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Pilot Study to Assess the Viability of a Rape Trauma Syndrome Questionnaire
Abstract
Studies have revealed that rape victims undergo a number of psychological symptoms following the attack, which constitute a specific syndrome termed the rape trauma syndrome (RTS). Evidence of the RTS has been admitted as scientific testimony in the prosecution of sexual offences and has been integral in their successful conviction. The present study aims to assess the viability of a questionnaire designed to identify the RTS in victims of alleged rape.
A 77-item rape trauma syndrome questionnaire (RTSQ) was developed and administered to 30 women who reported rape and 57 nurses who formed the control group. The data were analysed using the Statistical Package for the Social Sciences (Windows Version 6.0).
Statistical analysis suggested that the questionnaire was internally consistent and effective in uncovering significant differences between rape victims and controls in their experience of rape trauma symptoms. Rape victims scored significantly higher than controls on the RTS scale. Those who faked rape were also found to endorse a greater number of the rape trauma symptoms than actual rape victims, as well as a greater number of fictitious and unlikely symptoms.
This pilot study confirmed the viability of the RTSQ and paves the way for a more rigorous examination of its reliability and validity. In the future, the questionnaire may be of use in ascertaining the veracity of victims' claims of rape in the conviction of sexual offences where circumstances are equivocal.
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Context Patients with unstable angina/non–ST-segment elevation myocardial
infarction (MI) (UA/NSTEMI) present with a wide spectrum of risk for death
and cardiac ischemic events.Objective To develop a simple risk score that has broad applicability, is easily
calculated at patient presentation, does not require a computer, and identifies
patients with different responses to treatments for UA/NSTEMI.Design, Setting, and Patients Two phase 3, international, randomized, double-blind trials (the Thrombolysis
in Myocardial Infarction [TIMI] 11B trial [August 1996–March 1998] and
the Efficacy and Safety of Subcutaneous Enoxaparin in Unstable Angina and
Non-Q-Wave MI trial [ESSENCE; October 1994–May 1996]). A total of 1957
patients with UA/NSTEMI were assigned to receive unfractionated heparin (test
cohort) and 1953 to receive enoxaparin in TIMI 11B; 1564 and 1607 were assigned
respectively in ESSENCE. The 3 validation cohorts were the unfractionated
heparin group from ESSENCE and both enoxaparin groups.Main Outcome Measures The TIMI risk score was derived in the test cohort by selection of independent
prognostic variables using multivariate logistic regression, assignment of
value of 1 when a factor was present and 0 when it was absent, and summing
the number of factors present to categorize patients into risk strata. Relative
differences in response to therapeutic interventions were determined by comparing
the slopes of the rates of events with increasing score in treatment groups
and by testing for an interaction between risk score and treatment. Outcomes
were TIMI risk score for developing at least 1 component of the primary end
point (all-cause mortality, new or recurrent MI, or severe recurrent ischemia
requiring urgent revascularization) through 14 days after randomization.Results The 7 TIMI risk score predictor variables were age 65 years or older,
at least 3 risk factors for coronary artery disease, prior coronary stenosis
of 50% or more, ST-segment deviation on electrocardiogram at presentation,
at least 2 anginal events in prior 24 hours, use of aspirin in prior 7 days,
and elevated serum cardiac markers. Event rates increased significantly as
the TIMI risk score increased in the test cohort in TIMI 11B: 4.7% for a score
of 0/1; 8.3% for 2; 13.2% for 3; 19.9% for 4; 26.2% for 5; and 40.9% for 6/7
(P<.001 by χ2 for trend). The pattern
of increasing event rates with increasing TIMI risk score was confirmed in
all 3 validation groups (P<.001). The slope of
the increase in event rates with increasing numbers of risk factors was significantly
lower in the enoxaparin groups in both TIMI 11B (P
= .01) and ESSENCE (P = .03) and there was a significant
interaction between TIMI risk score and treatment (P
= .02).Conclusions In patients with UA/NSTEMI, the TIMI risk score is a simple prognostication
scheme that categorizes a patient's risk of death and ischemic events and
provides a basis for therapeutic decision making.
To assess the prognostic value of minor myocardial damage in patients presenting with chest pain without myocardial infarction.
The relative risk of suffering a cardiac event in the next six months was assessed in patients with minor myocardial damage assessed by the cardiac markers CK-MB, myoglobin, and troponin T.
Emergency department of a large university hospital.
In 128 consecutive patients with chest pain, acute myocardial infarction (by WHO criteria) was ruled out; of these, 39 had a rise and fall of one or more markers, indicating minor myocardial damage. The presence of a documented history of coronary artery disease was assessed on admission.
24 patients had a subsequent event (cardiac death, acute myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting) in the next six months. An abnormal troponin T predicted a subsequent event while abnormal CK-MB or myoglobin did not. The relative risk for troponin T was 2.8 (95% confidence interval: 1.0 to 7.9), for myoglobin 1.0 (0.3 to 3.2), and for CK-MB 0.9 (0.2 to 3.4). A documented history of coronary artery disease predicted subsequent events with a relative risk of 3.9 (1.3 to 11.3).
Troponin T was the only marker that predicted future events, but a documented history of coronary artery disease was the best predictor in patients in whom an acute myocardial infarction had been ruled out.
In patients with acute coronary syndromes, it is desirable to identify a sensitive serum marker that is closely related to the degree of myocardial damage, provides prognostic information, and can be measured rapidly. We studied the prognostic value of cardiac troponin I levels in patients with unstable angina or non-Q-wave myocardial infarction.
In a multicenter study, blood specimens from 1404 symptomatic patients were analyzed for cardiac troponin I, a serum marker not detected in the blood of healthy persons. The relation between mortality at 42 days and the level of cardiac troponin I in the specimen obtained on enrollment was determined both before and after adjustment for baseline characteristics.
The mortality rate at 42 days was significantly higher in the 573 patients with cardiac troponin I levels of at least 0.4 ng per milliliter (21 deaths, or 3.7 percent) than in the 831 patients with cardiac troponin I levels below 0.4 ng per milliliter (8 deaths, or 1.0 percent; P < 0.001). There were statistically significant increases in mortality with increasing levels of cardiac troponin I (P < 0.001). Each increase of 1 ng per milliliter in the cardiac troponin I level was associated with a significant increase (P = 0.03) in the risk ratio for death after adjustment for the base-line characteristics that were independently predictive of mortality (ST-segment depression and age > or = 65 years).
In patients with acute coronary syndromes, cardiac troponin I levels provide useful prognostic information and permit the early identification of patients with an increased risk of death.
Based upon personal observations during the last war, an analysis of pertinent literature, and recent insights into ordinary neuroses, the author presents a pathodynamic viewpoint of traumatic war neuroses according to pre-traumatic, traumatic, and early and late post-traumatic phases. Treatment should combine attempts to desensitize the patient to all memories of the war with medication to subdue the hyper-active affect and motor systems involved in emergency control. "A further requirement is to… restore the patient's lost ability to take pleasure in spontaneous activity and to enjoy initiative." (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The purpose of the following paper is to review results of recent empirical studies on victim reactions following rape and response to treatment. Results focus on three major research projects run concurrently in Atlanta, Pittsburgh and Charleston, as well as several smaller studies. The Atlanta study is described in detail and sampling bias is discussed. Short-term reactions are described and defined as those occurring during the first 3 months post-assault. During this time, most symptoms return to normal levels in most victims. Intermediate reactions, 3 months to one year post-assault, are described under four headings: depression, social adjustment, sexual functioning, and fear and anxiety. At the end of this interval, victims still score significantly higher than nonvictims on measures of fear and anxiety. Long-term reactions, defined as those continuing longer than one year post-assault, are discussed under four headings. No firm conclusions can be drawn as to the long-term symptoms experienced by victims versus nonvictims. Section IV reviews factors associated with adjustment to the assault. Factors within the rape situation are not clearly predictive of adjustment, but psychiatric history prior to the assault and amount of social support following the assault are predictive. In section V, empirical studies of behavior therapy with rape victims are reviewed. While all these studies were successful, they suffer from methodological flaws. Difficulties in doing rape research are discussed. Lastly, section VI offers a theoretical explication which draws on crisis theory to account for short-term and intermediate reactions and differential rates of recovery, and which draws on classical conditioning theory to account for continued high levels of fear and anxiety and selective anhedonia.
Behavioral science studies conducted on rape victims reveal a posttraumatic stress disorder which follows the attack known as rape trauma syndrome. Evidence of rape trauma syndrome can be very useful in explaining the behavior of rape victims. Rape trauma syndrome can help corroborate the victim's assertion of lack of consent and also help the jury understand the typical reactions of rape victims. Courts have held that expert testimony of rape trauma syndrome is admissible as evidence of (i) lack of consent, (ii) the amount of damages in civil suits, (iii) a defense to culpable behavior, and (iv) an explanation for behavior of the victim that is inconsistent with the claim of rape. Rape trauma syndrome meets the requirements for admissibility when it is used for the proper purpose and with adequate safeguards to prevent any unfair prejudice. Based on case precedent on the admissibility of rape trauma syndrome as scientific expert testimony, rape trauma syndrome should be admissible if (i) the evidence presented only shows the typical reactions to rape and does not make any legal conclusions as to whether the victim was raped, (ii) the expert is qualified, (iii) a proper foundation is laid, (iv) liberal cross-examination of the expert is allowed, and (v) the defense can introduce its own expert testimony on rape trauma syndrome.
The authors interviewed and followed 146 patients admitted during a one yr period to the emergency ward of a city hospital with a presenting complaint of having been raped. Based upon an analysis of the 92 adult women rape victims in the sample, they document the existence of a rape trauma syndrome and delineate its symptomatology as well as that of two variations, compounded reaction and silent reaction. Specific therapeutic techniques are required for each of these 3 reactions. Crisis intervention counseling is effective with typical rape trauma syndrome; additional professional help is needed in the case of compounded reaction; and the silent rape reaction means that the clinician must be alert to indications of the possibility of rape having occurred even when the patient never mentions such an attack.
This study assesses the prevalence and characteristics of sexual assault among women patients attending two family medicine residency training clinics.
Two hundred four consecutive women patients 18 years and older were asked to complete a questionnaire; one hundred eighty-eight (92.2%) agreed.
Fifty-four (28.7%) of the 188 women patients reported some type of sexual assault. Approximately 15% of patients reported being victims of rape; 8% reported attempted rape, and 5.3% reported forced sexual contact. Twelve (41.4%) of the 29 rape victims indicated that they had been raped more than once. Only 24% of rape and attempted rape victims reported the incident to police, 18.2% sought medical attention, and 21% sought counseling.
Family physicians should be aware of the prevalence of sexual assault in their practices and should understand proper questioning, management, counseling, and referral of patients.
Studies have demonstrated that troponin T is a strong independent indicator of a poor prognosis in patients with unstable coronary artery disease. Up to the present, no study has compared the prognostic value of troponin T with that of troponin I in the same cohort of patients.
Patients (n=516) suspected of having unstable coronary artery disease were investigated. Follow-up was done after 30 days, and the occurrences of cardiac death, acute myocardial infarction, refractory angina pectoris, and recurrent angina pectoris were registered. Elevated levels of troponin T (> or = 0.10 microg/L) were associated with an increased risk of cardiac death at 30 days compared with patients with normal levels, 3.2% versus 0.4% (P=.014). Troponin I values above the chosen cutoff (2.0 microg/L) were similarly found to be an indicator of increased risk of cardiac death, 3.2% versus 0.7% (P=.026). With regard to the composite end point of cardiac death/acute myocardial infarction, the troponins were strong independent indicators of adverse outcome.
In patients suspected of having unstable coronary artery disease, both troponin T and troponin I provide independent prognostic information with regard to cardiac death and acute myocardial infarction.
Controversy exists as to the clinical roles and relative specificities of cardiac troponin T or I in patients with unstable angina pectoris (UAP). We measured troponin T and I levels on admission in 123 patients with UAP. Of the 107 patients with normal creatine kinase during the first 24 hours, troponin T and I were elevated in 14 and 13 patients, respectively. At 30 days, 5 of 14 patients (36%) with elevated troponin T and 3 of 93 patients (3.2%) with normal troponin T had acute myocardial infarction (odds ratio [OR], 16.7; 95% confidence interval [CI] 3.4 to 81.5; p <0.001). Of 13 patients with elevated troponin I, 5 patients (39%) and 3 of 94 patients (3.2%) with normal troponin I had acute myocardial infarction (odds ratio, 21.7; 95% CI 4.3 to 110; p <0.001). No deaths occurred within 30 days. Both markers demonstrated equivalent sensitivity (63%) and specificities (troponin T: 91%; troponin I: 92%) for myocardial infarction. Meta-analysis of 12 published troponin T and 9 troponin I studies in patients with UAP produced risk ratios of 4.2 (95% CI 2.7 to 6.4, p <0.001) for troponin I compared with 2.7 (95% CI 2.1 to 3.4, p <0.001) for troponin T. Comparison of the sensitivities and specificities of both markers using summary receiver operating characteristic curves showed no significant difference in their abilities to predict acute myocardial infarction and cardiac death. Troponin T and I show similar prognostic significance for acute myocardial infarction or death in the same patients with UAP. The 2 markers are equally sensitive and specific, as confirmed by meta-analysis, and this supports a role in risk stratification.
To design a strategy for cardiac injury marker testing in the diagnosis of acute myocardial infarction.
Prospective study. Group I (n=54 patients): evaluation of clinical performance. Specimens collected at 0, 3, 6, and 12 (+/-1.5) hours after presentation. World Health Organization criteria were used for diagnosis of acute myocardial infarction. Group II (n=57 patients): evaluation of temporal evolution. Time intervals 0 to 1.5, 1.5 to 4.5, 4.5 to 7.5, and 7.5 to 13.5 hours. Patients identified by positive creatine kinase-MB (CK-MB) mass or myoglobin. Fourteen patients in Group I qualified for Group II. Hence, the total number of patients was 97.
A team of laboratorians and clinicians at the University of California, Davis, hospital assessed the clinical performance and temporal evolution of serial CK-MB isoform, troponin I, and troponin T results in comparison to parallel CK-MB mass and myoglobin results.
Group I: sensitivity, specificity, and positive and negative predictive values. Group II: the time interval of the first positive result for each cardiac injury marker. Strategy and conclusions were based on study results and a literature review.
Emergency department patients with acute onset of chest pain and other complaints, possibly indicative of myocardial ischemia, who were under evaluation for admission.
Twenty-seven cases of acute myocardial infarction were documented. Group I: troponin I had the highest specificity (100%) and the highest positive predictive value (100%); troponin I, troponin T, and CK-MB mass had the highest sensitivity (90.0%); and the negative predictive values of troponin I, troponin T, and CK-MB mass were comparable (97.8%, 97.6%, and 97.6%, respectively). Group II: early diagnosis (within 1.5 hours) was provided by both CK-MB isoforms and CK-MB mass, and then by myoglobin and troponins, in order of decreasing frequency.
Creatine kinase-MB mass, myoglobin, and troponin I were selected as the cardiac injury markers of choice at our institution. The strategy calls for serial testing of myoglobin and CK-MB mass initially-and serially if warranted by heightened clinical suspicion--with troponin I added if indicated for (1) specific confirmation, (2) late presentation, or (3) risk stratification.
This multicenter study evaluated the Biosite Triage(R) Cardiac Panel as a quantitative, multimarker, whole blood system for the detection of acute myocardial infarction (MI). Optimum cutoffs for the discrimination of acute MI (n = 192 patients, 59 with MI) as determined by ROC curve analyses were as follows: 0.4 microgram/L for cardiac troponin I (cTnI); 4.3 microgram/L for the creatine kinase MB isoenzyme (CK-MB); and 107 microgram/L for myoglobin. The Triage Panel showed the following concordances for detection or rule-out of MI compared with established devices: cTnI >89%; CK-MB >81%; myoglobin >69%. No significant differences were present between methods for the same marker. Diagnostic efficiencies demonstrated comparable sensitivities and specificities for the diagnosis of MI in patients presenting with symptoms compared with the Dade, Beckman, and Behring CK-MB, cTnI, and myoglobin assays; the ratio of sensitivity to specificity for each marker was as follows: cTnI, 98%:100%; CK-MB, 95%:91%; myoglobin, 81%:92%. The areas under the ROC curves for the Biosite myoglobin, CK-MB, and cTnI were 0.818, 0.905, and 0.970, respectively; the areas were significantly different, P <0.05. In patients with skeletal muscle injury and renal disease, the Triage cTnI showed 94% and 100% specificity, respectively. The Triage panel offers clinicians a whole blood, point-of-care analysis of multiple cardiac markers that provides excellent clinical sensitivity and specificity for the detection of acute MI.
Millions of patients present annually with chest pain, but only 10% to 15% have myocardial infarction. Lack of diagnostic sensitivity and specificity of clinical and conventional markers prevents or delays treatment and leads to unnecessary costly admissions. Comparative data are lacking on the new markers, yet using all of them is inappropriate and expensive.
The Diagnostic Marker Cooperative Study was a prospective, multicenter, double-blind study with consecutive enrollment of patients with chest pain presenting to the emergency department. Diagnostic sensitivity and specificity and frequency of increase in patients with unstable angina were determined for creatine kinase-MB (CK-MB) subforms, myoglobin, total CK-MB (activity and mass), and troponin T and I on the basis of frequent serial sampling for </=24 hours. Of 955 patients with chest pain, 119 (12.5%) had infarction identified by use of CK-MB mass, and 203 (21%) had unstable angina. CK-MB subforms were most sensitive and specific (91% and 89%) within 6 hours of onset, followed by myoglobin (78% and 89%). For late diagnosis, total CK-MB activity (derived from subforms) was the most sensitive and specific (96% and 98%) at 10 hours from onset, followed by troponin I (96% and 93%), but not until 18 hours, and troponin T (87% and 93% at 10 hours). In unstable angina, CK-MB subforms were increased in 29.5%, myoglobin in 23.7%, troponin I in 19.7%, and troponin T in 14.8%. All markers were increased in 99 patients. With each marker as the diagnostic standard, CK-MB subforms and myoglobin remained the most sensitive for early diagnosis.
The CK-MB subform assay alone or in combination with a troponin reliably triages patients with chest pain and should lead to improved therapy and reduced cost.
Earlier, rapid evaluation in chest pain units may make patient care more efficient. A multimarker strategy (MMS) testing for several markers of myocardial necrosis with different time-to-positivity profiles also may offer clinical advantages.
We prospectively compared bedside quantitative multimarker testing versus local laboratory results (LL) in 1005 patients in 6 chest pain units. Myoglobin, creatine kinase-MB, and troponin I were measured at 0, 3, 6, 9 to 12, and 16 to 24 hours after admission. Two MMS were defined: MMS-1 (all 3 markers) and MMS-2 (creatine kinase-MB and troponin I only). The primary assessment was to relate marker status with 30-day death or infarction. More patients were positive by 24 hours with MMS than with LL (MMS-1, 23.9%; MMS-2, 18.8%; LL, 8.8%; P=0.001, all comparisons), and they became positive sooner with MMS-1 (2.5 hours, P=0.023 versus LL) versus MMS-2 (2.8 hours, P=0.026 versus LL) or LL (3.4 hours). The relation between baseline MMS status and 30-day death or infarction was stronger (MMS-1: positive, 18.8% event rate versus negative, 3.0%, P=0.001; MMS-2: 21.9% versus 3.2%, P=0.001) than that for LL (13.6% versus 5.5%, P=0.038). MMS-1 discriminated 30-day death better (positive, 2.0% versus negative, 0.0%, P=0.007) than MMS-2 (positive, 1.8% versus negative, 0.2%; P=0.055) or LL (positive, 0.0% versus negative, 0.5%; P=1.000).
Rapid multimarker analysis identifies positive patients earlier and provides better risk stratification for mortality than a local laboratory-based, single-marker approach.
We sought to evaluate quantitatively the evidence on the diagnostic performance of presentation and serial biochemical markers for emergency department diagnosis of acute cardiac ischemia (ACI), including acute myocardial infarction (AMI) and unstable angina.
We conducted a systematic review and meta-analysis of the English-language literature published between 1966 and December 1998. We examined the diagnostic performance of creatine kinase, creatine kinase-MB, myoglobin, and troponin I and T testing. Diagnostic performance was assessed by using estimates of test sensitivity and specificity and was summarized by summary receiver-operating characteristic curves.
Only 4 studies were found that evaluated all patients with ACI; 73 were found that focused only on a diagnosis of AMI. To diagnose ACI, presentation biomarker tests had sensitivities of 16% to 19% and specificities of 96% to 100%; serial biomarker tests had sensitivities of 31% to 45% and specificities of 95% to 98%. Considering only the diagnosis of AMI, presentation biomarker tests had summary sensitivities of 37% to 49% and summary specificities of 87% to 97%; serial biomarker tests had summary sensitivities of 79% to 93% and summary specificities of 85% to 96%. Variation of test sensitivity was best explained by test timing. Longer symptom duration or time between serial tests yielded higher sensitivity.
The limited evidence available to evaluate the diagnostic accuracy of biomarkers for ACI suggests that biomarkers have very low sensitivity to diagnose ACI. Thus, biomarkers alone will greatly underdiagnose ACI and will be inadequate to make triage decisions. For AMI diagnosis alone, multiple testing of individual biomarkers over time substantially improves sensitivity, while retaining high specificity, at the expense of additional time. Further high-quality studies are needed on the clinical effect of using biomarkers for patients with ACI in the ED and on optimal timing of serial testing and in combination with other tests.
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