Manchester VA Medical Center

Differential conditioning was assessed in 15 medication-free individuals meeting Diagnostic and Statistical Manual of Mental Disorders (4th ed.; American Psychiatric Association, 1994) criteria for chronic posttraumatic stress disorder (PTSD) and 18 trauma-exposed individuals who never developed PTSD (non-PTSD). Conditioned stimuli (CSs) were colored circles, and the unconditioned stimulus was a "highly annoying" electrical stimulus. Individuals with PTSD had higher resting heart rate (HR) and skin conductance (SC) levels and produced larger SC orienting responses. During conditioning, the PTSD group showed larger differential SC, HR, and electromyogram responses to the reinforced vs. nonreinforced stimuli (CS+ vs. CS-) compared with the non-PTSD group. Only PTSD participants continued to show differential SC responses to CS+ vs. CS- during extinction trials. Results suggest that individuals with PTSD have higher sympathetic nervous system arousal at the time of conditioning and are more conditionable than trauma-exposed individuals without PTSD.

The present study was designed to investigate the relationship among physiologic concordance, patient-perceived therapist empathy, and social-emotional process during psychotherapy. Simultaneous measures of skin conductance (SC) were obtained from 20 unique and established patient-therapist dyads during a live therapy session followed by patient ratings of therapist empathy. Paired SC data of hypothetical dyads were used to test the reliability of the proposed measure of SC concordance. Observer microanalyses of social-emotional process were used to compare short segments of high versus low physiologic concordance. Results show a significant positive correlation (r=0.47, p=0.03) between SC concordance and patient ratings of perceived therapist empathy. Microanalyses suggest that during moments of high versus low SC concordance, there were significantly more positive social-emotional interactions for both patients and therapists (p=0.01). The results support a biological model of perceived patient empathy and patient-therapist social-emotional process during psychotherapy.

Recent studies have reported memory deficits and reduced hippocampal volumes in posttraumatic stress disorder (PTSD). The goal of the current research was to use functional neuroimaging and a validated explicit memory paradigm to examine hippocampal function in PTSD. We used positron emission tomography (PET) and a word-stem completion task to study regional cerebral blood flow (rCBF) in the hippocampus in 16 firefighters: 8 with PTSD (PTSD group) and 8 without PTSD (Control group). During PET scanning, participants viewed three-letter word stems on a computer screen and completed each stem with a word they had previously encoded either deeply (High Recall condition) or shallowly (Low Recall condition). Relative to the Control group, the PTSD group exhibited significantly smaller rCBF increases in the left hippocampus in the High vs Low Recall comparison. However, this finding reflected relatively elevated rCBF in the Low Recall condition in the PTSD group. Collapsing across High and Low Recall conditions, (1) the PTSD group had higher rCBF in bilateral hippocampus and left amygdala than the Control group, and (2) within the PTSD group, symptom severity was positively associated with rCBF in hippocampus and parahippocampal gyrus. The groups did not significantly differ with regard to accuracy scores on the word-stem completion task. The PTSD group had significantly smaller right (and a trend for smaller left) hippocampal volumes than the Control group. The results suggest an abnormal rCBF response in the hippocampus during explicit recollection of nonemotional material in firefighters with PTSD, and that this abnormal response appears to be driven by relatively elevated hippocampal rCBF in the comparison condition.

The authors examined the relation between intelligence and posttraumatic stress disorder (PTSD) by studying the association among precombat intelligence, current intelligence, and self-reported PTSD symptoms. Military aptitude test results were obtained in 59 PTSD and 31 non-PTSD Vietnam combat veterans who had undergone a psychodiagnostic interview and current intelligence testing. People with lower precombat intelligence were more likely to develop PTSD symptoms as assessed by the Clinician-Administered PTSD Scale even after adjustment for extent of combat exposure. The association between current intelligence and PTSD was no longer significant after adjusting for precombat intelligence. These results suggest that lower pretrauma intelligence increases risk for developing PTSD symptoms, not that PTSD lowers performance on intelligence tests.

OBJECTIVE: A review was performed to investigate the frequency of occurrence and outcome of patients who have retained surgical sponges. METHODS: Closed case records from the files of the Medical Professional Mutual Insurance Company (ProMutual, Boston, MA) involving a claim of retained surgical sponges were reviewed for a 7-year period. RESULTS: Retained sponges occurred in 40 patients, comprising 48% of all closed claims for retained foreign bodies. A falsely correct sponge count after an abdominal procedure was documented in 76% of these claims. Ten percent of claims involved vaginal deliveries and minor non-body cavity procedures, for which no sponge count was performed. Total indemnity payments were $2,072,319, and defense costs were $572,079. In three cases, the surgeon was deemed responsible by the court despite the nursing staff's admitting liability and evidence presented that the surgeon complied completely with the standard of care. A wide range of indemnity payments was made despite a remarkable similarity of outcome in the patients studied. CONCLUSIONS: Despite the rarity of the reporting of a retained surgical sponge, this occurrence appears to be encountered more commonly than generally is appreciated. Operating teams should ensure that sponges be counted for all vaginal and any incisional procedures at risk for retaining a sponge. In addition, the surgeon should not unquestioningly accept correct count reports, but should develop the habit of performing a brief but thorough routine postprocedure wound/body cavity exploration before wound closure. The strikingly similar outcome for most patients would argue for a standardized indemnity payment being made without the need for adversarial legal procedures.

Declarative memory impairment is a frequent complaint of patients suffering from posttraumatic stress disorder (PTSD). We assessed memory, attention, visual spatial skills, and executive function in Vietnam combat veterans with (n = 19) and without (n = 13) PTSD. Although PTSD subjects demonstrated a "generalized impairment" relative to non-PTSD subjects on a majority of tasks, only attention and memory provided unique and independent prediction of PTSD versus non-PTSD status. Our findings suggest that memory functioning represents a neurocognitive domain of specific relevance to the development of PTSD in trauma-exposed individuals, which can be distinguished from generalized attentional impairment as well as the effects of trauma exposure severity, IQ, comorbid depression, history of alcohol use, and history of developmental learning problems.

Rapidly evolving brain neuroimaging techniques such as magnetic resonance imaging (MRI) and positron emission tomography (PET) are proving fruitful in exploring the pathogenesis and pathophysiology of posttraumatic stress disorder (PTSD). Structural abnormalities in PTSD found with MRI include nonspecific white matter lesions and decreased hippocampal volume. These abnormalities may reflect pretrauma vulnerability to develop PTSD, or they may be a consequence of traumatic exposure, PTSD, and/or PTSD sequelae. Functional neuroimaging symptom provocation and cognitive activation paradigms using PET measurement of regional cerebral blood flow have revealed greater activation of the amygdala and anterior paralimbic structures (which are known to be involved in processing negative emotions such as fear), greater deactivation of Broca's region (motor speech) and other nonlimbic cortical regions, and failure of activation of the cingulate cortex (which possibly plays an inhibitory role) in response to trauma-related stimuli in individuals with PTSD. Functional MRI research has shown the amygdala to be hyperresponsive to fear-related stimuli in this disorder. Research with PET suggests that cortical, notably hippocampal, metabolism is suppressed to a greater extent by pharmacologic stimulation of the noradrenergic system in persons with PTSD. The growth of knowledge concerning the anatomical and neurochemical basis of this important mental disorder will hopefully eventually lead to rational psychological and pharmacologic treatments.

We used psychophysiologic techniques to assess responses to imagery of psychologically stressful past experiences in medication-free Vietnam combat veterans classified, on the basis of DSM-III-R criteria into posttraumatic stress disorder (PTSD; n = 7) or non-PTSD anxiety disorder (anxious; n = 7) groups. Scripts describing each individual's combat experiences were recorded and played back in the laboratory. Ss were instructed to imagine the events the scripts portrayed while heart rate, skin conductance, and frontalis electromyogram were recorded. PTSD Ss' physiologic responses were higher than those of anxious Ss. A discriminant function derived from a previous study of PTSD and mentally healthy combat veterans identified 5 of the 7 current PTSD Ss as physiologic responders and all 7 of the anxious Ss as nonresponders. Results of this study replicate and extend results of the previous study and support the validity of PTSD as a separate diagnostic entity.

The authors evaluated eyeblink and autonomic components of the acoustic startle response in combat-related posttraumatic stress disorder (PTSD). Thirty-seven Vietnam combat veterans with current PTSD and 19 combat veterans without PTSD were exposed to 15 consecutive 95-dB, 500-ms, 1000-Hz tones with 0-ms rise and fall times, while orbicularis oculi electromyogram, skin conductance, and heart rate responses were measured. PTSD veterans produced larger averaged electromyographic and heart rate responses, and a slower decline in skin conductance responses, across the 15 tone presentations compared to non-PTSD veterans. Results of this study provide laboratory support for an exaggerated startle response in PTSD and replicate and extend previous findings of increased autonomic responses to loud tone stimuli in this disorder.

Neuropsychological deficits have been reported among trauma survivors with posttraumatic stress disorder (PTSD). It is often assumed that these cognitive difficulties are toxic consequences of trauma exposure. Alternatively, they may reflect preexisting characteristics that contribute to the likelihood of developing PTSD. To address this possibility, the authors evaluated cognitive performance in monozygotic twin pairs who were discordant for combat exposure. Pairs were grouped according to whether the combat-exposed brother developed PTSD. The combat-unexposed cotwins of combat veterans with PTSD largely displayed the same performance as their brothers, which was significantly lower than that of non-PTSD combat veterans and their brothers. The results support the notion that specific domains of cognitive function may serve as premorbid risk or protective factors in PTSD.

A biological abnormality found to be associated with posttraumatic stress disorder (PTSD) may be, among other things, a pretrauma vulnerability factor, that is, it may have been present prior to the event's occurrence and increased the individual's likelihood of developing PTSD upon traumatic exposure. Alternately, it may be an acquired PTSD sign, that is, it may have developed after the traumatic exposure, along with the PTSD. We have studied pairs of Vietnam combat veterans and their noncombat-exposed, identical twins in an effort to resolve these competing origins. Combat veterans were diagnosed as current PTSD or non-PTSD (i.e., never had). Average heart rate responses (HRRs) to a series of sudden, loud-tone presentations were larger in Vietnam combat veteran twins with PTSD, but these larger responses were not shared by their noncombat-exposed cotwins, whose responses were similar to those of the non-PTSD combat veterans and their noncombat-exposed cotwins. These results suggest that larger HRRs to sudden, loud tones represent an acquired sign of PTSD. In contrast, increased neurological soft signs (NSSs), diminished hippocampal volume, and presence of abnormal cavum septum pellucidum (CSP) were found in Vietnam combat veteran twins with PTSD and their "high-risk," unexposed cotwins compared to Vietnam combat veteran twins without PTSD and their "low-risk," unexposed cotwins. These results support the conclusion that the latter abnormalities represent antecedent, familial vulnerability factors for developing chronic PTSD upon exposure to a traumatic event.

INTRODUCTION: Animal and human research suggests that the development of posttraumatic stress disorder (PTSD) may involve the overconsolidation of memories of a traumatic experience. Previous studies have attempted to use pharmaceutical agents, especially the β-adrenergic blocker propranolol, to reduce this overconsolidation. AIMS: In this randomized, placebo-controlled study of the efficacy of propranolol in reducing the development of PTSD, we optimized dosages and conducted both psychophysiological and clinical assessments 1 and 3 months after the traumatic event. Forty-one emergency department patients who had experienced a qualifying acute psychological trauma were randomized to receive up to 240 mg/day of propranolol or placebo for 19 days. At 4 and 12 weeks post-trauma, PTSD symptoms were assessed. One week later, participants engaged in script-driven imagery of their traumatic event while psychophysiological responses were measured. RESULTS: Physiological reactivity during script-driven traumatic imagery, severity of PTSD symptoms, and the rate of the PTSD diagnostic outcome were not significantly different between the two groups. However, post hoc subgroup analyses showed that in participants with high drug adherence, at the 5-week posttrauma assessment, physiological reactivity was significantly lower during script-driven imagery in the propranolol than in the placebo subjects. CONCLUSIONS: The physiological results provide some limited support for a model of PTSD in which a traumatic conditioned response is reduced by posttrauma propranolol. However, the clinical results from this study do not support the preventive use of propranolol in the acute aftermath of a traumatic event.

OBJECTIVE: Neuroimaging studies have revealed functional abnormalities in the anterior cingulate cortex in posttraumatic stress disorder (PTSD). The goal of this study was to determine whether hyperresponsivity of the dorsal anterior cingulate in PTSD is an acquired characteristic or a familial risk factor. METHOD: Using a case-control twin design, the authors studied combat-exposed veterans with PTSD (N=12) and their identical combat-unexposed co-twins (N=12), as well as combat-exposed veterans without PTSD (N=14) and their identical combat-unexposed co-twins (N=14). Participants underwent functional MRI during completion of the Multi-Source Interference Task, which reliably activates the dorsal anterior cingulate. RESULTS: Combat-exposed veterans with PTSD and their unexposed co-twins had significantly greater activation in the dorsal anterior cingulate and tended to have larger response time difference scores, as compared to combat-exposed veterans without PTSD and their co-twins. Dorsal anterior cingulate activation in the exposed twins was positively correlated with their PTSD symptom severity. Dorsal anterior cingulate activation in the unexposed twins was positively correlated with their combat-exposed co-twins' PTSD symptom severity, but not with depression or alcohol use severity in the combat-exposed co-twins. CONCLUSIONS: Hyperresponsivity in the dorsal anterior cingulate appears to be a familial risk factor for the development of PTSD following psychological trauma.

Nefazodone is an antidepressant medication which received approval from the Food and Drug Administration for treatment of major depressive disorder in 1994. This article summarizes the pharmacodynamics, pharmacokinetics, adverse effects, and drug interactions of nefazodone as well as its administration and dosing schedule. The potential efficacy of nefazodone in treating anxiety, premenstrual syndrome, chronic pain conditions, and sleep disturbances also is summarized. Nefazodone has a favorable side effects profile which makes it an attractive alternative option for patients who withdraw from treatment when they develop adverse effects to other available antidepressants.

Heart rate, skin conductance, and left lateral frontalis and corrugator facial electromyogram responses were measured during script-driven imagery of personal childhood sexual abuse (CSA) and other life experiences among women with and without Diagnostic and Statistical Manual of Mental Disorders (3rd ed., rev., American Psychiatric Association, 1987)--diagnosed posttraumatic stress disorder (PTSD) resulting from CSA. Women with current PTSD (n = 29) showed larger physiologic responses than those who never had PTSD (n = 18) during personal sexual abuse imagery but not during imagery of stressful, nonabuse-related life experiences. Responses of individuals with lifetime, but not current, PTSD (n = 24) fell between the other groups. An a priori discriminant function, derived from physiologic responses of previously studied individuals, correctly classified 66% of women with current PTSD and 78% of women who never had PTSD.

Cerebral blood flow was recorded (using positron emission tomography) while middle-aged subjects viewed or visualized pictures of neutral or aversive stimuli, and then determined whether auditorily presented statements correctly described the stimuli. Visualizing aversive stimuli enhanced cerebral blood flow, relative to visualizing neutral stimuli, in areas 17 (right) and 18 (bilateral), as well as the anterior insula (bilateral) and middle frontal cortex (left). Areas 17 and 18 have been identified as supporting the representations that underlie the experience of imagery, and the anterior insula is a major cortical recipient of input from the autonomic nervous system. Perceiving aversive stimuli enhanced cerebral blood flow, relative to neutral stimuli, in area 46, the angular gyrus and area 19, area 47, and the middle temporal gyrus (all in the left hemisphere). All of these areas have previously been implicated in visual object identification. It is striking that negative emotion did not modulate activation in any areas in the same way during imagery and perception.

Serum concentration of hepatic enzymes are linked to liver dysfunction, metabolic and cardiovascular diseases. We perform genetic analysis on serum levels of alanine transaminase (ALT), alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) using data on 437,438 UK Biobank participants. Replication in 315,572 individuals from European descent from the Million Veteran Program, Rotterdam Study and Lifeline study confirms 517 liver enzyme SNPs. Genetic risk score analysis using the identified SNPs is strongly associated with serum activity of liver enzymes in two independent European descent studies (The Airwave Health Monitoring study and the Northern Finland Birth Cohort 1966). Gene-set enrichment analysis using the identified SNPs highlights involvement in liver development and function, lipid metabolism, insulin resistance, and vascular formation. Mendelian randomization analysis shows association of liver enzyme variants with coronary heart disease and ischemic stroke. Genetic risk score for elevated serum activity of liver enzymes is associated with higher fat percentage of body, trunk, and liver and body mass index. Our study highlights the role of molecular pathways regulated by the liver in metabolic disorders and cardiovascular disease.

This study examined whether witnessing death and injury could produce psychophysiologically responsive posttraumatic stress disorder (PTSD). Participants consisted of medication-free female Vietnam nurse veterans with a diagnosis of current PTSD (n = 17) and who never had PTSD (n = 21), related to their military service. Individualized scripts describing personal traumatic military nursing events, a standard military nursing event, and other life events were tape recorded and played back to the participant while heart rate, skin conductance, and facial electromyograms were recorded. Nurses with PTSD showed significantly larger physiologic responses than non-PTSD nurses only during imagery of military-related nursing events. The groups' self-reported emotional responses did not differ during imagery. Psychophysiologic results support the proposition that witnessing death and serious injury to others is sufficiently stressful to cause PTSD.

Pierre Janet's classic contribution to the understanding of obsessive-compulsive disorder, Obsessions and Psychasthenia (1903), remains untranslated as well as unappreciated by American psychiatry, despite increasing recognition of the importance of this mental health problem. Herein the work is summarized and discussed. Although it tends to be remembered for its theoretical ideas, most of which have become dated, the most valuable aspect of Obsessions and Psychasthenia is its clinical discoveries. These include the important role played in the disorder by symptoms that are closely related to, but yet cannot properly be called, obsessions and compulsions (the "forced agitations"); the underlying psychasthenic mental state; and the obsessive-compulsive person's specific failure to adapt to reality. Despite the passage of nearly a century, these observations, and Janet's suggestions regarding treatment, are as timely now as when they were made.

"Spirituality in Patient Care." Chaplaincy Today, 18(2), pp. 54–55