Cultic Studies Review, Vol. 5, No. 6, 2006, Page 8
amygdala and the prefrontal cortex (PFC). The PFC is part of the neo-cortex, which evolved
later in time the PFC functions to organize, plan, reason, and judge information coming in.
The information and its significance then goes on to the amygdala. In contrast to the more
direct thalamus-amygdala route ―this pathway permits a more detailed and accurate
representation of the stimulus.‖ (Applegate &Shapiro, p. 186.) However, because of its
evolutionary heritage, the more primitive pathway is much quicker. (According to van der
Kolk, there is only one synapse between the thalamus and amygdala ―low road,‖ while there
are seven synapses from the thalamus to the PFC, the ―high road‖ [2000]). The amygdala
scans the data to see whether it resembles other fearful events and, if so, sends signals to
the adrenal glands to get those fight-or-flight hormones pumping. The body goes into a
hyperaroused state characteristic of PTSD before the PFC has a chance to determine the
actual significance of the cue—i.e., is this really a dangerous situation? Thus, the woman
discussed above reacts unconsciously and automatically first, before the PFC can kick in and
reality-test the situation—i.e., is this her husband whom she loves, or is this the early
perpetrator making sexual advances that disgust her?
Research on PTSD confirms that hippocampal volume is lower in people who develop PTSD
following a trauma compared to those similarly exposed who do not develop the disorder
(van der Kolk, 2003). Therefore, the files of those who develop PTSD are less likely to be in
chronological order because of the lower number of hippocampal neurons. However, the
causal direction has not been definitively established to date in other words, does chronic
stress burn out hippocampal neurons, in turn resulting in PTSD (see, for example, Bremner
&Narayan, 1998), or do people who develop PTSD have smaller hippocampal volume to
begin with? Tempting though it may be to presume the former, recent research seems to
point in the other direction—i.e., that people with smaller hippocampi prior to the trauma
are more likely than others to develop PTSD when traumatically exposed (Lyons, 2006).
However, this finding, that people with reduced hippocampal volume are more at risk for
PTSD, does not resolve the nature/nurture controversy because it does not necessarily
mean they are born with a smaller hippocampus. Prior trauma, such as a childhood history
of abuse, might explain the hippocampal reduction. In fact, Bremner and colleagues (1998)
tested this hypothesis and found that the left hippocampus in survivors of childhood physical
and sexual abuse was 12 percent smaller than that in controls. On the other hand, other
studies (e.g., DeBellis et al., 1999 and Carrion et. al, 2001) failed to confirm these findings.
Research on humans is appropriately hampered in resolving these issues since we can‘t
induce trauma intentionally and then see what happens.
The False Memory Controversy
Impairment of the hippocampus during trauma also lends support to the controversial
phenomenon of delayed recall (a.k.a. ―recovered‖ or ―false‖ memory). In psychotherapy, as
patients begin to talk about their earlier trauma, hippocampal activation occurs and memory
fragments are consolidated into an integrative whole. Implicit memory circuits link up with
explicit memory circuits to form a coherent neural network. In this way, a previously
―forgotten‖ memory, or one that had lain in shadow, may come to consciousness or be
further clarified.
Conversely, we also know that children can be suggestible and many variables influence
accurate recall (age, interval between occurrence and recall, stress arousal levels, etc.—
Doris, 1991). For example, Goldberg (1997) has shown how ―false memories‖ can be
implanted by therapists with an agenda, and how unconscious processes can influence
autobiographical (explicit) memory. Additionally, Herman (1992) has pointed out how
people with certain diagnostic traits (e.g., Borderline Personality Disorder) may lay claim to
recovered memories as they attempt to organize and make sense of their symptoms.
Nevertheless, because dissociated memories are sometimes implicit memories, a
amygdala and the prefrontal cortex (PFC). The PFC is part of the neo-cortex, which evolved
later in time the PFC functions to organize, plan, reason, and judge information coming in.
The information and its significance then goes on to the amygdala. In contrast to the more
direct thalamus-amygdala route ―this pathway permits a more detailed and accurate
representation of the stimulus.‖ (Applegate &Shapiro, p. 186.) However, because of its
evolutionary heritage, the more primitive pathway is much quicker. (According to van der
Kolk, there is only one synapse between the thalamus and amygdala ―low road,‖ while there
are seven synapses from the thalamus to the PFC, the ―high road‖ [2000]). The amygdala
scans the data to see whether it resembles other fearful events and, if so, sends signals to
the adrenal glands to get those fight-or-flight hormones pumping. The body goes into a
hyperaroused state characteristic of PTSD before the PFC has a chance to determine the
actual significance of the cue—i.e., is this really a dangerous situation? Thus, the woman
discussed above reacts unconsciously and automatically first, before the PFC can kick in and
reality-test the situation—i.e., is this her husband whom she loves, or is this the early
perpetrator making sexual advances that disgust her?
Research on PTSD confirms that hippocampal volume is lower in people who develop PTSD
following a trauma compared to those similarly exposed who do not develop the disorder
(van der Kolk, 2003). Therefore, the files of those who develop PTSD are less likely to be in
chronological order because of the lower number of hippocampal neurons. However, the
causal direction has not been definitively established to date in other words, does chronic
stress burn out hippocampal neurons, in turn resulting in PTSD (see, for example, Bremner
&Narayan, 1998), or do people who develop PTSD have smaller hippocampal volume to
begin with? Tempting though it may be to presume the former, recent research seems to
point in the other direction—i.e., that people with smaller hippocampi prior to the trauma
are more likely than others to develop PTSD when traumatically exposed (Lyons, 2006).
However, this finding, that people with reduced hippocampal volume are more at risk for
PTSD, does not resolve the nature/nurture controversy because it does not necessarily
mean they are born with a smaller hippocampus. Prior trauma, such as a childhood history
of abuse, might explain the hippocampal reduction. In fact, Bremner and colleagues (1998)
tested this hypothesis and found that the left hippocampus in survivors of childhood physical
and sexual abuse was 12 percent smaller than that in controls. On the other hand, other
studies (e.g., DeBellis et al., 1999 and Carrion et. al, 2001) failed to confirm these findings.
Research on humans is appropriately hampered in resolving these issues since we can‘t
induce trauma intentionally and then see what happens.
The False Memory Controversy
Impairment of the hippocampus during trauma also lends support to the controversial
phenomenon of delayed recall (a.k.a. ―recovered‖ or ―false‖ memory). In psychotherapy, as
patients begin to talk about their earlier trauma, hippocampal activation occurs and memory
fragments are consolidated into an integrative whole. Implicit memory circuits link up with
explicit memory circuits to form a coherent neural network. In this way, a previously
―forgotten‖ memory, or one that had lain in shadow, may come to consciousness or be
further clarified.
Conversely, we also know that children can be suggestible and many variables influence
accurate recall (age, interval between occurrence and recall, stress arousal levels, etc.—
Doris, 1991). For example, Goldberg (1997) has shown how ―false memories‖ can be
implanted by therapists with an agenda, and how unconscious processes can influence
autobiographical (explicit) memory. Additionally, Herman (1992) has pointed out how
people with certain diagnostic traits (e.g., Borderline Personality Disorder) may lay claim to
recovered memories as they attempt to organize and make sense of their symptoms.
Nevertheless, because dissociated memories are sometimes implicit memories, a
