMBINANT formation of new combinations of genes RECONSTITUTION putting back together the original parts or elements RECUR happen again REFRACTORY not responding to treatment REGENERATION re-growth of a structure or of lost tissue REGIMEN pattern of giving treatment RELAPSE the return of a disease REMISSION disappearance of evidence of cancer or other disease RENAL pertaining to the kidneys REPLICABLE possible to duplicate RESECT remove or cut out surgically RETROSPECTIVE STUDY looking back over past experience

SARCOMA a type of cancer SEDATIVE a drug to calm or make less anxious SEMINOMA a type of testicular cancer (found in the male sex glands) SEQUENTIALLY in a row, in order SOMNOLENCE sleepiness SPIROMETER an instrument to measure the amount of air taken into and exhaled from the lungs STAGING an evaluation of the extent of the disease STANDARD OF CARE a treatment plan that the majority of the medical community would accept as appropriate STENOSIS narrowing of a duct, tube, or one of the blood vessels in the heart STOMATITIS mouth sores, inflammation of the mouth STRATIFY arrange in groups for analysis of results (e.g., stratify by age, sex, etc.) STUPOR stunned state in which it is difficult to get a response or the attention of the subject SUBCLAVIAN under the collarbone SUBCUTANEOUS under the skin SUPINE lying on the back SUPPORTIVE CARE general medical care aimed at symptoms, not intended to improve or cure underlying disease SYMPTOMATIC having symptoms SYNDROME a condition characterized by a set of symptoms SYSTOLIC top number in blood pressure; pressure during active contraction of the heart

TERATOGENIC capable of causing malformations in a fetus (developing baby still inside the mother’s body) TESTES/TESTICLES male sex glands THROMBOSIS clotting THROMBUS blood clot TID three times a day TITRATION a method for deciding on the strength of a drug or solution; gradually increasing the dose T-LYMPHOCYTES type of white blood cells TOPICAL on the surface TOPICAL ANESTHETIC applied to a certain area of the skin and reducing pain only in the area to which applied TOXICITY side effects or undesirable effects of a drug or treatment TRANSDERMAL through the skin TRANSIENTLY temporarily TRAUMA injury; wound TREADMILL walking machine used to test heart function

UPTAKE absorbing and taking in of a substance by living tissue

VALVULOPLASTY plastic repair of a valve, especially a heart valve VARICES enlarged veins VASOSPASM narrowing of the blood vessels VECTOR a carrier that can transmit disease-causing microorganisms (germs and viruses) VENIPUNCTURE needle stick, blood draw, entering the skin with a needle VERTICAL TRANSMISSION spread of disease

WBC white blood cell

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Importance of host feeding in the biological control of insect pests: case study of egg parasitoid species (hymenoptera: chalcidoidea: trichogrammatidae).

Simple Summary

Graphical Abstract

1. Introduction

2. materials and methods, 2.1. biological material, 2.2. experimental design and procedures, 2.2.1. experiment 1: t. achaeae – t. brassicae interaction, 2.2.2. experiment 2: functional response of t. achaeae and t. brassicae, 2.2.3. experiment 3: effect of t. achaeae – t. brassicae interaction on the functional response, 3.1. t. achaeae–t. brassicae interaction, 3.2. functional response, 3.3. effect of t. achaeae–t. brassicae interaction on the functional response, 4. discussion.

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Author Contributions

Data availability statement, conflicts of interest.

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Species	Parameters	Values (±SE)	Confidence Interval (P = 0.05)		Best-Fit Model
Species	Parameters	Values (±SE)	Lower Limit	Upper Limit	Best-Fit Model
T. achaeae	P (interception)	3.506 ± 0.571	−3.745	10.758	Type II
T. achaeae	P (linear)	−0.477 ± 0.036	−0.938	−0.017	Type II
T. brassicae	P (interception)	1.660 ± 1.1250	−3.181	6.501	Type I
T. brassicae	P (linear)	−0.022 ± 0.050	−0.235	0.191	Type I

Species	Functional Response	Parameters (±SE)		Statistical Parameters
Species	Functional Response	a′/ (day )/(per-unit)	T (day)	d.f.	R	AIC
T. achaeae	Type I	0.809 ± 0.113	—	5	0.859	2.564
	Type II	9.996 ± 4.973	0.018 ± 0.001	5	0.998	2.336
	Type III	64.830 ± 22.355	0.018 ± 0.003	5	0.997	3.463
T. brassicae	Type I	1.043 ± 0.044	—	5	0.994	2.564
	Type II	2.653 ± 1.220	0.011 ± 0.003	5	0.981	8.608
	Type III	0.137 ± 0.064	0.015 ± 0.001	5	0.982	8.417

Species	Parameters	Values (±SE)	Confidence Interval (P = 0.05)		Best-Fit Model
Species	Parameters	Values (±SE)	Lower Limit	Upper Limit	Best-Fit Model
T. achaeae	P (interception)	3.586 ± 2.010	−5.046	12.218	Type I
T. achaeae	P (linear)	−0.047 ± 0.077	−0.380	0.285	Type I
T. brassicae	P (interception)	0.024 ± 0.402	−5.133	5.085	Type I
T. brassicae	P (linear)	0.075 ± 0.028	−0.282	0.431	Type I

Species	Functional Response	Parameters (±SE)		Statistical Parameters
Species	Functional Response	a′/ (day )/(per-unit)	T (Day)	d.f.	R	AIC
T. achaeae	Type I	0.879 ± 0.072	—	5	0.949	8.658
	Type II	1.652 ± 0.789	0.007 ± 0.002	5	0.960	10.072
	Type III	0.121 ± 0.011	0.014 ± 0.001	5	0.935	12.439
T. brassicae	Type I	0.951 ± 0.065	—	5	0.972	7.601
	Type II	0.805 ± 0.419	0.003 ± 0.001	5	0.965	11.322
	Type III	0.034 ± 0.018	0.008 ± 0.002	5	0.932	13.341

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Share and Cite

Cabello, T.; Gallego, J.R.; Lopez, I.; Gamez, M.; Garay, J. Importance of Host Feeding in the Biological Control of Insect Pests: Case Study of Egg Parasitoid Species (Hymenoptera: Chalcidoidea: Trichogrammatidae). Insects 2024 , 15 , 496. https://doi.org/10.3390/insects15070496

Cabello T, Gallego JR, Lopez I, Gamez M, Garay J. Importance of Host Feeding in the Biological Control of Insect Pests: Case Study of Egg Parasitoid Species (Hymenoptera: Chalcidoidea: Trichogrammatidae). Insects . 2024; 15(7):496. https://doi.org/10.3390/insects15070496

Cabello, Tomas, Juan Ramón Gallego, Inmaculada Lopez, Manuel Gamez, and Jozsef Garay. 2024. "Importance of Host Feeding in the Biological Control of Insect Pests: Case Study of Egg Parasitoid Species (Hymenoptera: Chalcidoidea: Trichogrammatidae)" Insects 15, no. 7: 496. https://doi.org/10.3390/insects15070496

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Early-Onset Schizophrenia With Predominantly Negative Symptoms: A Case Study of a Drug-Naive Female Patient Treated With Cariprazine

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Schizophrenia case studies: putting theory into practice

Case study 1: A man who suddenly stops smoking

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Case 2: A woman with constipation

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Case 3: A mother is concerned for her son who is talking to someone who is not there

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