Pharmacology for Post-Traumatic Stress Disorder Related to Childhood Sexual Abuse: A Literature Review

Kreidler, Maryhelen C., Briscoe, Leslie A., Beech, Rhonda R., Perspectives in Psychiatric Care

TOPIC. Post-traumatic stress disorder (PTSD) related to pharmacotherapy responses in general and specifically to noncombat symptomatology related to childhood sexual abuse.

PURPOSE. To explore findings related to pharmacological advances in the treatment of PTSD and relate the findings to the treatment of childhood sexual abuse.

SOURCES. Published literature.

CONCLUSIONS. The literature on pharmacotherapy for PTSD in general and childhood trauma and PTSD in particular is small and inconsistent, but we need to be aware of any and all advances.

Search terms: Neurobiology, pharmacotherapy, sexual abuse, PTSD, trauma

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During both world wars, the Korean War, and the Vietnam War, there was recognition of the similarities of the impact of trauma on soldiers (Braun, 1993; Solomon, 1993). In 1984, criteria describing the posttraumatic stress disorder (PTSD) syndrome were published in the Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. (DMS-III) (American Psychiatric Association [APA], 1984), providing an organized schema to demonstrate the relationship between trauma and PTSD.

In recent years, the literature has identified the post-trauma response of victims to life events other than war. Trauma can be an acute, one-time event, such as a natural disaster; a man-made disaster involving fire, nuclear power, or toxic chemicals; airline crashes; or traumas such as rape, physical assault, and terrorist attacks (Kleinman, 1989). Traumatic events also can be chronic, such in the Holocaust (van der Kolk & Fisher, 1995), childhood neglect and abuse (Chu, 1997), combat, or being a prisoner of war (Bremner & Brett, 1997). For the purpose of this article, childhood sexual abuse (CSA) is defined as intrafamilial or extrafamililial sexual imposition involving a child under 18 years of age. Sexual imposition includes behaviors that range from exhibitionism, voyeurism, or seductive speech to fondling, sodomy, oral-genital contact, and intercourse.

The DSM-IV-TR (APA, 2000) identified three symptom clusters for the client with PTSD. The first is reexperiencing symptoms such as intrusive memories, nightmares, and dissociative flashbacks. The second cluster is hyperarousal/hyperactivity symptoms such as tension, irritability, anxiety, vigilance, poor sleep, and impaired concentration. Avoidant symptoms that make up the third cluster include emotional numbing, social isolation, and lack of life progress.

The prevalence of PTSD varies according to source and definition. The DSM-IV-TR (APA, 2000) reports it affecting 8% of the adult population in the United States. Among individuals with one or more traumatic events, a prevalence of 23.6% to 25% showed evidence of PTSD (Breslau, Davis, Andreskin, & Peterson, 1991; Green, 1994). A study of 4,000 adult female civilians revealed that 69% had exposure to traumatic events (Resnick, Kilpatrick, Dansky, Saunders, & Best, 1993). The National Co-Morbidity Survey (Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995) reported rates of exposure to one or more traumatic events to be 51.2% in females and 60.6% in males. Women, although seemingly less exposed to trauma than men, consistently suffer more PTSD symptoms as a result of exposure to trauma. This may be related to the types of trauma women are more likely to experience such as rape, sexual abuse, and battering. Herman (1992) suggested an expanded version of the disorder called complex PTSD for victims of prolonged or early childhood trauma, since they exhibit considerable affect dysregulation. Wolfsdorf and Zlotnick (2001) define affect dysregulation as the inability to adaptively manage or tolerate intense emotion, van der Kolk et al. (1996) investigated the complexity of adaptation to trauma and found 77% of participants with early childhood trauma suffer affect dysregulation compared with 37% of disaster survivors.

Rarely does PTSD occur in isolation. Co-morbidity with depression, substance abuse, eating disorders, generalized anxiety, bipolar disorder, and countless other Axis I and Axis II diagnoses is the rule, rather than the exception. Researchers' attempts to provide pure samples to control for extraneous factors may well exclude generalization to the actual population of PTSD sufferers. The intent of this article is to examine the literature and to identify those studies that have dealt with PTSD and pharmacotherapy in general and with non-combat-related PTSD symptoms specifically (primarily from childhood sexual abuse), and specific responses to psychopharmacology.

Literature Review

Neurobiology of Post-Traumatic Stress Disorder

Several systems have been identified in the neurobiology of PTSD. These include neurotransmitter abnormalities, neuroendocrine alterations, and changes in functional neuroanatomy. A general finding in PTSD is that different systems are sensitized and that there is an increased release of noradrenaline and increased autonomic activity. In response to excessive adrenergic function, there may be postsynaptic down-regulation of adrenergic receptors with close interconnections between the raphe nucleus (RN) and the locus coeruleus (LC). The dopamine system also may be sensitized (Charney, Deutch, Krystal, Southwick, & David, 1993).

The two brain structures that appear to be particularly involved in PTSD are the amygdala and the hippocampus. The amygdala receives input from the thalamus and cortex and sends messages to the brainstem, hypothalamus, and striatum. Serotonin may act indirectly on amygdala pathways or at the level of the amygadala itself. The central nucleus of the amygdala integrates fear responses, projecting to the hypothalamic-pituitary axis (HPA) (Kent, Coplan, & Gorman, 1998). The amygdala circuits respond to repeated trauma in a way that prevents the extinction of the fear response. Thus emotions at a later time may inhibit the proper evaluation of an experience and cause an inappropriate response. Studies have suggested that repeated subthreshold electrical stimulation within the brain, known as kindling, can be applied to PTSD (Hageman, Andersen, & Jorgensen, 2001; van der Kolk, 2001). It is hypothesized that repeated traumatization or a trauma followed by intrusive reexperiences might kindle limbic nuclei, leading to behavioral changes seen in this disorder.

The hippocampus receives input and responds to both the amygdala and the cortex. It may be involved in mediating memories of traumatic events and learned responses to cues. Studies have demonstrated the death of hippocampal neurons and shrinkage of the hippocampus after exposure of animals to chronic stress (O'Brien, 1997). There also have been human studies that demonstrate amygdala and hippocampal involvement in PTSD (Rauch et al., 1996; Schuff et al., 2001; Stein, Koverola, Hanna, Torchia, & McClarty, 1998). Several studies using magnetic resonance imaging also have suggested that reduced hippocampal volume is evident in abused subjects (Bremner et al., 1997; Nishizawa, Benkelfat, & Young, 1997; Stein et al., 1998).

Increased levels of corticotropin-releasing factor occur with repeated trauma or intrusive reexperiencing of events. Although increased release of cortisol might be expected in PTSD patients, studies demonstrate decreased cortisol blood levels (Yehuda & …

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Publication information: Article title: Pharmacology for Post-Traumatic Stress Disorder Related to Childhood Sexual Abuse: A Literature Review. Contributors: Kreidler, Maryhelen C. - Author, Briscoe, Leslie A. - Author, Beech, Rhonda R. - Author. Journal title: Perspectives in Psychiatric Care. Volume: 38. Issue: 4 Publication date: October-December 2002. Page number: 135+. © Nursecom, Inc. Jan 2009. COPYRIGHT 2002 Gale Group.

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