Elsevier

Psychiatry Research

Volume 109, Issue 2, 15 March 2002, Pages 171-179
Psychiatry Research

Event-related potential dysfunction in posttraumatic stress disorder: the role of numbing

https://doi.org/10.1016/S0165-1781(02)00003-3Get rights and content

Abstract

The purpose of this study was to examine the relationship between disturbance in event-related potentials (ERPs) and symptom clusters in posttraumatic stress disorder (PTSD). ERPs were recorded in 17 unmedicated civilian PTSD patients and 17 age- and sex-matched controls during a conventional auditory oddball task. PTSD symptom clusters (re-experiencing, active avoidance, numbing, hyperarousal) were correlated with ERP measures. The PTSD group showed ERP disturbances to target stimuli (reduced P200 and P300 and increased N200 amplitude, increased N200 and P300 latency) and reduced P200 amplitude to common stimuli compared to the control group. A significant negative correlation was found between the intensity of numbing symptoms and parietal P300 amplitude. This study replicates findings of disturbed N200 and P300 components in PTSD, reflecting impairments in stimulus discrimination and attention. The finding that numbing was associated with reduced attention processing (P300) is consistent with models positing a relationship between disordered arousal and attention in PTSD.

Introduction

Attentional disturbances are commonly reported in posttraumatic stress disorder (PTSD; Buckley et al., 2000). Event related potentials (ERPs) may reflect these attentional disturbances. P300 amplitude is an ERP component that is inversely related to stimulus probability, perceptual certainty, and meaning or significance (Pritchard, 1981, Johnson, 1986). P300 amplitude is generally accepted to reflect the allocation of attentional resources (Pritchard, 1981, Polich and Kok, 1995) and the updating of working memory (Donchin and Coles, 1988). In PTSD, P300 amplitude is increased to trauma-relevant (Attias et al., 1996, Stanford et al., 2001) or novel stimuli (Kimble et al., 2000) and reduced to neutral auditory stimuli (McFarlane et al., 1993, Charles et al., 1995, Boudarene and Timsit-Berthier, 1997, Metzger et al., 1997). Increased P3 amplitude in PTSD is thought to reflect an attentional bias towards threat stimuli (Buckley et al., 2000, Stanford et al., 2001) and reduced P3 amplitude to reflect a consequent reduction in attentional resources directed to non-threatening stimuli (Litz and Keane, 1989, Metzger et al., 1997).

Disturbances in pre-attentive processes have been observed in PTSD. For example, PTSD patients reveal reduced sensory gating (Neylan et al., 1999) and increased mismatch negativity (Morgan and Grillon, 1999) to neutral auditory stimuli. These findings are thought to reflect a heightened central nervous system reactivity to stimulus detection and change. A neuropsychological model suggests such hyperactivity to all stimuli may lead to difficulties discriminating relevant from irrelevant stimuli (Kolb, 1987). N200 is an ERP component reflecting multiple neural processes associated with stimulus discrimination and classification (Näätänen, 1990). N200 amplitude is influenced by attention and task difficulty (Näätänen, 1992), and N200 latency is thought to reflect stimulus discrimination time (Ritter et al., 1979, Näätänen and Picton, 1986).

Many ERP oddball studies in PTSD have restricted their analyses to P300, thus potentially ignoring earlier sensory and stimulus discrimination difficulties. Oddball studies that have examined N200 report equivocal findings. An early study reported increased N200 latency and reduced P300 amplitude to targets and distractor tones in an unmedicated, non-combat PTSD group (McFarlane et al., 1993). This finding was interpreted to reflect difficulties with discriminating relevant from irrelevant stimuli, and it was speculated that these difficulties might relate to autonomic hyperreactivity. In contrast, a second three-tone oddball study in Vietnam veterans failed to report N200 differences. It needs to be noted, however, that ERPs may be affected by time since trauma, medication, and type of trauma (Metzger et al., 1997). Whereas the first study (McFarlane et al., 1993) examined N200 in an unmedicated, non-combat sample an average of 2 years after trauma and compared them to a non-traumatized control group, the second study examined Vietnam veterans approximately 20 years post-trauma and compared them to a traumatized control group. To examine the validity of these findings, potential disturbances in N200 need to be investigated in an unmedicated and relatively acute PTSD group.

Biological models predict chronic hyperarousal in PTSD may underlie this central nervous system hyperreactivity and deficient stimulus discrimination (Kolb, 1987). Central to the notion of disordered arousal in PTSD is the proposition that numbing symptoms (reduced interest, social withdrawal, emotional numbing) may reflect compensatory mechanisms associated with hyperarousal (Foa et al., 1995). Consistent with this proposal are factor-analytic findings that re-experiencing symptoms are clustered with active avoidance, and hyperarousal symptoms are associated with numbing (Foa et al., 1995, Buckley et al., 1998, Taylor et al., 1998). The only study that has examined the relationship between ERPs and PTSD symptom clusters reported positive associations between hyperarousal and avoidance symptom clusters and P300 amplitude to emotional word stimuli, but no associations with words and re-experiencing symptoms (Blomhoff et al., 1998).

The aim of the present study was to index the extent of impaired stimulus discrimination in an unmedicated, non-combat PTSD group and to correlate disturbances in information processing with specific PTSD symptoms. According to Kolb's model (1987), we predicted an impaired stimulus discrimination in PTSD, indexed by increased N200 latency and reduced P300 amplitude, and significant correlations between hyperarousal and numbing and ERP disturbances.

Section snippets

Patients

Seventeen PTSD patients (6 male, 11 female) who were victims of non-sexual assault (n=11) or motor vehicle accidents (n=6) were recruited through the PTSD Unit at Westmead Hospital and 17 age- and sex-matched controls were recruited from the community. All participants were free from psychoactive medications for at least 4 weeks. Exclusion criteria included neurological, panic, psychotic or major depressive disorder, head injury, or substance abuse. The average time since trauma was 10 months

Patient characteristics

Groups did not differ in age (PTSD=38.4 years, S.D.=9.2; controls=37.9 years, S.D.=9.8), education (PTSD=12.7 years, S.D.=3.3; controls=12.6 years, S.D.=1.6), or alcohol use (PTSD=2.7, S.D.=2.7; controls=1.6, S.D.=1.5). As expected, the PTSD group had higher levels of state anxiety [PTSD=52.5, S.D.=10.2; controls=31, S.D.=6.8: F(1, 32)=52, P<0.001] and trait anxiety [PTSD=58.1, S.D.=9.3; controls=33.9, S.D.=5: F(1,32)=883.7, P<0.001].

Behavioral measures

PTSD patients had significantly slower reaction times to

Discussion

The PTSD group showed decreased P200 and P300 amplitude, increased N200 amplitude and an increase in RT, N200 and P300 latency. These findings confirm previous reports of reduced P300 amplitude (McFarlane et al., 1993, Charles et al., 1995, Boudarene and Timsit-Berthier, 1997, Metzger et al., 1997), increased RTs (McFarlane et al., 1993, Attias et al., 1996, Boudarene and Timsit-Berthier, 1997), and increased P300 latency in PTSD (Boudarene and Timsit-Berthier, 1997). The increased N200 latency

Acknowledgements

This research was funded by the National Health and Medical Research Council and an Australian Postgraduate Award.

References (34)

  • L.J Metzger et al.

    Auditory event-related potentials to tone stimuli in combat-related Posttraumatic Stress Disorder

    Biological Psychiatry

    (1997)
  • C.A Morgan et al.

    Abnormal mismatch negativity in women with sexual assault-related Posttraumatic Stress Disorder

    Biological Psychiatry

    (1999)
  • T.C Neylan et al.

    Sensory gating in posttraumatic stress disorder: reduced auditory P50 suppression in combat veterans

    Biological Psychiatry

    (1999)
  • J Polich et al.

    Cognitive and biological determinants of P300: an integrated review

    Biological Psychology

    (1995)
  • M.S Stanford et al.

    Impact of threat relevance on P3 event-related potentials in combat-related post-traumatic stress disorder

    Psychiatry Research

    (2001)
  • Babor T.F., De la Fuente J.R., Saunders J., Grant M., 1989. The Alcohol Use Disorders Test: Guidelines of Use in...
  • M Boudarene et al.

    Interest of event-related potentials in assessment of posttraumatic stress disorder

    Annals of the New York Academy of Sciences

    (1997)
  • Cited by (0)

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