Psychological Bulletin, 2009,135(6)- 909-42

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Linking Dimensional Models of Internalizing Psychopathology toNeurobiological Systems: Affect-Modulated Startle as an

Indicator of Fear and Distress Disorders and Affiliated Traits

Uma Vaidyanathan, Christopher J. Patrick, and Bruce N. CuthbertUniversity of Minnesota

Integrative hierarchical models have sought to account for the extensive comorbidity between variousinternalizing disorders in terms of broad individual difference factors these disorders share. However,such models have been developed largely on the basis of self-report and diagnostic symptom data.Toward the goal of linking such models to neurobiological systems, we reviewed studies that haveemployed variants of the affect-modulated startle paradigm to investigate emotional processing ininternalizing disorders as well as personality constructs known to be associated with these disorders.Specifically, we focused on four parameters of startle reactivity: fear-potentiated startle, inhibition of startle in the context of pleasant stimuli, context-potentiated startle, and general startle reactivity. On thebasis of available data, we argue that these varying effects index differing neurobiological processes

related to mood and anxiety disorders that are interpretable from the standpoint of dimensional modelsof the internalizing spectrum. Further, we contend that these empirical findings can feed back into andhelp reshape conceptualizations of internalizing disorders in ways that make them more amenable toneurobiological analysis.

Keywords: startle blink, internalizing disorders, neurobiology of internalizing disorders

In the two decades that have passed since the finding of affect-modulated startle was initially reported in humans (Vrana, Spence,& Lang, 1988), an extensive literature has developed on the use of this measure for investigating affective individual differences inrelation to psychopathology (cf. Cook, 1999; Grillon & Baas,

2003; Patrick & Bernat, 2006). In particular, startle reflex modu-lation has been examined in relation to traits associated with fear,neuroticism, and negative affectivity and in relation to disordersinvolving an excess of emotional reactivity (e.g., phobias, panic,posttraumatic stress, and depression) as well as those involvingputative emotional deficits (e.g., psychopathy, schizophrenia).This line of research is important because much is known about theneurobiological substrates of startle modulation effects. Alongsidethis work, systematic efforts have been devoted during the past 20years to the development of integrative dimensional models of psychopathology (e.g., Clark & Watson, 1991; Kendler, Prescott,Myers, & Neale, 2003; Krueger, 1999; Krueger, Markon, Patrick,Benning, & Kramer, 2007; Mineka, Watson, & Clark, 1998;Watson, 2005) that incorporate the well-known phenomenon of diagnostic comorbidity and provide a framework for understand-

ing common as well as distinctive factors contributing to varyinginterrelated disorders. However, these models have been con-structed largely on the basis of diagnostic and self-report data, andlinkages to findings on neurobiology have been speculative for themost part. Our aim in the current article is to review what is known

about variations in affect-modulated startle in relation to anxietyand mood (internalizing) disorders and affiliated trait constructs,with the aim of linking this work to existing dimensional modelsof internalizing psychopathology. A comprehensive review of thiskind is important for advancing our understanding of the neurobi-ological foundations of internalizing disorders and traits and pro-viding insights into how conceptualizations of psychopathologicsyndromes can be refined to make them more amenable to neuro-biological analysis (cf. Hyman, 2007).

Focus of the Current Review

Psychological disorders involving mood and anxiety symptomsexhibit systematic co-occurrence (comorbidity) that has been in-terpreted as reflecting core emotional processes that these disor-ders have in commonbroadly subsumed under the rubric of negative affectivity (Clark & Watson, 1991; Mineka et al., 1998;Watson, 2005). The internalizing disorders, so called because theyare thought to represent problematic thoughts and/or behaviorsdirected toward the self or a tendency to internalize psychologicaldistress, are a family of disorders in which high levels of fear,anxiousness, and misery are observed (cf. Krueger, 1999). Theyinclude several of the anxiety disorders along with major depres-sive disorder and dysthymia, as described within the Diagnosticand Statistical Manual of Mental Disorders (4th ed., text rev.; DSM-IV-TR ; American Psychiatric Association [APA], 2000).

Uma Vaidyanathan, Christopher J. Patrick, and Bruce N. Cuthbert,Department of Psychology, University of Minnesota.

This study was supported by National Institute of Mental Health GrantMH072850 and by funds from the Hathaway endowment at the Universityof Minnesota.

Correspondence concerning this article should be addressed to UmaVaidyanathan or Christopher J. Patrick, Department of Psychology, Uni-versity of Minnesota, Elliott Hall, 75 East River Road, Minneapolis, MN55455. E-mail: [email protected] or [email protected]

Psychological Bulletin 2009 American Psychological Association2009, Vol. 135, No. 6, 909942 0033-2909/09/$12.00 DOI: 10.1037/a0017222

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Personality traits in the domain of negative affectivity have beenconceptualized as general substrates for varying forms of internal-izing psychopathology (Clark & Watson, 1999). Several influen-tial theories, including Tellegens (1985) three-factor model of personality, Clark and Watsons (1991) tripartite model of anxietyand depression, and Grays (1981) neurobiological theory of mo-

tivation, have sought to account for the comorbidity of thesedisorders in terms of common personality traits that contribute toeach. From a neurobiological standpoint, one major construct of interest in this regard has been sensitivity of the brains defensivemotivational system, which can be viewed as a core substrate forindividual differences in negative affectivity (e.g., Patrick & Ber-nat, 2006; Rosen & Schulkin, 1998). The current article focuses onhuman research to date that has employed the startle blink reflex asa measure of defense system activation to investigate individualdifferences in emotional reactivity associated with internalizingpsychopathology and affiliated personality constructs. 1

Previous integrative reviews dealing with the topic of internal-izing disorders (e.g., Clark & Watson, 1991; Mineka et al., 1998)have focused primarily on phenotypic aspects of these disorders,including patterns of diagnostic comorbidity among them andoverlapping associations they exhibit with particular personalitytraits. In contrast, the current article focuses on the biologicalmechanisms implicated in these disordersin particular, reactivityof the brains defensive motivational system as indexed by poten-tiation of the startle probe reflexrather than exclusively onpsychometric or diagnostic constructs (e.g., personality traits, DSM disorders). Our major aims in this review are to (a) integratefindings from existing published studies of internalizing syn-dromes employing startle probe methodology and (b) link thesefindings to current conceptualizations of the structure of internal-izing disorders and affiliated trait constructs. As discussed infurther detail below, we opted for an integrative, descriptive ap-

proach here rather than a quantitative, meta-analytic approach inorder to highlight and discuss marked variations in sample char-acteristics and methodology that will need to be considered infurther research.

Our review opens with a synopsis of studies of startle modula-tion effects in relation to varying anxiety and mood disorders,followed by a survey of such effects in relation to trait constructsassociated with these disorders. A brief analysis of startle modu-lation findings for the syndrome of psychopathy is also provided.Given substantial evidence for affective (in particular, fear) defi-cits in psychopathy, a survey of findings in this area in conjunctionwith those for phobic disorders provides evidence for continuity of effects on emotion-modulated startle across a broad dispositionalfear continuum. The review concludes with a discussion of startleresearch findings in relation to integrative hierarchical conceptu-alizations of internalizing psychopathology.

Internalizing Psychopathology and Affiliated TraitDispositions: EmpiricalConceptual Background

Analyses of patterns of comorbidity among the various inter-nalizing disorders have revealed that their interrelations can beaccounted for by an overarching factor that subsumes two distinctbut correlated dimensions, one encompassing fear syndromes andthe other anxiousmisery syndromes (cf. Krueger, 1999). Highlevels of fearfulness in relation to specific stimuli characterize the

first dimension, around which disorders such as simple phobias,social phobia, and panic disorder can be organized. The otherdimension is marked by more pervasive negative activation andhigh levels of dysphoriaanxiousness and misery (Krueger, 1999)or distress (Watson, 2005)and encompasses major depressivedisorder, dysthymia, and generalized anxiety disorder (GAD; see

also Kendler et al., 2003). More recent research (e.g., Cox, Clara,& Enns, 2002) has also located posttraumatic stress disorder(PTSD) within this latter cluster of internalizing disorders.

Other theories have sought to account for the observed comor-bidity among these disorders and the distinctive features of each interms of shared versus unique personality traits that are implicatedin them. For example, in Clark and Watsons (1991) tripartitemodel, high negative affectdefined as enhanced proneness tonegative states including anxiousness, irritability, and stress reac-tivityserves as a general distress factor that is present in bothanxiety and mood disorders. Each type of disorder, additionally,has components that are specific to it: Anxiety disorders entailphysiological hyperarousal, whereas low positive affect or anhe-donia (defined as a reduced capacity to experience pleasurableactivation or enjoyment in life) is considered specific to depres-sion. Similarly, Tellegens (1985) three-factor model of personal-ity posits high negative emotionality (NEM) as a common dispo-sitional factor involved in depression and anxiety disorders andlow positive emotionality as playing a specific role in depression.Another related conceptualization is Grays (1981) notion of thebehavioral inhibition system (BIS), which is postulated to inhibitmovement toward goals in the face of cues signaling punishmentor possible danger. According to Gray, individuals with a hypo-active BIS system show low levels of trait anxiety, whereas thosepossessing an oversensitive BIS system exhibit high levels of anxiety, fear, frustration, and sadness, predisposing them towardanxiety disorders and depression. In addition, Gray hypothesizedthe existence of a behavioral activation system (BAS) that issensitive to signals of reward, nonpunishment, and avoidance of harm, and accounts for positive states such as joy and hope. Fromthe standpoint of Grays model, hypoactivity of the BAS can beviewed as a distinctive substrate for depression.

Although there are similarities among the personality constructsidentified as relevant by each theory, they nonetheless differenough that direct comparisons between studies that use differentpersonality measures may not always be possible. This complexityis compounded further by variations in experimental parameterssuch as the type of emotion-eliciting stimuli used in the study(pictures, imaginal stimuli, shock, etc.), subject exclusionary cri-teria (e.g., comorbid psychopathology such as other anxiety dis-

orders, depression, and psychotic disorders), assessment strategy(e.g., groups with or without psychopathology as determined by DSM criteria, extreme groups on Fear Survey Schedule or Beck Depression Inventory), and other potential confounding variables

1 Grillon and Baas (2003) previously reviewed findings from affect-startle studies of internalizing psychopathology conducted up to 2002. Inaddition to updating coverage of mood and anxiety disorder studies, thecurrent review covers findings from startle studies of trait constructsaffiliated with internalizing disorders and advances a conceptual frame-work within which existing work in these areas can be integrated and guidefuture research.

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such as medication use. Additionally, differences in statisticalmethodology (e.g., correlational analyses that accommodate infor-mation about degree of psychopathology vs. t tests that focus ondiscrete group differences) and definition of operational variables(e.g., baseline startle response operationalized as reactivity dur-ing neutral pictures in some studies and as reactivity during inter-

trial intervals [ITIs] in others) complicate matters even further.Such marked discrepancies necessitate a qualitative review of studies in this area rather than a quantitative one.

Task Paradigms for Assessing Affect-Modulated Startle

The startle blink reflex is a basic protective (defensive) reactionthat occurs when an individual encounters an abrupt, intensestimulus. Research has shown the startle blink reflex to be aversatile measure that can be evoked by a variety of stimuli andthat is sensitive to (modulated by) both emotional and attentionalinfluences.

In studies examining variations in emotion-modulated startle,subjects are typically exposed to intermittent stimuli that areemotionally evocative, and during periods of exposure, the blink response to an intervening auditory probe stimulus is measured.For example, in the frequently used affective picture-startle para-digm, subjects are presented with photographic images depicting arange of emotional objects or scenes such as babies, animals,insects, buildings, kitchen utensils, guns, physical injury, sickness,etc. Abrupt acoustic probes (e.g., 50-ms, 95110-dB broadbandnoise bursts with immediate rise time) are delivered intermittentlyduring picture-viewing intervals, and eyeblink reactions to theprobe stimuli are measured with electromyographic sensors (forguidelines on processing eyeblink response data, see Blumenthal etal., 2005). The blink reflex has been found to be reliably modu-lated by the affective valence of the foreground picture stimulus,

with healthy control subjects generally exhibiting enhanced (po-tentiated) magnitude of blink response during unpleasant picturesrelative to neutral and attenuated (inhibited) reactivity duringpleasant scenes relative to neutral (cf. Lang, Bradley, & Cuthbert,1990; Vrana et al., 1988).

Lang et al. (1990) advanced a motivational priming hypothesisto account for this bidirectional impact of foreground emotionalvalence on the startle reflex. According to this model, aversive andpleasurable affective scenes lead to activation of defensive andappetitive motivational states, respectively, in the viewer (e.g.,Greenwald, Cook, & Lang, 1989; Lang, Greenwald, Bradley, &Hamm, 1993). Because the startle reflex is inherently a defensive(protective) response, it demonstrates augmentation when theviewer is in a preexisting defensive motivational state (i.e., arisingfrom exposure to an aversive foreground). In contrast, pleasantforeground stimuli instigate an appetitive (approach) state that isinconsistent with the defensive startle reflex, leading to inhibitionof the probe-elicited blink response. On average, startle responseselicited during processing of neutral foregrounds (i.e., outside thecontext of appetitive or defensive mobilization) fall in betweenthese two extremes.

A variant of the affect-startle modulation paradigm is the affec-tive imagery procedure in which startle probe stimuli are deliveredduring periods in which subjects imagine pleasant, unpleasant, andneutral scenes. Notably, studies using this procedure have gener-ally demonstrated the largest magnitude of startle reactivity during

unpleasant scenes, followed by pleasant scenes and then by neutral(e.g., Miller, Patrick, & Levenston, 2002; Witvliet & Vrana, 1995),indicating general enhancement of startle reactivity for emotion-ally arousing scenes (regardless of valence) versus low-arousalneutral scenes. This pattern of results has been interpreted asreflecting concurrent, contrasting effects of depth of imaginal

engagement and defensive versus appetitive activation on startlereactivity within this context (Miller et al., 2002). 2

Yet another variant of the affect-modulated startle paradigmentails delivery of startle probe stimuli during exposure to condi-tioned aversive stimuli. This procedure has been used especially instudies investigating PTSD. Studies of this kind usually include aninitial habituation phase in which subjects are exposed to simplenonaffective visual cues (e.g., colored lights) that are paired pre-dictably or unpredictably with an aversive stimulus, leading to cueconditioning (e.g., Jovanovic, Norrholm, Fennell, et al., 2009;Morgan, Grillon, Southwick, Davis, & Charney, 1995). Startlereactivity is then measured in subsequent phases, during periods inwhich conditioned stimuli are either present or absent. An alter-native to this paradigm involves assessing reactivity to startleprobes alone (e.g., Orr, Lasko, Shalev, & Pitman, 1995; Shalev,Orr, Peri, Schreiber, & Pitman, 1992) or to probes under instructedthreat of shock (e.g., Grillon, Morgan, Davis, & Southwick, 1998b;Pole, Neylan, Best, Orr, & Marmar, 2003) or in conditions of darkness (e.g., Grillon, Morgan, Davis, & Southwick, 1998a), withthe idea that such manipulations are sufficiently potent to evokedefensive reactivity on their own, without any prior conditioning.These latter procedures (e.g., context-potentiated startle, reactivityto probes alone) differ from picture viewing or imaginal process-ing paradigms in that startle modulation is examined for aversivecuing alone in relation to nonaffective (neutral) cuing.

However, despite notable differences as mentioned, a commonfeature of these varying task paradigms is that each includes

measurement of changes in startle blink reactivity as a function of induced motivational states. Because of its utility as an index of negative affect reactivity in particular, startle reflex modulationhas been employed in numerous studies of internalizing disordersand affiliated personality traits. Some studies have also examineddeviations in positive emotional reactivity within picture-viewingand imagery paradigms, particularly in relation to depression.

Given the variety of startle modulation effects to be discussed inthis review, some clarification of terminology is called for tominimize confusion and permit comparisons of modulatory pat-terns across differing studies. In the following pages, generalstartle reactivity refers to average startle reactivity in the absenceof or without regard to foreground stimulus manipulations, if

present. The term thus encompasses blink reactivity in probe-aloneparadigms, startle reactivity during ITIs of a task procedure, andmean reactivity across all trial conditions within a particular study.(The expression baseline startle reactivity has also been com-monly used in the literature. Although the term implies reactivityin the absence of an explicit task manipulation, this expression hasin fact been applied to conditions of various other types in theliterature, including reactivity during ITIs, reactivity to neutralforeground stimuli, and reactivity in nonthreatening contexts. We

2 For a thorough review of studies investigating anxiety disorders thatused this paradigm, see Lang and McTeague (2009).

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have opted for the term general startle reactivity because it moreaptly encompasses these varying operationalizations.) The termvalence-modulated startle effect (also referred to as linear startleeffect ) refers to the normative pattern of startle blink modulationobserved across stimulus valence conditions (unpleasant neu-tral pleasant) in picture-viewing paradigms. Emotion-modulated

startle refers to the increase (potentiation) or decrease (inhibition)in the magnitude of blink startle during viewing of an affectiveforeground relative to a neutral comparison condition. Context- potentiated startle refers to the increase in startle reactivity instressful contexts in an experiment (e.g., attachment of shock electrodes, suggesting that shocks may occur later in the experi-ment, but are not imminent) compared with a more neutral con-dition within the same experiment.

Neurobiology of the Defensive Motivational System andProcesses Indexed by Startle Modulation

As mentioned earlier, the startle response is considered a basicdefensive reflex that functions as a behavioral interrupt to directattention to the stimulus that caused the startle response (Graham,1979). Though it was initially theorized that the blink reflexindexed an arousal-engagement dimension (i.e., the more arousingand engaging the foreground stimulus, the greater the inhibition of startle to a probe in a differing stimulus modality), research onaffective valence and startle modulation led to a revision of thisperspective. Lang, Bradley, and Cuthbert (1997) postulated a cas-cade of defensive responses that occur in mammals upon exposureto an explicit aversive stimulus. According to this theory, differingphysiological systems respond in a progressive manner as the levelof defensive activation increases with increasing imminence of danger. At lower levels of activation, evident during initial stagesof an encounter with a potential threat, the startle reflex first

decreases as a function of early attentional processing of threatcues. Then, as the threat becomes clearer and more imminent andactivation of the defensive system increases, the magnitude of thestartle response increases as well.

The increase in startle that occurs during exposure to an explicitaversive cue has a known neurobiological basis. Upon presentationof an acoustic startle probe, an obligatory reflex circuit is activatedin which stimulus input is transmitted from the cochlear rootneurons to the nucleus reticularis pontis caudalis (nRPC), which inturn activates motor neurons to instigate the startle response.However, this circuit also receives input from secondary neuralpathways that can alter (modulate) the basic startle reflex. Re-search with rodents has revealed two distinct systems, both asso-ciated with the amygdala, that modulate the startle response as afunction of negative emotional states (see Davis, 1998; Davis,Walker, & Lee, 1997). One of these is a short-term (phasic) fearsystem, associated with the central nucleus of the amygdala (CeA),which is responsive to explicit threat cues. Fear-potentiated startleis mediated by this system (i.e., by a pathway from the CeA to thenRPC). The other system, a tonic negative arousal system, isassociated with the extended amygdalain particular, the bednucleus of the stria terminalis (BNST). This BNST system medi-ates persisting increases in startle reactivity associated with longerlasting emotional stressors. While acknowledging some interrela-tionship between the two systems (e.g., intense or repeated acti-vation of the amygdala by stressful events may lead to longer term

activation of the BNST via processes such as kindling; cf. Rosen& Schulkin, 1998), Davis and colleagues (Davis, 1998; Davis etal., 1997) posited that these systems play differing roles in fear andanxiety states, with the amygdala more important for cue-specificfear and the BNST more important for nonspecific anxiety. Inhumans, phasic enhancement of startle during aversive cuing (i.e.,

fear-potentiated startle) has been interpreted as reflecting activa-tion of the central amygdala (Lang et al., 1990), whereas tonicenhancement of startle associated with a stressful context (i.e.,context-potentiated startle) has been interpreted as reflecting ac-tivity in the BNST (Grillon & Davis, 1997). On the other hand,startle inhibition during exposure to pleasant stimuli is thought tobe mediated by the nucleus accumbens (NAC). For example,Koch, Schmid, and Schnitzler (1996) demonstrated that the NACplays a crucial role in reducing fear-potentiated startle in thepresence of a conditioned reward stimulus in rats. However, theprecise mechanism by which the NAC accomplishes this in conjunction with the neural circuitry for fear-potentiated startle re-mains to be determined.

In summary, attempts to map out the neurobiology of the acous-tic startle reflex have shown that it is a variegated system involvinginterconnections among several brain structures. An obligatorystartle reflex, regardless of foreground stimulus valence, is insti-gated by the basic brainstem circuit upon exposure to an intenseabrupt noise or other rapid-onset stimulus. Fear-potentiated startleis mediated by connections from structures such as the CeA andBNST to the nRPC node of the brainstem circuit, with the formermore associated with phasic fear response and the latter with tonicanxiety response. Startle responses to pleasant stimuli appear to bemoderated additionally by input from the NAC. Although the basicstructures involved in this circuit are clear, further research isrequired to understand the interplay of these various structures inproducing startle response modulation, in particular startle inhibi-

tion during processing of pleasurable foreground stimuli.

Startle Reflex Modulation and InternalizingPsychopathology

Startle modulation has been frequently used to study internal-izing disorders and affiliated personality traits. A recent review byGrillon and Baas (2003) provided a broad summary of the use of the startle reflex in studying various forms of psychopathologyincluding internalizing and externalizing disorders, psychotic dis-orders, and personality pathology. The objective of this priorreview was to summarize findings for differing startle modulationeffects in relation to varying specific disorders. The central aim of the current review is different from this. Beyond providing anupdated survey of findings in this area, our goal is to integratestartle findings for varying diagnostic syndromes and affiliatedindividual difference constructs into a hierarchicaldimensionalframework (cf. Watson, 2005), in order to facilitate understandingof prior research findings and guide future research in theseinterrelated domains.

Although several variants of the startle paradigm have been usedto study internalizing psychopathology, theoretical considerationshave informed the use of certain procedures with particular disor-ders. For example, the picture-viewing startle task has been usedmost frequently in studies of phobic disorders and dispositionalfearfulness (see Table 1). Because phobias by definition are char-



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acterized by extreme levels of fear (i.e., defense system activation)to specific environmental stimuli considered aversive, phobic subjects would be expected to show heightened startle potentiationreflecting enhanced activation of the phasic fear (amygdala) sys-temduring exposure to such stimuli. As discussed in detailbelow, this hypothesis has received substantial support across

many published studies to date.However, in the disorder of PTSD, for which exaggerated startleserves as a specific diagnostic criterion, studies have tended tofocus on reactivity to startle probes alone without any other fore-ground stimuli (e.g., Orr et al., 1995, 2003; Shalev et al., 1992).Related work by Grillon and colleagues has posited that thisenhancement of startle in PTSD is dependent on the presence of anaversive context, and these researchers have investigated startlereactivity in experimental situations that are manipulated to bestressful or unpleasant in some manner, compared with a neutralexperimental context (e.g., Grillon & Morgan, 1999; Grillon et al.,1998b). Startle studies of depression, on the other hand, havepredominantly employed affect-modulated startle paradigms, astheoretical accounts of depression emphasize both a deficiency inpositive affect and an excess of negative affect (e.g., Allen,Trinder, & Brennan, 1999; Dichter, Tomarken, Shelton, & Sutton,2004).

Differing hypotheses can be advanced regarding deviations instartle modulation in individuals with internalizing disorders of these types. One possibility is that individuals with disorders suchas PTSD or major depression may show enhanced startle potenti-ation during viewing of threatening scenes, as is the case forphobic disorders. On the other hand, if increased fear-potentiatedstartle reflects an augmentation of cue-specific fear that is uniqueto phobic or fear disorders, a different pattern of results might beexpected for the anxiousmisery syndromes. Given that disordersof this type are marked by high levels of free-floating anxiety,

enhanced general startle reactivity or increased startle reactivity inrelation to aversive or unfamiliar situations (i.e., enhanced contextpotentiation) might be expected. Alternatively, if anxiety levels areabnormally high and persistent across time, the startle response toabrupt probe stimuli might be generally diminished. The basis forthis prediction comes from Seligmans (1975) conceptualization of learned helplessness, in which repeated exposure to unavoidablenegative stimulation leads to a general lack of behavioral reactiv-ity, even when avenues of escape subsequently become available.Yet another possibility is that the lack of positive affectivityapparent in disorders of this type might be associated in particularwith a lack of normal inhibition of startle during viewing of pleasurable stimulieither alone or in conjunction with enhancedaversive startle potentiation or general sensitization of startle re-activity.

With these considerations in mind, in this review we seek tohighlight consistent patterns of findings in studies to date that haveexamined startle modulation effects in samples of individualsselected for the presence of internalizing disorders or personalitytraits affiliated with these disorders.

Phobic Disorders

Phobias are characterized by clinically significant anxietyevoked by specific feared stimuli (e.g., snakes, spiders, socialsituations). Because the mechanism of the fear-potentiated startle

effect is most directly relevant to cue-specific fear disorders, earlystudies focused on startle potentiation during aversive cuing insubjects with specific phobias. As reviewed by Grillon and Baas(2003), early studies in this area (de Jong, Merckelbach, & Arntz,1991; de Jong, Visser, & Merckelbach, 1996; Vrana, Constantine,& Westman, 1992) attempted to use the blink reflex as an indicator

of treatment success by assessing it pre- and postintervention insubjects with specific phobia. Results were in the predicted direc-tion, with phobic subjects showing reduced fear-potentiated startleduring viewing of fear-relevant stimuli after completion of treat-ment sessions, suggesting that the blink reflex could indeed beused as an outcome measure. Hamm and colleagues (Globisch,Hamm, Esteves, & O hman, 1999; Hamm, Cuthbert, Globisch, &Vaitl, 1997) compared startle reactivity during picture viewing inphobic subjects and nonphobic controls. Findings from these twostudies indicated that phobic subjects showed greater startle po-tentiation during processing of phobic scenes, compared withnonphobic controls. These results provide further support for thehypothesis that phobic subjects exhibit greater levels of defensivereactivity than controls during exposure to aversive stimuli.

A more recent study by McTeague et al. (2009) investigatedaversive startle potentiation in treatment-seeking patients diag-nosed with social phobia compared with healthy controls. Theauthors used an imagery paradigm in which subjects visualizedneutral and fearful scenes, with startle probes presented at unpre-dictable points during image processing. Scripts for fear scenesconsisted of standardized scenarios involving social threat andnonsocial threat along with personalized scenes based on subjectsown worst fears. The social phobic group was subdivided into acircumscribed subgroup, for whom social anxiety was limited toperformance contexts alone, and a generalized subgroup, forwhom fear of social situations were more pervasive. Comparedwith the circumscribed subgroup, the generalized subgroup

showed greater comorbidity with mood-related (depressive) disor-ders, indicating a larger component of distress or generalizednegative affectivity (cf. Watson, 2005) in this subgroup.

Findings from the imagery assessment indicated startle potenti-ation for fearful scenes relative to neutral scenes in healthy con-trols as well as socially phobic individuals; however, generalstartle reactivity across all imagery scenes (regardless of content)was greater for patients than controls. Healthy controls showedpotentiation only during imagery of personalized fear and nonso-cial threat scenes relative to neutral scenes. In contrast, patientsdemonstrated significant startle potentiation for social threatscenes (standard as well as personalized). This effect was drivenby the generalized social phobic group, rather than the circum-scribed social phobic group, suggesting pervasive defensive reac-tivity across all aversive scenarios. However, this finding of per-vasive potentiation was limited to generalized social phobicpatients without comorbid depression. Subjects who met criteriafor depression as well as social phobia demonstrated potentiationof startle only for personalized fear scenes (i.e., not for standardsocial threat or nonthreat scenes), suggesting that the presence of depression may operate to blunt defensive mobilization to threatcues except when the threat is potent or imminent (see next sectionon depression).

Although the aforementioned studies all found evidence of heightened startle potentiation for individuals with phobic feardisorders, two other studies did not. One of these (de Jong, Arntz,



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& Merckelbach, 1993) contrasted startle reactivity in phobic subjects exposed to unpleasantfearful, pleasant, and neutral condi-tions (a live spider, appetizing food, and a block of wood, respec-tively) in pre- and posttreatment assessments. Although blink responses for the spider condition decreased significantly from thepre- to the posttreatment assessment, phobic subjects did not show

the expected pattern of valence-modulated startle in either thepretreatment or immediate posttreatment assessment. In anotherstudy that failed to show fear-potentiated startle in phobic subjects(Merckelbach, de Jong, Leeuw, & van den Hout, 1995), spiderphobics and healthy controls were presented with backwardlymasked phobic stimuli (spider scenes) along with nonphobicscenes (i.e., pictures of flowers, mushrooms, and snakes), withprobes delivered after offset of the masking stimulus. It is unclearwhy these authors did not find any differences between groups.

In summary, with the exception of the two studies discussedabove, research to date has generally demonstrated greater fear-potentiated startle among phobic subjects, in comparison withcontrols. Additionally, one study (McTeague et al., 2009) reportedblunted defensive reactivity as indexed by startle potentiation tostandardized (i.e., nonpersonally relevant) threat scenes in patientswith generalized social phobia and depression.

Panic Disorder With or Without Agoraphobia

Recurrent unexpected panic attacks causing significant clinicalimpairment are the defining characteristic of panic disorder. Thesemay or may not co-occur with agoraphobia, which entails anxietyabout situations from which escape is difficult. Analyses of inter-relations among DSM disorders, as determined by structured clin-ical interviews (e.g., Cox et al., 2002; Krueger, 1999), have indi-cated that panic disorder coheres more closely with the phobicdisorders than with depression or PTSD. This is somewhat unex-

pected, as a diagnosis of panic disorder requires at least twouncued or unexpected panic attacks not tied to any specific stim-ulusa phenomenon that appears more indicative of nonspecificanxiety (as seen in the distress disorders) than cue-specific fear. Onthe whole, as described below, findings from startle modulationstudies are more consistent with the notion of panic disorder as adistress syndrome, although evidence from at least one studysuggests that there may be a subgroup of panic patients whorespond more like phobic individuals.

Melzig, Weike, Zimmermann, and Hamm (2007) examinedstartle response potentiation in subjects with panic disorder com-pared with diagnosis-free controls in two aversive conditions:threat of shock and darkness. The experiment consisted of anadaptation or habituation phase followed by a darklight phase inwhich startle probes, but no shocks, were delivered. This wasfollowed by a darklight phase that included periods entailingthreat of shock interspersed with safe (no shock) periods. No groupdifferences in general startle reactivity were evident during theadaptation phase, darklight condition, or darklight plus safeshock condition, nor did groups differ in degree of startle poten-tiation during dark versus light or shock versus safe conditions.However, when patients with panic disorder were subdivided intothose with comorbid depression and those without, those withcomorbid depression failed to show significant startle potentiationduring threat versus safe periods, whereas panic patients withoutdepression did show significant potentiation. Indeed, panic pa-

tients without depression showed a trend toward even strongerthreat versus safe potentiation than control subjects. In addition toMcTeague et al.s (2009) study, these findings provide furtherevidence that the presence of comorbid depression mitigatesagainst robust cue-specific startle potentiation.

In another study, Cuthbert et al. (2003) compared general startle

reactivity during ITIs and potentiation during aversive imagery intreatment-seeking patients diagnosed with varying anxiety disor-ders (specific phobia, social phobia, and panic disorder with ago-raphobia) as well as healthy controls. Subjects imagined scriptedneutral, and standardized and personalized fearful scenes. Startlepotentiation was defined as mean blink reactivity for the fearversus neutral imagery conditions. Across all groups, significantstartle potentiation was observed for fearful imagery scenes as awhole. However, for personal fear scenes, significant startle po-tentiation was observed in patients with specific and social phobiaand in controls but not in patients with panic disorder. Instead,panic patients showed a trend (approaching significance) towardgreater general startle reactivity (measured as startle reactivityduring ITI) relative to controls and patients diagnosed with eitherspecific phobia or social phobia. These results provide evidence of deficient cue-specific startle potentiation coupled with enhancedgeneral startle reactivity in patients with panic disorder.

In a follow-up to this study, Lang, McTeague, and Cuthbert(2007) used a similar imagery paradigm to examine startle reac-tivity in patients diagnosed with specific phobia, social phobia,panic disorder with agoraphobia, and/or GAD and a no-disordercontrol group. Specific phobics showed the greatest startle poten-tiation during imagery of fearful scenes relative to startle duringITIs, followed by those with social phobia, panic disorder withagoraphobia, and GAD. Additionally, scores on a measure of traitanxiousness (akin to negative affectivity or general distress;Watson, 2005; Watson & Tellegen, 1985) showed an inverse

relationship with fear-potentiated startle, such that subjects withthe highest levels of trait anxiousness showed the smallest degreeof startle potentiation for personal fear scenes. These results againsuggest that panic disorder in patient samples is more similar toGAD and depression than to the phobic disorders. These data alsoindicate that reductions in fear-potentiated startle may be charac-teristic of the anxiousmisery subgroup of internalizing disorders.

Grillon et al. (2008) conducted a study examining startle reac-tivity in patients with panic disorder (screened to exclude individ-uals with comorbid depression) and control subjects. Startle probeswere delivered during three conditions: a neutral condition inwhich visual cues were presented without accompanying aversivestimuli, a predictable aversive condition in which the occurrence of the aversive stimuli was signaled by distinctive visual cues (i.e.,cues different from those in the other two conditions), and anunpredictable aversive condition that included noncontingent vi-sual cues. Startle probes were delivered during cue presentationperiods and during ITIs in each condition. Although all subjectsdemonstrated startle potentiation during predictable and unpredict-able conditions relative to the neutral condition, panic patientsalone showed a significant increase in startle reactivity to ITIprobes occurring within the unpredictable aversive condition rel-ative to the neutral condition. The authors interpreted this asevidence that nonspecific (contextual) fear associated with unpre-dictability of aversive events represents a key component in panicdisorder.



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An earlier study by Grillon, Ameli, Goddard, Woods, and Davis(1994) examined startle reflex potentiation in patients diagnosedwith panic disorder in a threat-of-shock paradigm. However, theresults of this study are somewhat unclear, as the primary findingwas that younger patients with panic disorder ( 40 years old),compared with age-matched controls, showed greater startle re-

sponse magnitudes across probes delivered during the threat peri-ods, whereas older subjects did not. The authors hypothesized thatthis could have been an effect of age or that older patients couldhave developed some sort of immunity, as manifested by relativelynormal startle reactivity. They interpreted the increased startle inyounger patients as indicating an effect of global context in theexperimental phase of the study, such that a stressful context led togenerally augmented startle among panic disorder patients.

In summary, studies conducted in this area generally suggestthat patients with panic disorder appear to be a diverse group withregard to startle reactivity. Findings from one study (Melzig et al.,2007) indicate that there may be a specific subgroup of panicpatients (i.e., those without comorbid depression) who show en-hanced cue-specific fear, akin to patients with specific phobias.Additionally, this study along with others suggests that patientswith panic disorder and agoraphobia, or comorbid panic and de-pression, show limited startle potentiation for aversive stimuli. Inother words, panic disorder appears to have characteristics that aresimilar to both the fear disorders and the anxiousmisery disorders,suggesting that it may not necessarily be best classified as a feardisorder alone.

PTSD

The DSM-IV-TR (APA, 2000) defines PTSD as the reexperi-encing of an extremely traumatic event accompanied by symptomsof increased arousal and by avoidance of stimuli associated with

the trauma (p. 429). Given that one of the diagnostic criteria forthis disorder is an exaggerated startle response, the startle blink reflex is an obvious candidate for study in individuals with PTSD.Indeed, a vast literature exists on physiological reactivity in PTSDin general and startle reactivity in particular. On the basis of thisextant research, three reviews (Grillon & Baas, 2003; Metzger etal., 1999; Pole, 2007) have concluded that there is evidence for thepresence of enhanced startle reactivity in subjects diagnosed withPTSD. Additionally, Grillon and Baas (2003) noted that this effectwas particularly evident in a stressful or aversive context (e.g., anexperimental situation, being exposed to shocks). Given thesecomprehensive preexisting reviews, we provide a brief summaryof the various studies in this field and their principal findings anddiscuss how these findings fit within the conceptual framework of the current review.

Following the line of reasoning that exaggerated startle is adiagnostic symptom of PTSD, a number of investigators haveexamined startle blink reactivity in PTSD to probes presentedalone, in the absence of other concurrent stimuli. Several studies of this type have reported evidence of increased startle reactivity insubjects with PTSD compared with control subjects (Butler et al.,1990; Cuthbert et al., 2003; Grillon et al., 1998a; Ladwig et al.,2002; Morgan, Grillon, Lubin, & Southwick, 1997; Morgan, Gril-lon, Southwick, Davis, & Charney, 1995; Morgan, Grillon, South-wick, Davis, & Charney, 1996; Morgan, Grillon, Southwick,Nagy, et al., 1995; Orr et al., 1995; Shalev et al., 1992; Shalev,

Peri, Orr, Bonne, & Pitman, 1997). However, in direct contrast,several others have found no evidence of increased blink reactivityin subjects with PTSD (Carson et al., 2007; Grillon, Morgan,Southwick, Davis, & Charney, 1996; Guthrie & Bryant, 2005;Jovanovic, Norrholm, Sakoman, Esterajher, & Kozaric-Kovacic,2009; Karl, Malta, Alexander, & Blanchard, 2004; Metzger et al.,

1999; Orr, Lasko, Metzger, & Pitman, 1997; Orr et al., 2003; Orr,Solomon, Peri, Pitman, & Shalev, 1997; Ross et al., 1989).In a conceptual reinterpretation of these findings, Grillon and

Baas (2003) proposed that the increased startle response observedin PTSD occurs as a function of the presence of a stressful oraversive experimental context. They posited that without this aver-sive priming, PTSD might not be associated with increased startlereactivity. Empirical support for this viewpoint derives from ex-periments that have induced stressful experimental contexts bymethods such as creating unpredictable conditions in which cuessignal the possible delivery of aversive stimuli (Grillon, Pine,Lissek, Rabin, & Vythilingam, 2009), attaching shock electrodesto subjects while mentioning that shocks would not be delivereduntil later (Grillon et al., 1998b; Pole et al., 2003), and assessingstartle reactivity in two sessions in which mild electric shocks wereadministered in the first session (Grillon & Morgan, 1999). Find-ings from these studies have generally indicated that subjects withPTSD show increased startle reactivity during the stressful phasesof these experiments but not in the nonstressful phases. Alongthese lines, Pole et al. (2009) reported that startle reactivity duringstressful versus neutral contexts in police officers without psycho-pathology prospectively predicted PTSD symptom severity 1 yearlater following exposure to trauma.

In a related line of research, Griffin (2008) and Shalev et al.(2000) investigated differences in startle reactivity after traumaexposure. Shalev et al. demonstrated that there were no differencesin general startle reactivity between subjects with and without

PTSD (diagnosed at 4 months after trauma) at 1 week posttrauma.However, at 1 and 4 months posttrauma, subjects with PTSD took longer to habituate to startle probes. Similarly, Griffin showed thatat 1 month posttrauma assessment, there were no differences instartle reactivity between subjects with and without PTSD. How-ever, at the 6-month follow-up, those diagnosed with PTSD hadgreater startle responses; this effect was due to increased startleblink reactivity for the PTSD group between the two assessments.The Griffin and Shalev et al. studies appear to suggest that abnor-malities in startle reactivity develop after trauma exposure, incontrast with Pole et al.s (2009) findings. It must be noted,however, that neither of the former studies included pretraumastartle assessments. Thus, definitive conclusions cannot be drawnregarding the development of abnormal startle reactivity followingtrauma exposure.

Another explanation for unusual startle reactivity in PTSD wassuggested by Miller and Litzs (2004) study, which examinedstartle reactivity during affective picture viewing in veterans di-agnosed with PTSD according to DSM (3rd ed., rev.; APA, 1987)criteria relative to non-PTSD control veterans. This study includedan interesting manipulation in which veterans were exposed to anontrauma-related stressor (threat of shock) followed by a trauma-related stressor (combat-related photographs presented with war-related sounds). At pretest and immediately following each of thetwo-stressor manipulations, subjects completed a standard picture-startle assessment that included varied pleasant and unpleasant



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scenes. Modulation scores for affective stimuli (trauma and non-trauma related) were calculated in relation to startle during ITIs.Subjects in both groups showed enhanced blink reactivity duringunpleasant compared with pleasant scenes and reduced blink re-activity during both pleasant and unpleasant scenes relative to ITI.Similar results were observed during both the preshock and post-

shock startle assessments. However, for the startle assessmentfollowing the trauma-related stressor, controls showed no signifi-cant difference in startle reactivity for pleasant versus unpleasantstimuli (with reactions for both affective contents reduced incomparison with ITIs), whereas veterans with PTSD showed sig-nificantly enhanced blink response during unpleasant pictures rel-ative to either ITIs or pleasant picture trials. Thus, results indicatedthat subjects with PTSD acted like phobic subjects from previousstudies once they had been primed by presentations of trauma-specific stimuli. The implication is that exposure to relevant aver-sive cues is required to precipitate increased startle reactivity inPTSD.

Cuthbert et al. (2003) attempted to explain elevated startle inPTSD from a slightly different standpoint by comparing patientswith PTSD against healthy controls and subjects with other anxietydisorders including specific phobias, social phobia, and panicdisorder with agoraphobia. Similar to patients with panic disorder,those with PTSD did not show significant blink potentiation fortheir specific fear scenes relative to standard neutral scenes. Like-wise, as mentioned earlier, patients with PTSD also tended todisplay enhanced general startle reactivity (measured as startlereactivity during ITI), relative to control subjects and patientsdiagnosed with either specific phobia or social phobia. The authorsinterpreted these findings in the context of elevated negativeaffectivity (as defined by scores on questionnaire measures of anxiety symptoms, fear and anxiety-related scales, depressivesymptoms, and comorbid diagnoses of depression). They noted

that controls, and patients with specific phobia or social phobia,were comparatively low in negative affectivity compared withpanic disorder or PTSD patients. It is interesting that the latter twogroups also showed the least startle potentiation during personalfear scenes. The authors posited that although a certain amount of negative affectivity predisposes subjects with phobias to increasedcue-specific fear reactivity (i.e., fear-potentiated startle), beingextremely high on negative affectivity appears to be associatedwith limited cue-specific fear reactivity. Of note, this pattern of results, together with the finding of greater general startle reactiv-ity for panic disorder and PTSD patients, is consistent with theresults of studies of panic disorder patients discussed earlier. Thesedata again suggest that patients with panic disorder may be moresimilar to patients with PTSD in terms of physiological reactivitythan they are to specific phobic patients.

Complicating this explanation, however, are studies that havefound no differences in fear-potentiated startle between subjectswith and without PTSD but only differences in context-potentiatedstartle (Grillon & Morgan, 1999; Grillon et al., 2009) or a lack of fear inhibition to safety cues (Grillon & Morgan, 1999; Jovanovic,Norrholm, Fennell, et al., 2009). Jovanovic, Norrholm, Fennell, etal. (2009) reported an additional intriguing result, showing that thelack of fear inhibition during safety cues was specifically related tothe reexperiencing and avoidance symptoms of PTSD and not tothe hyperarousal symptoms, suggesting that the various symptomdimensions of PTSD are differentially associated with startle re-

activity. Additionally, as one further twist in this complex litera-ture, two studies have reported an opposite pattern of decreasedstartle reactivity in subjects with PTSD (Medina, Mejia, Schell,Dawson, & Margolin, 2001; Ornitz & Pynoos, 1989).

In summary, there have been numerous studies using varyingtypes of experimental paradigms that have investigated startle

blink responding in PTSD. Although several interesting explana-tions have been proposed for the range of results reported in thesestudies, the reasons for differences in findings across studies is notreadily apparent. Even though it is difficult to draw strong con-clusions at this point, as with our review of the studies in this fieldand prior meta-analytic reviews by Metzger et al. (1999) and Pole(2007), the general trend of results suggests that PTSD is associ-ated with exaggerated startle reactivity. However, it is unclearwhether this increased reactivity occurs primarily in aversive con-texts, as Grillon et al. (1998b) have suggested, or whether it occurspervasively across contexts. Results for fear-potentiated startle(i.e., augmentation in relation to specific fear-relevant cues) appeareven more mixed, with some studies showing no difference instartle reactivity for fear-relevant versus neutral conditions insubjects with PTSD and others showing enhanced fear-potentiation in PTSD patients subsequent to an aversive primingmanipulation (e.g., exposure to trauma-related cues).

Some of these divergences in findings may reflect proceduraldifferences across studies. For example, it is unclear whetherstartle reactivity under threat of shock is equivalent to blink reactivity while imagining an aversive scene. It can be argued thatalthough context-conditioning experiments attempt to differentiatebetween fear-potentiated startle and context-potentiated startle,studies of this type do not lend themselves readily to such differ-ential analysis insofar as context-conditioning paradigms focus onassessment of startle reactivity during the anticipation of aversivestimulus events, either cued or uncued. In contrast, affect-imagery

and affect-startle paradigms do not rely on conditioning or antic-ipation effects but rather assess startle reactivity directly in thepresence of the aversive stimulus, making them more suitable forassessing fear-potentiated startle.

Conversely, it could be debated whether affect-imagery andaffect-picture studies of patient samples have assessed generalstartle reactivity adequately. Some studies of this type (e.g., Cuth-bert et al., 2003; Lang et al., 2007; Miller & Litz, 2004) haveincluded presentation of startle probes during ITIs, whereas others(e.g., Allen et al., 1999; Kumari, Kaviani, Raven, Gray, & Check-ley, 2001) have examined differences in mean startle reactivityacross all foreground stimulus trials between patient and controlgroups. Although it could be assumed that startle reactivity toprobes occurring within ITIs or across stimulus trials overallindexes something akin to reactivity to probes alone (i.e., in theabsence of any foreground stimulus), this assumption has not beensystematically evaluated and thus should be considered provisionaland in need of verification.

Another source of discrepancies in results could be the presenceof comorbid diagnoses. As can be seen in Table 2, participantsamples in the different PTSD studies varied widely with regard tothe comorbid disorders they experienced. However, not all studiesassessed and/or attempted to control for comorbid disorders. Of those that did (in most cases for depression or panic disorder), allreported that results were unaffected by the presence of additional

(text continues on page 925 )



12/34

T a b l e 2

S u m m a r y o f S t u d i e s E x a m i n i n g A f f e c t - M o d u l a t e d S t a r t l e R e a c t i v i t y i n P o s t t r a u m a t i c S t r e s s D i s o r d e r

C a t e g o r y

E x p e r i m e n t a l p a r a d i g m

D i a g n o s t i c i n s t r u m e n t

S u b j e c t s

C o m o r b i d d i a g n o s i s

M e d i c a t i o n a

K e y r e s u l t

S t u d i e s i n v e s t i g a t i n g

g e n e r a l s t a r t l e

B u t l e r e t a l . (

1 9 9 0 )

S t a r t l e p r o b e a l o n e

D S M - I I

I - R

1 3 P T S D

, 1 2 c o m b a t c o n t r o l s N o c o m o r b i d d i a g n o s i s

A

G r e a t e r s t a r t l e

i n P T S D f o r 9 5 -

a n d 1 0 0 - d B

p r o b e s b u t n o t

o t h e r p r o b e

i n t e n s i t i e s .

S h a l e v e t a l . (

1 9 9 2 )


S C I D - R

1 4 P T S D ; 1 4 o t h e r a n x i e t y

d i s o r d e r s ( 7 P D

, 3 G A D

, 4

O C D ) ; 1 5 s u b j e c t s w i t h

t r a u m a e x p o s u r e b u t n o

p s y c h o p a t h o l o g y ; 1 9 w i t h

n o t r a u m a e x p o s u r e o r

p s y c h o p a t h o l o g y

P T S D : 2 A A

, 1 M D

C

T r e n d t o w a r d l a r g e r g e n e r a l s t a r t l e

i n P T S D

.

M o r g a n , G r i l l o n ,

S o u t h w i c k , N a g y , e t

a l . (

1 9 9 5 )


S C I D - R

1 8 P T S D

, 1 1 c o m b a t c o n t r o l s 5 p a s t a n d c u r r e n t P D

, 1 5

p a s t M D

B

G e n e r a l s t a r t l e g r e a t e r i n P T S D

.

N o d i f f e r e n c e i n r e s u l t s d u e t o

P D d i a g n o s i s

.

O r r e t a l . (

1 9 9 5 )


S C I D - R

3 7 P T S D

, 1 9 c o m b a t c o n t r o l s P T S D : 1 B P

I I , 1

4 M D

,

7 D Y S , 1 p s y c h o t i c

d i s o r d e r n o t o t h e r w i s e

s p e c i f i e d , 6 A A

, 7 S A

,

6 P D w i t h o u t A G O

, 7

S O , 2

S P , 3

O C D

, 2

G A D

, 6 b o r d e r l i n e

p e r s o n a l i t y , 2

A S P D ;

c o m b a t c o n t r o l s : 1

M D

, 2 D Y S , 2 A A

, 1

P D w i t h o u t A G O

, 2

S O , 1

G A D

, 1

b o r d e r l i n e p e r s o n a l i t y

D


t h a n c o m b a t c o n t r o l s

. N o

d i f f e r e n c e s d u e t o c o m o r b i d

d i s o r d e r . M

e d i c a t i o n u s e h a d n o

e f f e c t o n r e s u l t s

.

M o r g a n e t a l . (

1 9 9 6 )


S C I D - R

1 0 P T S D

, 7 c o m b a t c o n t r o l s

,

1 5 c i v i l i a n c o n t r o l s

2 A A

B


t h a n c i v i l i a n a n d c o m b a t

c o n t r o l s

. C i v i l i a n a n d c o m b a t

c o n t r o l s n o t d i f f e r e n t f r o m e a c h

o t h e r .

M o r g a n e t a l . (

1 9 9 7 )


S C I D - R

1 3 P T S D

, 1 6 c o n t r o l s

6 P D w i t h o u t A G O

, 1 1

M D

B


g r o u p t h a n c o n t r o l s f o r l e f t e y e

b u t n o t r i g h t e y e . T

h i s e f f e c t

m o r e d r i v e n b y r e c e n t - P

T S D

g r o u p a n d n o t l o n g - s t a n d i n g

P T S D g r o u p . N o d i f f e r e n c e i n

r e s u l t s d u e t o c o m o r b i d P D o r

M D

.


1 9 9 7 )


S C I D - R

P a t i e n t s r e f e r r e d f o r t r a u m a -

r e l a t e d d i s t r e s s : 3 0 w i t h

P T S D

, 2 8 w i t h o u t P T S D

P T S D : 1 2 M

D , 4

P D , 1

d i s s o c i a t i v e d i s o r d e r ;

w i t h o u t P T S D : 1 8 p a s t

P T S D

, 5 M D

, 2

a d j u s t m e n t d i s o r d e r

B


t h a n n o n - P T S D

.

L a d w i g e t a l . (

2 0 0 2 )


D i a g n o s t i c c h e c k l i s t

r e c o m m e n d e d b y W H O

1 1 P T S D

, 1 9 c o n t r o l s ; a l l

s u b j e c t s h a d p e r i t r a u m a t i c

d i s s o c i a t i o n

N o n e n o t e d

A


t h a n c o n t r o l s

. ( t a b l e c o n t i n u e s )



13/34

T a b l e 2 ( c o n t i n u e d )

C a t e g o r y



S u b j e c t s



K e y r e s u l t

R o s s e t a l . (

1 9 8 9 )


D S M - I I

I - R

9 P T S D

, 9 c o n t r o l s

4 M D

, 3 G A D

, 2 D Y S , 2

A S P D

B

N o d i f f e r e n c e s b e t w e e n g r o u p s .

G r i l l o n e t a l . (

1 9 9 6 )


S C I D - R

1 9 P T S D

, 1 0 c o m b a t

c o n t r o l s

, 1 6 c i v i l i a n

c o n t r o l s

M D a n d O C D

e x c l u s i o n a r y c r i t e r i a , 4

P D , 1

0 A A

B

N o d i f f e r e n c e s a m o n g g r o u p s .

O r r , L

a s k o

, e t a l . ( 1 9 9 7 )

N o n s t a r t l i n g p r o b e s

a l o n e

S C I D - R

2 0 P T S D

, 1 9 c o m b a t c o n t r o l s N o n e n o t e d , a

p a r t f r o m

p a s t A A o r S A

B


O r r , S

o l o m o n , e

t a l . ( 1 9 9 7 ) S t a r t l e p r o b e a l o n e

S C I D - R

1 9 c u r r e n t P T S D

, 7 4 c o m b a t

c o n t r o l s

P T S D : 5 G A D ; 6 c u r r e n t

M D ; c o m

b a t c o n t r o l s :

2 G A D , 2 c u r r e n t M D

C


M e t z g e r e t a l . (

1 9 9 9 )


S C I D - R

5 7 w o m e n w i t h h i s t o r y o f

c h i l d s e x u a l a b u s e : 2 1

c u r r e n t P T S D

, 2 3 l i f e t i m e

b u t n o t c u r r e n t P T S D

, 1 3

n e v e r P T S D

C u r r e n t P T S D : 2 B P , 5

M D

, 5 D Y S , 5 P D

, 3

A G O

, 7 S O

, 8 S P

, 3

G A D

, 1 s o m a t o f o r m , 3

e a t i n g d i s o r d e r , 1

S A ;

l i f e t i m e P T S D : 1 M D

,

1 D Y S , 1 P D

, 1 S P

, 2

e a t i n g d i s o r d e r ; n e v e r

P T S D : 1 P D

, 1 S O

, 1

S P , 2

S A , 1

A A

D


M e d i c a t i o n u s e h a d n o e f f e c t o n

r e s u l t s

.

O r r e t a l . (

2 0 0 3 )


C A P S

M o n o z y g o t i c t w i n s

d i s c o r d a n t f o r c o m b a t

e x p o s u r e a n d P T S : 5 0

P T S D

, 5 3 c o n t r o l t w i n s

C o m o r b i d i t y n o t e d ,

t h o u g h d e t a i l s n o t

p r o v i d e d

C


K a r l e t a l . ( 2 0 0 4 )


w i t h n e u t r a l , s t a r t l e ,

a n d t r a u m a - r e l a t e d

s o u n d s ; p r e - a n d

p o s t t r e a t m e n t

a s s e s s m e n t

C A P S

1 7 m o t o r v e h i c l e a c c i d e n t

s u r v i v o r s : 1 0 P T S D

, 3

s u b s y n d r o m e , 4 n o n - P T S D ;

s u b j e c t s r a n d o m l y a s s i g n e d

t o t r e a t m e n t o r c o n t r o l

w a i t l i s t

N o n e n o t e d

A

N o d i f f e r e n c e s a m o n g g r o u p s a t

p r e t r e a t m e n t . N o d i f f e r e n c e s

b e t w e e n s t a r t l e a n d t r a u m a -

r e l a t e d s o u n d s i n g r o u p s .

D e c r e a s e d g e n e r a l s t a r t l e i n

t r e a t m e n t g r o u p c o m p a r e d w i t h

w a i t l i s t c o n t r o l s

.

G u t h r i e a n d B r y a n t ( 2 0 0 5 )

S t a r t l e p r o b e a l o n e ;

E M G

a c t i v i t y

a s s e s s e d p r e - a n d

p o s t t r a u m a

C A P S

3 5 t r a u m a - e x p o s e d

f i r e f i g h t e r s , 3 6 n o n t r a u m a

e x p o s e d c o n t r o l s

N o n e n o t e d

B

N o d i f f e r e n c e s b e t w e e n g r o u p s . I

n

b o t h g r o u p s , m e a n p r e t r a u m a

s t a r t l e a c t i v i t y p r e d i c t i v e o f

m e a n p o s t t r a u m a s t a r t l e a c t i v i t y

.

C a r s o n e t a l . (

2 0 0 7 )


C A P S a n d S C I D

N u r s e s w i t h V i e t n a m W a r

r e l a t e d P T S D : 3 9 c u r r e n t

P T S D

, 4 0 p a s t P T S D

, 4 9

e x p o s e d b u t n o P T S D

C u r r e n t g r o u p : 2 o t h e r

B P , 1 6 M

D , 4

D Y S , 7

P D , 1

A G O

, 6 S O

, 5

S P , 1

O C D

, 1

u n d i f f e r e n t i a t e d

s o m a t o f o r m , 4

b i n g e -

e a t i n g d i s o r d e r , 2

A A ;

p a s t g r o u p : 2 P D

, 1

S P , 1

b o d y d y s m o r p h i c

d i s o r d e r ; n o P T S D : 2

M D

, 2 D Y S , 4 S P

, 1

b i n g e - e a t i n g d i s o r d e r

D


M e d i c a t i o n u s e h a d n o e f f e c t o n

r e s u l t s

.

( t a b l e c o n t i n u e s )



14/34

T a b l e 2 ( c o n t i n u e d )

C a t e g o r y



S u b j e c t s



K e y r e s u l t

J o v a n o v i c , N o r r h o l m ,

S a k o m a n , e

t a l . ( 2 0 0 9 )


C A P S

4 5 P T S D

, 3 3 c o n t r o l s

E x c l u s i o n a r y c r i t e r i a

i n c l u d e d S A o r B P

A


S o m e e v i d e n c e f o r i m p a i r e d

h a b i t u a t i o n a c r o s s t r i a l s i n

P T S D

.


2 0 0 0 )


E M G

a c t i v i t y

a s s e s s e d 1 w e e k , 1

m o n t h , a n d 4 m o n t h s

p o s t t r a u m a

C A P S a n d S C I D - R

2 1 P T S D a l o n e , 1 5 P T S D

a n d M D

, 1 6 M D a l o n e ,

1 6 6 n e i t h e r P T S D n o r M D

N o n e n o t e d

e x c e p t f o r

M D

A

N o d i f f e r e n c e a m o n g g r o u p s a t 1

w e e k p o s t t r a u m a . A t 1 - a n d

4 - m o n t h p o s t t r a u m a , P T S D t o o k

l o n g e r t o h a b i t u a t e t o s t a r t l e .

N o d i f f e r e n c e a m o n g g r o u p s

b e c a u s e o f M D

.

G r i f f i n ( 2 0 0 8 )


E M G

a c t i v i t y

a s s e s s e d 1 m o n t h

a n d 6 m o n t h s

p o s t t r a u m a

C A P S a n d S C I D

4 0 r a p e o r t r a u m a s u r v i v o r s ;

P T S D c l a s s i f i c a t i o n b a s e d

o n d i a g n o s i s a t 6 - m o n t h

f o l l o w - u p

A t 1 - m o n t h

p o s t t r a u m a :

2 6 w o m e n w i t h P T S D

s y m p t o m

d i a g n o s i s , 1 2

P T S D s y m p t o m a n d

M D

, 1 M D o n l y ; a t

6 - m o n t h p o s t t r a u m a :

1 6 w o m e n w i t h P T S D

,

5 P T S D a n d M D

, 4

M D o n l y

B

N o d i f f e r e n c e s i n s t a r t l e a t 1 -

m o n t h p o s t t r a u m a a s s e s s m e n t .

P T S D g r o u p h a d l a r g e r s t a r t l e

a t 6 - m o n t h f o l l o w - u p t h a n n o n -

P T S D

. T h i s w a s d u e t o i n c r e a s e

i n s t a r t l e f o r P T S D g r o u p .

O r n i t z a n d P y n o o s ( 1 9 8 9 )


D S M - I I

I

6 P T S D

, 6 c o n t r o l s

N o n e n o t e d

B

G e n e r a l s t a r t l e i n P T S D l e s s t h a n

c o n t r o l s

.

M e d i n a e t a l . (

2 0 0 1 )


L A S C

4 6 w o m e n e x p o s e d t o h i g h

l e v e l s o f c h i l d h o o d

c o r p o r a l p u n i s h m e n t a n d

h i g h l e v e l s o f p a r t n e r

a g g r e s s i o n

N o n e n o t e d

A

P T S D s y m p t o m s c o r e n e g a t i v e l y

c o r r e l a t e d w

i t h g e n e r a l s t a r t l e .

S t u d i e s i n v e s t i g a t i n g c o n t e x t -

p o t e n t i a t e d , f e a r -

p o t e n t i a t e d , a n d / o r

g e n e r a l s t a r t l e

M o r g a n , G r i l l o n ,

S o u t h w i c k , D a v i s

, e t a l .

( 1 9 9 5 )

S t a r t l e p r o b e p r e s e n t e d

a l o n e

a n d d u r i n g

a n t i c i p a t i o n o f

a v e r s i v e s t i m u l i a n d

r e c o v e r y p h a s e s

S C I D - R

9 P T S D

, 1 0 c o n t r o l s

4 P D

, 5 A A

A

G r e a t e r g e n e r a l s t a r t l e i n P T S D

d u r i n g p r o b e a l o n e a n d

a n t i c i p a t i o n

p h a s e s b u t n o t

r e c o v e r y p h a s e . E v i d e n c e

r e g a r d i n g F P S u n c l e a r , a s

s i g n i f i c a n t l y g r e a t e r F P S i n

P T S D d r i v e n b y 1 s u b j e c t .

G r i l l o n e t a l . (

1 9 9 8 a )

S t a r t l e p r o b e d u r i n g

a d a p t a t i o n p h a s e a n d

l i g h t a n d d a r k n e s s

c o n d i t i o n s

S C I D - R

1 9 P T S D

, 1 3 c o m b a t

c o n t r o l s

, 2 0 c i v i l i a n

c o n t r o l s

B P a n d S A

e x c l u s i o n a r y

c r i t e r i a

B

N o d i f f e r e n c e s

a m o n g g r o u p s

d u r i n g a d a p t a t i o n . S t a r t l e d u r i n g

d a r k n e s s a n d l i g h t c o n d i t i o n s

g r e a t e r i n P T S D t h a n c o m b a t a n d

c i v i l i a n c o n t r o l s . N o d i f f e r e n c e s

i n c o n t e x t - p o t e n t i a t e d s t a r t l e

( s t a r t l e d u r i n g d a r k n e s s l

i g h t )

b e t w e e n P T S D a n d c o m b a t

c o n t r o l s . H o w e v e r , P

T S D s h o w e d

g r e a t e r c o n t e x t - p o t e n t i a t e d s t a r t l e

t h a n c i v i l i a n

c o n t r o l s .

( t a b l e c o n t i n u e s )

922 VAIDYANA

Psychological Bulletin, 2009,135(6)- 909-42

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Transcript of Psychological Bulletin, 2009,135(6)- 909-42