Abstract
Posttraumatic stress disorder (PTSD) is highly comorbid with schizophrenia and may be associated with higher levels or lower levels of negative symptoms. In the current study, we attempted to clarify the relationship between PTSD and negative symptoms by examining the proportion of patients meeting various negative symptom criteria in a sample of patients diagnosed with schizophrenia alone or schizophrenia and comorbid PTSD. Results indicated that the presence of PTSD in schizophrenia was associated with increased secondary negative symptoms, with the deficit syndrome (DS) and primary negative symptoms associated with lower rates of current and lifetime diagnoses of PTSD. Furthermore, the deficit/nondeficit classification provided greater differentiation of PTSD symptoms than did negative symptoms defined more broadly using the Scale for the Assessment of Negative Symptoms or primary vs secondary distinctions. These findings suggest that DS patients are at a uniquely low risk for PTSD.
Keywords: schizophrenia, deficit syndrome, negative symptoms, trauma, PTSD
Introduction
Anxiety and trauma have long been thought to play a role in the development and maintenance of psychosis. However, few studies have examined the co-occurrence of anxiety disorders and schizophrenia.1 Of the major anxiety disorders identified in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV),2 lifetime prevalence rates have been estimated to be at least moderate in individuals diagnosed with schizophrenia: obsessive compulsive disorder (1.9%–35.0%), generalized anxiety disorder (2.5%–16.7%), panic disorder (3.3%–20.0%), social phobia (8.2%–36.3%), specific phobia (2.5%–13.6%), agoraphobia (3.8%–6.7%), and posttraumatic stress disorder (PTSD) (19.0%–66.0%).3–5 Of the anxiety disorders, PTSD has received relatively little attention, despite the presumed role of trauma and psychological stress in predicting onset and relapse in schizophrenia.6 Within the limited literature examining trauma and psychosis, individuals with schizophrenia carrying a comorbid PTSD diagnosis have been found to have more frequent violent thoughts, behaviors, and feelings, heightened paranoia, and greater severity of delusions and hallucinations.7–9 Negative beliefs about the self and others may mediate the relationship between trauma and paranoia, and re-experiencing symptoms may mediate the link between trauma and hallucinations.10 Comorbid PTSD has also been associated with a number of poor outcomes, including lower quality of life,5,11 higher rates of suicidal ideation and behavior,12 and increased utilization of medical services.11 Thus, PTSD and trauma seem to have a clear link with functional disability and positive symptoms of schizophrenia.
It is less clear whether symptoms of PTSD are associated with the negative symptoms of schizophrenia, with some studies reporting an increased incidence of negative symptoms13–15 and others reporting decreased negative symptoms.8,16–18 One explanation for these discrepant findings might be that patient samples differed with regard to the prevalence of patients whose negative symptoms could be considered primary or secondary features of the illness. Primary negative symptoms are those that are idiopathic to the disease process itself, while secondary negative symptoms are those that arise from secondary factors, such as depression, anxiety, and medication effects. Patients displaying primary negative symptoms that are persistent for a period of 12 months or longer are further classified as meeting criteria for “deficit syndrome (DS) schizophrenia.”19
If PTSD is associated with increased severity of negative symptoms, one would expect that these negative symptoms would be due to secondary causes. Although not directly stated, such a possibility has been alluded to in previous studies, where it has been suggested that negative symptoms may sometimes occur as an anxiety reaction in response to a traumatic event.7 For example, it is possible that flat affect may reflect symptoms of emotional numbing often seen in PTSD or that limited social interaction and poor eye-contact may be indicative of purposeful avoidance that occurs as part of a PTSD reaction, rather than symptoms of emotional withdrawal. In such cases, negative symptoms would not be considered primary manifestations of the disease process of schizophrenia itself but rather secondary to symptoms associated with anxiety and trauma.
It is also equally plausible to expect that patients with PTSD would be highly unlikely to display negative symptoms that are primary in nature. Consistent with this notion is evidence showing that patients with primary and enduring negative symptoms, such as those with the DS,19 are at reduced risk for experiencing a number of negative emotions (as measured by clinical ratings) that are commonly associated with PTSD (eg, depression, guilt, hostility, and anxiety).20–24 For DS patients and for those with primary negative symptoms, it is possible that the diminished frequency and intensity of negative emotional experience buffer against the development of PTSD when traumatic events are encountered. Similarly, increased secondary negative symptoms would be expected when a diagnosis of PTSD is present in schizophrenia.
At first glance, it would seem that reduced prevalence of PTSD in patients with primary negative symptoms and those with the DS would be tautological; however, this is not the case for several reasons. First, there is mixed evidence with regard to whether DS patients report experiencing reduced negative affect, with several studies using clinical rating scales indicating reduction in various negative emotions23,25,26 while other studies using questionnaires and laboratory-based measures have found contradictory results indicating that deficit patients actually have elevated levels of negative emotional experience.27–30 Given these mixed results, and the lack of focused investigations examining primary and secondary negative symptoms when PTSD is present in schizophrenia, it is not currently possible to draw definitive conclusions regarding whether DS patients do in fact have reduced levels of negative emotion or rather have elevated levels of negative affect and similarly whether their experience of negative emotions would buffer them from developing PTSD or put them at higher risk for it. Second, it is unclear whether the diminished emotional range seen in DS patients reflects a reduced capacity to experience emotion (ie, reduced intensity) or rather a reduced frequency of emotional experiences in their daily lives. It may be that when confronted with an emotional stimulus that carries enough salience, such as a traumatic event, that event is capable of generating a viable emotional experience that would not occur during the normal course of the patient's life. It is possible that clinician-based interviews reflect this decreased frequency of emotional experience, despite the fact that these patients are capable of experiencing negative emotion when confronted with salient environmental stimuli. Third, even if patients with primary negative symptoms experience less negative emotion at the time of interview/testing (which is unclear and potentially confounded by methodological influences), this does not in fact preclude them from having a lifetime diagnosis of PTSD. It is possible that DS patients could have developed PTSD before developing psychosis or before developing negative symptoms. It is unknown whether the presumed inability to experience emotion that is seen in the DS exists prior to the onset of psychosis or whether such impairments develop later in the course of the illness. As such, it is unclear whether DS patients would in fact be at reduced risk for developing PTSD throughout the lifetime. However, this is an interesting question given that traumatic experiences are not simply limited to adulthood and an area that warrants investigation in future studies. Fourth, not all DS patients have diminished emotional experience. Rather, some have prominent symptoms of avolition31 with normal emotional experience when interviewed using clinical measures such as the Schedule for the Deficit Syndrome (SDS). Thus, one cannot definitively say that any observed reductions in the rate of individuals with schizophrenia and comorbid PTSD who exhibit primary negative symptoms or meet criteria for the DS is tautological.
Greater knowledge of the characteristics placing individuals with schizophrenia at risk for PTSD would significantly advance schizophrenia research and treatment, allowing for more efficient allocation of intervention resources and clarification of the effects of trauma on the course of illness. In the current study, we selected samples of schizophrenia patients with and without current/lifetime diagnoses of PTSD and examined the prevalence of patients within the PTSD groups who met criteria for various negative symptom classifications. Individuals with schizophrenia with and without PTSD were divided into groups based on the severity and cause of negative symptoms using a number of criteria, including (1) high and low negative symptoms defined using the Scale for the Assessment of Negative Symptoms (SANS), (2) presence of primary vs secondary negative symptoms, and (3) presence or absence of DS schizophrenia. Comparisons were conducted to determine the prevalence of individuals with and without diagnoses of PTSD who fell into these various negative symptom classifications. Based upon previous research, it was hypothesized that secondary negative symptoms would be associated with higher rates of PTSD, while primary negative symptoms would be associated with decreased prevalence of current and lifetime PTSD. It was further hypothesized that the deficit-nondeficit classification would predict PTSD diagnosis better then negative symptom classifications made based upon high-low SANS and primary/secondary classifications alone, reflecting the importance of the persistence factor delineated in the DS diagnosis.
Methods
Participants
Participants in the current study included 70 chronic outpatients diagnosed with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR), schizophrenia.2 Patients were on average 42.4 years old and had 11.9 years of education. The sample was approximately 57.1% male and 45.7% Caucasian. Mean age of onset was 20.4 years. Mean Brief Psychiatric Rating Scale (BPRS)32 total scores were 42.14, indicating that patients were experiencing a moderate level of symptoms at the time of evaluation. Approximately 8.6% of patients were prescribed conventional antipsychotics and 91.4% were prescribed atypical antipsychotics.
Patients were divided into schizophrenia with comorbid PTSD (SZ + PTSD) and schizophrenia without comorbid PTSD (SZ − PTSD) for both lifetime and current diagnoses. For current PTSD diagnoses, SZ + PTSD and SZ − PTSD did not significantly differ on age, education, race, or chlorpromazine equivalent dosage.33 There was a significantly greater proportion of females then males in the SZ + PTSD group. Analysis of the lifetime SZ + PTSD and SZ − PTSD groups also indicated that groups did not differ on relevant demographics, except for a greater proportion of females in the SZ + PTSD group.
Patients were recruited from a local community outpatient mental health center in Nevada and were identified by their treating psychiatrist for inclusion in the study if they carried a primary clinical diagnosis of DSM-IV-TR schizophrenia. All patients were recruited from the community and received monetary compensation for their participation. They were told that they were volunteering to participate in a study examining symptoms, cognition, and emotional functioning. The participation rate of patients referred by treating physicians was moderately high (∼70%).
Diagnoses of schizophrenia and PTSD were further confirmed using the Structured Clinical Interview for DSM-IV (SCID).34 Additionally, treating psychiatrists and other program staff were consulted, and medical records were thoroughly reviewed to inform Axis I diagnoses. PTSD diagnoses were supplemented by information gathered from the Life Events Checklist from the Clinician Administered PTSD Scale (CAPS). Exclusionary criteria included (1) English as secondary language, (2) history of traumatic brain injury or condition that would affect central nervous system function, (3) diagnosis of mental retardation, (4) use of medications that could produce significant cognitive effects (other than those prescribed to treat schizophrenia), and (5) corrected vision worse than 20/50.
Measures
Measures included in the current study were designed to evaluate clinical diagnosis, traumatic experience, and schizophrenia symptomology.
Clinical Diagnosis and Symptom Assessment.
The SCID34 was administered to determine Axis I psychiatric diagnosis and identify clinical symptoms. All SCID modules were administered; however, only data from the Psychotic and Anxiety disorder modules were examined in the current study. Interrater reliability of the SCID has been shown to be excellent (kappa = .85, range = .71–.97), and diagnostic accuracy, as compared with consensus diagnosis, has been found to be very accurate (82%).35 A study conducted by Fennig et al36 suggests that the SCID-I is a valid instrument for the diagnosis of schizophrenia, as SCID schizophrenia diagnosis displayed good sensitivity (.89), specificity (.96), and agreement (.86) when compared with best-estimate diagnosis made by psychiatrists on first-admission psychotic patients.
The Life Events Checklist from the CAPS37 was administered to all participants. The CAPS is a structured clinical interview measuring major PTSD categories and has been found to have excellent psychometric properties and diagnostic utility.38 The life events checklist assesses whether participants have experienced, witnessed, or learned about 17 common traumatic life events (eg, natural disaster, fire or explosion, serious injury, or harm). Scores are used to estimate the number of traumatic exposures an individual has experienced in a lifetime. In the current study, events endorsed by participants were followed up by questioning to determine whether events were experienced as traumatic and whether events resulted in a traumatic response.
Clinical rating scales completed to assess symptoms of schizophrenia included the SDS,39 SANS,40 Scale for the Assessment of Positive Symptoms (SAPS),41 BPRS,32 and Abnormal Involuntary Movement Scale.42
Procedure
The aforementioned clinical measures were administered as part of a larger battery of symptom, affective neuroscience, and neuropsychological tests. Demographic, diagnostic, and symptom ratings were obtained prior to administration of the neurocognitive tests for all patients. Evaluations typically lasted from 3 to 4 h, and breaks were afforded as needed to diminish fatigue and maintain effort. Evaluations were conducted by experienced doctoral students who were extensively trained to complete procedures in a reliable and valid manner. Evaluations occurred in a quiet and private setting, and procedures were approved by the University Institutional Review Board.
Classification of Negative Symptom Subgroups
Individuals with schizophrenia were divided into various negative symptom subgroups to determine the association between negative symptoms and PTSD. Three classifications were used: (1) high SANS total vs low SANS total, (2) primary vs secondary, and (3) deficit vs nondeficit. High and low negative symptom classification was determined using a median split on the SANS total score. The high negative symptom group had a mean SANS total score of 67.0 (SD = 22.0) and the low negative symptom group received a score of 22.9 (SD = 10.8) (F = 111.09, P < .001).
Primary vs secondary negative symptom distinctions were made using the SDS. Patients were considered to meet criteria for the secondary negative symptom group if they received a score of 2 or greater (moderate severity) on at least 1 of the 6 SDS subscales, and if the symptoms did not meet SDS criteria for being considered primary. Patients who received a score of 2 or greater, as well as a judgment that the symptoms were considered primary on any of the 6 SDS subscales, were designated as falling into the primary negative symptom group. In the event that patients received both primary and secondary ratings for SDS subscales meeting severity criteria, these patients were considered to display secondary negative symptoms. This procedure was implemented to obtain a “purer” group of primary negative symptom patients that would be closer in presentation to DS patients, which would allow for a comparison of deficit vs primary symptoms and, thus, directly assess the effects of the stability criteria of the DS on PTSD comorbidity. This classification resulted in 21 primary and 15 secondary negative symptom patients.
The SDS was used to separate schizophrenia patients into DS and nondeficit syndrome (ND) subgroups. This procedure resulted in the identification of 15 DS and 55 ND schizophrenia patients. DS and ND groups were compared on relevant demographic and clinical features to ensure the validity of the DS classification. Analysis of variance (ANOVA) and chi-square analyses examining variables relevant to DS status suggested that DS and ND patients displayed clinical and demographic features consistent with the DS literature. Specifically, DS and ND patients did not significantly differ on education or age, and both groups had a higher percentage of males than females. There was a trend toward significant differences in ethnicity, where African Americans made up a somewhat greater proportion of the DS than ND sample. DS and ND groups did not differ on age of onset, extrapyramidal symptom severity as measured by the Abnormal Involuntary Movement Scale total score (DS: mean [M] = 7.5, SD = 6.5; ND: M = 5.1, SD = 5.8; F = 1.9, P = .17), or daily antipsychotic medication dosage. DS and ND patients were also prescribed a similar regiment of antipsychotic medication. More severe total SANS negative symptoms and less severe SAPS total positive symptoms were found in the DS group, and no differences were found for BPRS disorganized symptoms (DS: M = 7.3, SD = 2.5; ND: M = 7.4, SD = 3.1; F = 0.01, P = .96). Additionally, DS patients received significantly lower scores on BPRS items assessing dysphoria: Anxiety (DS: M = 1.73, SD = 1.03; ND: M = 3.22, SD = 1.61; F = 11.45, P < .001), Guilt (DS: M = 1.13, SD = 0.52; ND: M = 2.89, SD = 1.76), Hostility (DS: M = 1.27, SD = 0.59; ND: M = 2.30, SD = 1.54), and Depression (DS: M = 1.07, SD = 0.26; ND: M = 1.98, SD = 1.56).
The various negative symptom patient classifications did not differ on age, education, percent of males, ethnicity, chlorpromazine equivalent dosage, or SAPS total scores. Groups were also prescribed a similar regiment of antipsychotic medications at the time of testing. Demographic and clinical characteristics are presented in table 1.
Table 1.
Demographic and Clinical Characteristics of Patient Groups
| Deficit (n = 15)—Mean (SD) | Nondeficit (n = 55)—Mean (SD) | Test Statistic | P Value | |
| Age (years) | 45.8 (12.5) | 41.5 (10.7) | F = 01.8 | .19 |
| Education (years) | 12.4 (01.7) | 11.8 (01.9) | F = 01.3 | 27 |
| Male | 60.0% | 56.4% | χ2 = 0.06 | .52 |
| Ethnicity | 26.7% | 50.9% | χ2 = 0.10 | .11 |
| CPZ dosage | 861 (572) | 712 (590) | χ2 = 0.67 | .42 |
| SANS total | 76.3 (23.3) | 36.6 (22.8) | F = 35.1 | <.001 |
| SAPS total | 21.9 (11.3) | 33.6 (19.0) | F = 5.15 | .03 |
| Prescribed conventional | 13.3% | 09.1% | F = 0.24 | .47 |
| Prescribed atypical | 93.3% | 90.9% | F = 0.09 | .62 |
| Primary (n = 21)—Mean (SD) | Secondary (n = 15)—Mean (SD) | |||
| Age | 46.6 (11.1) | 40.5 (7.6) | F = 3.40 | .07 |
| Education | 12.1 (01.7) | 12.2 (01.8) | F = 0.01 | .97 |
| Male | 66.7% | 53.3% | χ2 = 0.66 | .32 |
| Ethnicity | 42.9% | 33.3% | χ2 = 02.4 | .66 |
| CPZ dosage | 811.7 (498) | 654 (678) | F = 0.64 | .43 |
| SANS total | 53.7 (24.6) | 50.1 (25.8) | F = 0.18 | .67 |
| SAPS total | 32.5 (19.1) | 35.9 (19.2) | F = 0.28 | .60 |
| Prescribed conventional | 14.0% | 13.0% | F = 0.60 | .94 |
| Prescribed atypical | 95.0% | 93.0% | F = 0.06 | .81 |
| High SANS (n = 35)—Mean (SD) | Low SANS (n = 35)—Mean (SD) | |||
| Age | 42.8 (12.1) | 41.9 (10.3) | F = 0.10 | .75 |
| Education | 11.9 (01.7) | 11.9 (02.1) | F = 0.02 | .90 |
| Male | 62.9% | 51.4% | χ2 = 0.93 | .24 |
| Caucasian | 37.1% | 54.3% | χ2 = 4.07 | .66 |
| CPZ dosage | 885.5 (699.8) | 600.3 (500.1) | F = 3.80 | .056 |
| SANS total | 67.0 (22.0) | 22.9 (10.8) | F = 111.09 | <.001 |
| SAPS total | 30.9 (16.1) | 31.4 (20.4) | F = 0.13 | .91 |
| Prescribed conventional | 14% | 6% | F = 01.4 | .28 |
| Prescribed atypical | 97% | 86% | F = 2.96 | .09 |
Results
Differences in Negative Symptom Severity Between Patients With and Without PTSD
As a first level of analysis, severity of negative symptoms was compared between schizophrenia patients with and without current and lifetime diagnoses of PTSD. Individual one-way ANOVAs comparing patients with current PTSD (SZ + PTSD) vs patients without current PTSD (SZ − PTSD) on SDS, SANS, and BPRS negative symptom items indicated a significant difference only for the SANS global blunted affect rating, such that SZ − PTSD had a greater severity of blunted affect.
Comparisons of SZ + PTSD lifetime and SZ − PTSD lifetime indicated significant differences for SDS blunted affect, SDS diminished emotional range, SDS diminished sense of purpose, SANS global affective flattening, and BPRS blunted affect. For each of these negative symptom items, SZ − PTSD was found to have a significantly greater severity of negative symptoms (see table 2).
Table 2.
Severity of Negative Symptoms in Patients With and Without PTSD
| SZ − PTSD |
SZ + PTSD |
F | P | |||
| Mean | SD | Mean | SD | |||
| Current PTSD | ||||||
| SDS blunted affect | 1.47 | 1.28 | 1.07 | 1.38 | 1.05 | .31 |
| SDS emotional range | 0.85 | 1.16 | 0.36 | 1.08 | 2.10 | .15 |
| SDS poverty of speech | 0.78 | 1.18 | 0.71 | 1.43 | 0.03 | .86 |
| SDS curbed interests | 0.98 | 1.19 | 0.93 | 1.26 | 0.22 | .88 |
| SDS sense of purpose | 1.11 | 1.33 | 1.14 | 1.26 | 0.36 | .55 |
| SDS social drive | 1.16 | 1.28 | 0.93 | 1.23 | 0.01 | .93 |
| SANS global affective flattening | 2.35 | 1.56 | 1.43 | 1.28 | 4.09 | .05 |
| SANS global alogia | 1.82 | 1.38 | 1.21 | 1.57 | 2.00 | .16 |
| SANS global avolition | 1.93 | 1.46 | 1.71 | 1.43 | 0.24 | .63 |
| SANS global anhedonia-asociality | 2.09 | 1.51 | 2.21 | 1.67 | 0.07 | .79 |
| BPRS emotional withdrawal | 2.64 | 1.86 | 2.36 | 2.09 | 0.24 | .63 |
| BPRS motor retardation | 2.05 | 1.52 | 2.00 | 1.66 | 0.01 | .91 |
| BPRS blunted affect | 3.25 | 2.06 | 2.29 | 1.97 | 2.50 | .11 |
| Lifetime PTSD | ||||||
| SDS blunted affect | 1.72 | 1.27 | 0.97 | 1.24 | 6.00 | .02 |
| SDS emotional range | 1.05 | 1.27 | 0.37 | 0.85 | 6.43 | .01 |
| SDS poverty of speech | 0.82 | 1.18 | 0.70 | 1.29 | 0.15 | .69 |
| SDS curbed interests | 1.13 | 1.28 | 0.77 | 1.07 | 1.55 | .22 |
| SDS sense of purpose | 1.31 | 1.35 | 0.87 | 1.14 | 5.70 | .02 |
| SDS social drive | 1.44 | 1.42 | 0.70 | 1.00 | 2.09 | .15 |
| SANS global affective flattening | 2.62 | 1.52 | 1.57 | 1.38 | 8.64 | <.001 |
| SANS global alogia | 1.85 | 1.44 | 1.50 | 1.43 | 0.98 | .33 |
| SANS global avolition | 1.97 | 1.60 | 1.77 | 1.25 | 0.34 | .56 |
| SANS global anhedonia-asociality | 2.33 | 1.54 | 1.83 | 1.48 | 1.83 | .18 |
| BPRS emotional withdrawal | 2.90 | 1.94 | 2.17 | 1.80 | 2.55 | .11 |
| BPRS motor retardation | 2.21 | 1.50 | 1.83 | 1.57 | 0.19 | .32 |
| BPRS blunted affect | 3.62 | 2.10 | 2.33 | 1.83 | 7.08 | .01 |
High vs Low SANS Total Negative Symptoms
Current and lifetime PTSD diagnoses were compared among high and low negative symptom groups. Mean percent of high and low negative symptom patients meeting DSM-IV diagnostic criteria for current and lifetime PTSD are presented in table 2. Results of a chi-square analysis for current PTSD diagnosis was nonsignificant, χ2 = 0.76, P = .28; however, the analysis of lifetime PTSD diagnosis approached significance, χ2 = 2.84, P < .07. Additionally, high and low SANS patients reported a similar number of total lifetime traumatic experiences on the Life Events Checklist, F = 0.20, P = .66 (see table 3).
Table 3.
Prevalence of Current and Lifetime PTSD Diagnoses and Mean Number of Self-Reported Traumatic Life Experiences
| % Current PTSD | % Lifetime PTSD | Total No. Traumatic Experiences—Mean (SD) | |
| Deficit vs nondeficit | |||
| Deficit (n = 15) | 0.0 | 6.7 | 4.1 (1.6) |
| Nondeficit (n = 55) | 27.3 | 54.5 | 4.9 (4.5) |
| Primary vs secondary | |||
| Primary (n = 21) | 14.3 | 23.8 | 4.4 (3.6) |
| Secondary (n = 15) | 40.0 | 53.3 | 6.1 (5.3) |
| High SANS vs low SANS | |||
| High (n = 35) | 12.1 | 34.3 | 4.5 (4.5) |
| Low (n = 35) | 25.7 | 54.3 | 5.0 (3.6) |
| Total | 21.4 | 44.3 | 4.8 (4.0) |
Primary vs Secondary Negative Symptoms
PTSD diagnosis was also examined in relation to primary and secondary negative symptoms as rated by the SDS. Results of a chi-square analysis approached significance for current, χ2 = 3.09, P = .08, and lifetime diagnoses, χ2 = 3.3, P = .07. The number of self-reported traumatic experiences as measured by the Life Events Checklist did not differ among patient groups, F = 1.2, P = .28, indicating that trend-level differences are not accounted for by number of prior traumatic experiences. Thus, there is a trend toward SZ + PTSD being more prevalent in patients whose negative symptoms are secondary vs those whose negative symptoms are primary. The mean percentage of primary and secondary negative symptom patients receiving PTSD diagnoses are presented in table 3.
DS vs ND Schizophrenia
Results of a chi-square analysis examining the relationship between current/lifetime PTSD and DS/ND diagnosis are presented in table 3. Results showed that both current SZ + PTSD, χ2 = 5.21 df = 70, P = .029, and lifetime SZ + PTSD, χ2 = 10.95, df = 70, P < .001, are significantly less likely to occur in DS then ND patients. Importantly, this reduced prevalence occurs despite a similar number of self-reported traumatic events on the Life Events Checklist, F = 0.56, df = 69, P = .46. Thus, PTSD is significantly more likely to be associated with the ND then DS form of schizophrenia, even when one accounts for previous traumatic exposure.
Discussion
In our sample of schizophrenia patients, current and lifetime PTSD diagnoses were estimated to be at 21.4% and 44.3%, respectively. These findings are consistent with other studies reporting PTSD comorbidity rates in schizophrenia (19%–66%) and provide further evidence that the occurrence of PTSD in schizophrenia is higher than the rate of PTSD in the general population (8%).4,5 The current findings extend previous research in a number of ways. First, with regard to the mixed findings reported in prior studies, with some indicating increased and others indicating decreased negative symptoms in SZ + PTSD, the current results provide tentative evidence supporting both these conclusions. Specifically, when SZ + PTSD patients were classified into high and low negative symptom groups based on a median split from the SANS, results indicated a tendency for lifetime diagnosis of comorbid PTSD to be associated with less severe negative symptoms (P = .07). Only the global blunted affect item from the SANS proved to differentiate those with and without current PTSD diagnoses. These findings do not support previous studies indicating that comorbid PTSD is associated with greater severity of negative symptoms in individuals with schizophrenia.
In contrast, when patients were divided according to the presence of primary vs secondary negative symptoms using the SDS, there was a tendency (P = .07) for patients with SZ + PTSD to be more likely to have secondary then primary negative symptoms, providing marginal support for our hypothesis that PTSD results in elevated negative symptoms only in patients whose negative symptoms are secondary. Thus, while these results should be considered preliminary in nature, they do suggest that the mixed results reported in prior studies may be largely due to methodological differences in the classification of negative symptoms that fail to consider whether negative symptoms are primary or secondary.
Analyses were also conducted to determine whether individuals with SZ + PTSD were more or less likely to be classified as having DS schizophrenia. Results indicated that patients with SZ + PTSD were significantly more likely to be classified ND then DS. These findings could not be attributed to DS patients having significantly fewer lifetime traumatic experiences, nor could they be attributed to group differences in demographics, severity of positive or disorganized symptoms, or length of illness. Furthermore, the deficit/nondeficit distinction provided greater differentiation of PTSD symptoms than did negative symptoms defined more broadly using the SANS or primary vs secondary classification made using the SDS. The fact that greater separation was found using deficit/nondeficit classifications than high/low and primary/secondary distinctions suggests that negative symptom stability and etiological factors unique to the DS may play a key role in buffering DS patients against the development of PTSD following traumatic exposure. Thus, findings suggest that in schizophrenia, a comorbid diagnosis of PTSD is more closely associated with more transient and secondary negative symptoms and that DS patients are uniquely at reduced risk for developing PTSD. This finding poses the interesting question of: What is it that puts DS patients at reduced risk for PTSD?
The mechanism behind lower prevalence of PTSD in patients with primary negative symptoms and the DS is unclear; however, there are a number of plausible explanations. One possibility is that the diminished experience of negative emotion buffers DS patients from developing PTSD after a traumatic experience. In other words, when confronted with an event that involves actual/threatened death or serious injury, deficit patients may fail to respond with highly intense negative emotion and thereby fail to pair negative affect with a traumatic episode. Similarly, it is possible that impairments in automatically detecting emotional information43 prevent DS patients from having attention drawn toward salient environmental stimuli that trigger the experience or re-experience of trauma. A third possibility is that DS patients, who have significantly reduced social drive, simply engage in fewer social interactions and, therefore, have lower rates of PTSD because they are exposed to fewer traumatic events. In the current study, this possibility was ruled out as the sole cause because DS patients reported a similar number of traumatic life events as ND patients. A fourth possibility is that neurocognitive impairment precludes DS patients from re-experiencing a salient traumatic event. A recent meta-analysis and new data presented by Cohen et al44 provided evidence that DS patients display generally reduced neuropsychological functioning when major neurocognitive domains were compared. It may be that impairments in basic attention, working memory, learning, retrieval-based memory, and/or executive functioning reduce the likelihood of having recurrent recollections of an experienced traumatic event or reduce the likelihood that internal or external cues that symbolize the traumatic event will trigger a viable traumatic experience.
The current findings have several limitations. First, generalizability is limited by the somewhat small sample of patients (n = 70) and subsequently reduced power. Our findings may also be limited to samples of chronic outpatients, such as those included in the current sample. Associations between PTSD/trauma and negative/DS symptoms may therefore differ in inpatient and first-episode populations. Additionally, while the SCID has established reliability and validity with regard to diagnosing DSM-IV Axis I disorders,35,36 other structured interviews such as the CAPS37 may have produced somewhat different findings with regard to the diagnosis of PTSD. It is also important to note that a causal inference cannot be drawn from the current findings and that a sequence of the developmental trajectory of PTSD cannot be inferred. It will be important for future studies to collect information regarding the sequence of psychopathology development. To summarize, results indicate that: (1) SZ + PTSD is associated with lower levels of primary negative symptoms, (2) SZ + PTSD is somewhat more likely to be associated with secondary then primary negative symptoms, and (3) individuals with SZ + PTSD are at significantly reduced risk for having DS.
Funding
The University of Nevada, Las Vegas (to D.N.A)
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