The Neurobiology of Trauma1
David Lisak, Ph.D.
University of Massachusetts Boston
(unpublished article, 2002)
The human brain is the product of millions of years of evolution. Much of its anatomy
and physiology is the legacy of our common ancestry with the other animals, and even
with the earlier life forms from which mammals evolved. One very significant legacy of
this evolutionary heritage is a highly developed capacity to experience fear.
Although 21st century humans look very much like the planet’s number one predator, the
vast majority of our time on earth has been spent as a prey species: mid-sized meals for
true predators, such as lions, leopards and saber-tooth tigers. Our survival depended on
our capacity to react instantaneously to the threat of attack from these formidable
animals. When a leopard makes its lunge, life or death may be decided in a millisecond.
Successful adaptation demanded the evolution of a system of hormones and
neurochemicals capable of instantaneously altering the body’s functioning, preparing it
for life-saving flight or savage fight, and for the capacity to freeze completely until either
flight or fight was chosen. This cascade of chemicals is the biological equivalent of
setting off an atomic bomb inside the body. Within a fraction of a second, heart rate,
blood pressure, breathing rate, blood distribution and pupil dilation are all fundamentally
altered.
This “fight or flight” response is triggered without any conscious intervention.
Conscious thought, although subjectively fast, actually is far too slow to beat the leopard.
Evolution demanded a system that by-passes the cortex – the brain’s center of higher and
integrative functioning. It demanded a system that is wired directly into the amygdala,
the brain’s “fear center.” So, when we see a threatening stimulus, like a gun for example,
our amygdala has received the information and triggered the fight or flight response long
before we say to ourselves, “there’s a gun!”
Not only can we react without the intervention of our cortex, we can also store a great
deal of information without it. In fact, once again, it has been crucial to our survival that
we be capable of encoding in memory particular stimuli, the recognition of which might
determine life or death, and to do so without cortical involvement. Imagine a zebra
bending down to drink at a water hole, every sense keenly alert for danger. Suddenly,
from out of the grass nearby, a blur of brown hide lunges out. The zebra instantly spins,
lunges and gallops away, alive for another hour. But thirst demands that it return to the
water hole. When it does, the particular stimuli that preceded the attack will now have
been etched into memory – not at the cortical level — but rather at far simpler, subcortical
levels. At the zebra’s second visit to the water hole, should a gust of wind
happen to sway the grass and cause a similar sound to that of the lion’s lunge, the poor
animal will flee with the same experience of terror as before. If zebras think, it may say
to itself, “that was just the wind,” but it will be 50 yards away when it does so.
Being creatures with complex brains, humans actually have multiple pathways to the
experience of fear. The amygdala route, the “low road” to fear, is the fastest. However,
we may also perceive something in the environment that is not instantly recognizable as a
threat. In such a case we rely on the “high road” to fear, the route that takes the
information into the cortical regions of the brain. There, more thorough analysis of the
stimulus is possible, and we can make a more deliberative determination of the nature of
the threat.
The human capacity to experience fear, so crucial to our species’ survival, is also the
cornerstone of our capacity to become traumatized. A human being who has not been
traumatized is capable of using both the “low” and “high” roads to fear. A moving car
that suddenly appears in the corner of one’s eye will activate the low road and allow us to
jump back onto the curb before being struck. The sight of a lion at the zoo will activate
the high road, allowing us to recognize that although its canines would surely rip us to
shreds, we are safely beyond its reach. The sound of a loud bang may well activate both
low and high roads, giving us a sudden start until we identify the sound as the backfire of
a car engine. A human being who has been traumatized, however, will have far less
flexibility in the activation of their fear system. For the traumatized human, the low road
to fear predominates.
Human beings who have been raped will, just like the zebra, carry with them a network
of neurons forever prepared to respond to the perception of any of the cues that were
present during the rape. It might be the sound of a man’s voice; the feel of hands on a
particular part of the body; or the look of anger in another’s eyes. The possibilities are
literally infinite. At the sound, touch or sight of those cues, the rape victim will
experience the same cascade of neurochemicals that were triggered during the actual
rape. Their heart will begin racing, their blood pressure will spike, their breathing will
accelerate. They may find themselves fleeing in terror from a supermarket because
someone unexpectedly touched them on the arm. They may find themselves frozen in
terror because a man said something hostile to them in a parking lot. Their reactions are
not conscious choices, not “hysterical” over-reactions, any more than is the zebra’s flight
from the sound of windblown grass. Both are reactions governed not by the cortex, not
by conscious thought, but rather by the “low road” of amygdala-based fear networks.
Traumatic Memory
The memory of a traumatic experience is not encoded in the same way as is a normal
experience. The powerful neurochemicals that trigger the fight or flight response have
far-reaching effects, including dramatic effects on the manner in which memories are
encoded. Often, a traumatized person cannot generate the kind of narrative memory that
we can normally muster for an important experience. Their memories are often
fragmented, out of sequence, and filled with gaps. They may recall very specific details
for particular aspects of the experience, and recall little or nothing for others. It is for this
reason – the neurobiology of traumatic memory – that great care must be taken in
interviewing trauma survivors. The fact that a traumatized person recalls a detail which
they earlier had not is not prima facie evidence of fabrication; it is the characteristic way
in which these types of memories are stored and recalled. The fact that they can recall
the texture of the rapist’s shirt, but cannot recall whether he was wearing a hat, is not
evidence that something is being hidden; it is a product of how the brain encodes
information during a trauma.
Once again, these characteristics of traumatic memory are not the consequence of
conscious choice or resistance. Rather, they are the consequence of the radically altered
neurochemical environment in which the memories were encoded.
To summarize, the rape victim, like any traumatized human, is left with a permanently
altered brain. As part of its legacy, trauma leaves its victims with fear networks etched
into the amygdala, networks that can be triggered by a multitude of cues that would
ordinarily not evoke fear. Trauma also leaves its victims with fragmented and
discontinuous memories of what happened to them. As a consequence of these legacies,
the rape victim faces enormous challenges in the judicial process. To participate in that
process – to endlessly recount their trauma, to appear in the court room where the rapist
sits – is equivalent to the zebra consciously choosing to return to the water hole where the
lion attacked. In both cases, a confrontation with the biological legacy of trauma is
inevitable. The zebra only does so out of absolute necessity; the rape victim’s choice
must be more conscious, and more deliberate.
1 For further information about the neurobiology of fear, see Joseph Ledoux, The
Emotional Brain, 1996, New York, Simon & Shuster. For detailed information about the
neurobiology of trauma, see Rachel Yehuda and Alexander C. McFarlane, Psychobiology
of Posttraumatic Stress Disorder, 1997, New York, Annals of the New York Academy of
Sciences, Volume 821.
