SCARS
THAT WON'T HEAL: THE NEUROBIOLOGY OF CHILD ABUSE
Maltreatment
at an early age can have enduring negative effects on a child's
brain development and function
Teicher,
M. H. (2002). Scars that Won’t Heal: The
Neurobiology of Child Abuse.
© Scientific American, 286(3), 68-75.
In
1994 Boston police were shocked to discover a malnourished four-year-old
locked away in a filthy Roxbury apartment, where he lived in dreadfully
squalid conditions. Worse, the boy's tiny hands were found to
have been horrendously burned. It emerged that his drug-abusing
mother had held the child's hands under a steaming-hot faucet
to punish him for eating her boyfriend's food, despite her instructions
not to do so. The ailing youngster had been given nomedical care
at all. The disturbing story quickly made national headlines.
Later placed in foster care, the boy received skin grafts to help
his scarred hands regain their function. But even though the victim's
physical wounds were treated, recent research findings indicate
that any injuries inflicted to his developing mind may never truly
heal.
Though an extreme example, the notorious case is
unfortunately not all that uncommon. Every year child welfare
agencies in the U.S. receive more than three million allegations
of childhood abuse and neglect andcollect sufficient evidence
to substantiate more than a million instances.
It
is hardly surprising to us that research reveals a strong link
between physical, sexual and emotional mistreatment of children
and the development of psychiatric problems. But in the early
1990s mental health professionals believed that emotional and
social difficulties occurred mainly through psychological means.
Childhood maltreatment was understood either to foster the development
of intrapsychic defense mechanisms that proved to be self-defeating
in adulthood or to arrest psychosocial development, leaving a
"wounded child" within. Researchers thought of the damage
as basically a software problem amenable to reprogramming via
therapy or simply erasable through the exhortation "Get over
it."
New
investigations into the consequences of early maltreatment, including
work my colleagues and I have done at McLean Hospital in Belmont,
Mass., and at Harvard Medical School, appear to tell a different
story. Because childhood abuse occurs during the critical formative
time when the brain is being physically sculpted by experience,
the impact of severe stress can leave an indelible imprint on
its structure and function. Such abuse, it seems, induces a cascade
of molecular and neurobiological effects that irreversibly alter
neural development.
Extreme Personalities
The aftermath of childhood abuse can manifest itself
at any age in a variety of ways. Internally it can appear as depression,
anxiety, suicidal thoughts or posttraumatic stress; it can also
be expressed outwardly as aggression, impulsiveness, delinquency,
hyperactivity or substance abuse. One of the more perplexing psychiatric
conditions that is strongly associated with early ill-treatment
is borderline personality disorder. Someone with this dysfunction
characteristically sees others in black-and-white terms, often
first putting a person on a pedestal, then vilifying the same
person after some perceived slight or betrayal. Those afflicted
are also prone to volcanic outbursts ofanger and transient episodes
of paranoia or psychosis. They typically have a history of intense,
unstable relationships, feel empty or unsure of their identity,
commonly try to escape through substance abuse, and experience
self-destructive or suicidal impulses.
While
treating three patients with borderline personality disorder in
1984, I began to suspect that their early exposure to various
forms of maltreatment had altered the development of their limbic
systems. The limbic system is a collection of interconnected brain
nuclei (neural centers) that play a pivotal role in the regulation
of emotion and memory. Two critically important limbic regions
are the hippocampus and the amygdala, which lie below the cortex
in the temporal lobe [see illustration on opposite page]. The
hippocampus is thought to be important in the formation and retrieval
of both verbal and emotional memories, whereas the amygdala is
concerned with creating the emotional content of memory--for example,
feelings relating to fear conditioning and aggressive responses.
My
McLean colleagues Yutaka Ito and Carol A. Glod and I wondered
whether childhood abuse might disrupt the healthy maturation of
these brain regions. Could early maltreatment stimulate the amygdala
into a state of heightened electrical irritability or damage the
developing hippocampus through excessive exposure to stress hormones?
We reasoned further that hippocampal harm or amygdaloid overexcitation
could produce symptoms similar to those experienced by patients
with temporal lobe epilepsy (TLE), which sporadically disrupts
the function of these brain nuclei. During TLE seizures, patients
remain conscious while experiencing a range of psychomotor symptoms
brought on by electrical storms within these regions. Associated
effects include the abrupt onset of tingling, numbness or vertigo;
motor-related
manifestations such as uncontrollable staring or twitching; and
autonomic symptoms such as flushing, nausea or the "pit in
your stomach'' feeling one gets in a fast-rising elevator. TLE
can also cause hallucinations or illusions in any of the five
senses. It is not unusual, for instance, for one afflicted with
this condition to experience Alice-in-Wonderland-like distortions
of the sizes or shapes of objects. Disconnected feelings of déjà
vu and mind-body dissociation are also common.
Abuse-Driven Brain Changes
To explore the relation between early abuse and dysfunction
of the limbic system, in 1984 I devised a checklist of questions
that assess the frequency with which patients experience TLE-related
symptoms. In 1993 my co-workers and I reported results from 253
adults who came to an outpatient mental health clinic for psychiatric
evaluation. Slightly more than half reported having been abused
physically or sexually, or both, as children. Compared with patients
who reported no ill-treatment, average checklist scores were 38
percent greater in the patients with physical (but not sexual)
abuse and 49 percent higher in the patients with sexual (but not
other physical) mistreatment. Patients who acknowledged both physical
and sexual abuse had average scores 113 percent higher than patients
reporting none. Maltreatment before age 18 had more impact than
later abuse, and males and females were similarly affected.
In
1994 our McLean research team sought to ascertain whether childhood
physical, sexual or psychological abuse was associated with brain-wave
abnormalities in electroencephalograms (EEGs), which provide a
more direct measure of limbic irritability than our checklist.
We reviewed the records of 115 consecutive admissions to a child
and adolescent psychiatric hospital to search for a link. We found
clinically significant brain-wave abnormalities in 54 percent
of patients with a history of early trauma but in only 27 percent
of nonabused patients. We observed EEG anomalies in 72 percent
of those who had documented histories of serious physical and
sexual abuse. The irregularities arose in frontal and temporal
brain regions and, to our surprise, specifically involved the
left hemisphere rather than both sides, as one would expect.
Our
findings dovetailed with a 1978 EEG study of adults who were victims
of incest. The study's author, Robert W. Davies of the Yale University
School of Medicine, and his team had found that 77 percent exhibited
EEG abnormalities and 27 percent experienced seizures.
Subsequent
work by other investigators using magnetic resonance imaging (MRI)
technology has confirmed an association between early maltreatment
and reductions in the size of the adult hippocampus. The amygdala
may be smaller as well. In 1997 J. Douglas Bremner, then at the
Yale University School of Medicine, and his colleagues compared
MRI scans of 17 adult survivors of childhood physical or sexual
abuse, all of whom had posttraumatic stress disorder (PTSD), with
17 healthy subjects matched for age, sex, race, handedness, years
of education, and years of alcohol abuse. The left hippocampus
of abused patients with PTSD was, on average, 12 percent smaller
than the hippocampus of the healthy control subjects, but the
right hippocampus was of normal size. Not surprisingly, given
the important role of the hippocampus in memory function, these
patients also scored lower on verbal memory tests than the nonabused
group.
In
1997 Murray B. Stein of the University of California at San Diego
also found left hippocampal abnormalities in 21 adult women who
had been sexually abused as children and who had PTSD or dissociative
identity disorder (also called multiple personality disorder,
a condition thought by some researchers to be common in abused
females). Stein determined that in these women the volume of the
left hippocampus was significantly reduced but that the right
hippocampus was relatively unaffected. In addition, he found a
clear correspondence between the degree of reduction in hippocampus
size and the severity of the patients' dissociative symptoms.
In 2001 Martin Driessen of Gilead Hospital in Bielefeld, Germany,
and his colleagues reported a 16 percent reduction in hippocampus
size and an 8 percent reduction in amygdala size in adult women
with borderline personality disorder and a history of childhood
maltreatment.
On
the other hand, when Michael D. De Bellis and his colleagues at
the University of Pittsburgh School of Medicine carefully measured
MRI images of the hippocampus in 44 maltreated children with PTSD
and 61 healthy control subjects in 1999, they failed to observe
a significant difference in volume.
My
McLean colleagues Susan Andersen and Ann Polcari and I obtained
similar results in our recently completed volumetric analysis
of the hippocampus in 18 young adults (18 to 22 years of age)
with a history of repeated forced sexual abuse accompanied by
fear or terror, who were compared with 19 healthy age-matched
controls. Unlike in previous studies, the control subjects were
not patients but were recruited from the general public and had
fewer mental health problems. We observed no differences in hippocampal
volume. Like Driessen's group, however, we did find a 9.8 percent
average reduction in the size of
the left amygdala, which correlated with feelings of depression
and irritability or hostility. We asked ourselves why the hippocampus
was smaller in abused subjects in studies from Bremner's, Stein's
and Dreissen's groups but normal in De Bellis's and in our own
investigations. Of the several possible answers, the most likely
is that stress exerts a very gradual influence on t he hippocampus,
so adverse effects may not be discernible at a gross anatomical
level until people get older.
Moreover,
animal studies by Bruce S. McEwen of the Rockefeller University
and Robert M. Sapolsky of Stanford University had previously demonstrated
the marked vulnerability of the hippocampus to the ravages of
stress. Not only is the hippocampus particularly susceptible because
it develops slowly, it also is one of the few brain regions that
continues to grow new neurons after birth. Further, it has a higher
density of receptors for the stress hormone cortisol than almost
any other area of the brain. Exposure to stress hormones can significantly
change the shape of the largest neurons in the hippocampus and
can even kill them. Stress also suppresses production of the new
granule cells (small neurons), which normally continue to develop
after birth.
Experiments
with rats by Christian Caldji, Michael J. Meaney of McGill University
and Paul M. Plotsky of Emory University have shown that early
stress reconfigures the molecular organization of these regions.
One major result is the alteration of the protein subunit structure
of GABA receptors in the amygdala [see illustration on next page].
These receptors respond to gamma aminobutyric acid, the brain's
primary inhibitory neurotransmitter, and GABA attenuates the electrical
excitability of neurons. Reduced function of this neurotransmitter
produces excessive electrical activity and can trigger seizures.
This discovery provides an elegant molecular explanation for our
findings of EEG abnormalities and limbic irritability in patients
with childhood abuse.
Left-Side Problems
The effect on the limbic system was only the most expected
consequence of childhood trauma. We were intrigued, however, by
our earlier observation that ill-treatment was associated with
EEG abnormalities in the left hemisphere. This inspired us to
examine the effect of early abuse on the development of the left
and right hemispheres. We chose to use EEG coherence, a sophisticated
quantitative analysis method that provides evidence about the
brain's microstructure--its wiring and circuitry. Conventional
EEG, in contrast, reveals brain function. The EEG coherence technique
accomplishes its task by generating a mathematical measure of
the degree of cross-correlation among the elaborate neuronal interconnections
in the cortex that process and modify the brain's electrical signals.
In general, abnormally high levels of EEG coherence are evidence
of diminished development among these neuron interchanges.
Our
research team used this technique in 1997 to compare 15 healthy
volunteers with 15 child and adolescent psychiatric patients who
had a confirmed history of intense physical or sexual abuse. Coherence
measures showed that the left cortices of the healthy control
subjects were more developed than the right cortices, a result
that is consistent with what is known about dominant hemisphere
anatomy--that is, right-handed people tend to be left-cortex dominant.
The maltreated patients, however, were notably more developed
in the right cortex than the left, even though all were right-handed
and hence
left-dominant. The right hemispheres of abused patients had developed
as much as the right hemispheres of the control subjects, but
their left hemispheres lagged substantially behind. This anomalous
result showed up regardless of the patient's primary diagnosis.
And although the effect extended throughout the entire left hemisphere,
the temporal regions were most affected, which suppor ted our
original hypothesis.
The left hemisphere is specialized for perceiving
and expressinglanguage, whereas the right hemisphere specializes
in processing spatial information
and in processing and expressingemotions--particularly negative
emotions. We had wondered whethermistreated children might store
their disturbing memories in the righthemisphere and whether recollecting
these memories mightpreferentially activate the right hemisphere.
To
test this hypothesis, Fred Schiffer worked in my laboratory at
McLean in 1995 to measure hemispheric activity in adults during
recall of a neutral memory and then during recall of an upsetting
early memory. Those with a history of abuse appeared to use predominantly
their left hemispheres when thinking about neutral memories and
their right when recalling an early disturbing memory. Subjects
in the control group used both hemispheres to a comparable degree
for either task, suggesting that their responses were more integrated
between the two hemispheres.
Because
Schiffer's research indicated that childhood trauma was associated
with diminished right-left hemisphere integration, we decided
to look for some deficiency in the primary pathway forinformation
exchange between the two hemispheres, the corpus callosum.In 1997
Andersen and I collaborated with Jay Giedd of the National Institute
of Mental Health to search for the posited effect. Togetherwe
found that in boys who had been abused or neglected, the middleparts
of the corpus callosum were significantly smaller than in the
control groups. Furthermore, in boys, neglect exerted a far greater
effect than any other kind of maltreatment. In girls, however,
sexual abuse was a more powerful factor, associated with a major
reduction in size of the middle parts of the corpus callosum.
These results were replicated and extended in 1999 by De Bellis.
Likewise, the effects of early experience on the development of
the corpus callosum have been confirmed by research in primates
by Mara M. Sanchez of Emory.
Our
latest finding had its roots in the seminal studies of Harry F.
Harlow of the University of Wisconsin-Madison. In the 1950s Harlow
compared monkeys raised by their mothers with monkeys reared by
wire or terrycloth surrogate mothers. Monkeys raised with the
surrogates became socially deviant and highly aggressive adults.
Working with Harlow, W. A. Mason of the Delta Primate Center in
Louisiana discovered that these consequences were less severe
if the surrogate mother was swung from side to side. J.W. Prescott
of the NationalInstitute of Child Health and Human Development
hypothesized that this
movement would be conveyed to the cerebellum, particularly the
middle part, called the cerebellar vermis, located at the back
of the brain just above the brain stem. Among other functions,
the vermis modulates the brain-stem nuclei that control the production
and release of the neurotransmitters norepinephrine and dopamine.
Like the hippocampus, this part of the brain develops gradual
ly and continues to create neurons after birth. It has an even
higher density of receptors for stress hormones than the hippocampus,
so exposure to such hormones can strongly affect its development.
Abnormalities
in the cerebellar vermis have recently been reported to be associated
with various psychiatric disorders, including manic-depressive
illness, schizophrenia, autism and attention deficit/hyperactivity
disorder. These maladies emerge from genetic and prenatal factors,
not childhood mistreatment, but the fact that vermal anomalies
seem to sit at the core of so many psychiatric conditions suggests
that this region plays a critical role in mental health.
Dysregulation
of the vermis-controlled neurotransmitters norepinephrine and
dopamine can produce symptoms of depression, psychosis and hyperactivity
as well as impair attention. Activation of the dopamine system
has been associated with a shift to a more left hemisphere-biased
(verbal) attentional state, whereas activation of the norepinephrine
system shifts attention to a more right hemisphere-biased (emotional)
state. Perhaps most curiously, the vermis also helps to regulate
electrical activity in the limbic system, and vermal stimulation
can suppress seizure activity in the hippocampus and amygdala.
R.G.
Heath, working at Tulane University in the 1950s, found that Harlow's
monkeys had seizure foci in their fastigial nuclei and hippocampus.
In later work with humans, he found that electrical stimulation
of the vermis reduced the frequency of seizures and improved the
mental health in a small number of patients with intractable neuropsychiatric
disorders. This result led my colleagues and me to speculate whether
childhood abuse could produce abnormalities in the cerebellar
vermis that contributed to psychiatric symptoms, limbic irritability
and gradual hippocampal degeneration.
To
begin to test this hypothesis, Carl M. Anderson recently worked
in tandem with me and with Perry Renshaw at the Brain Imaging
Center atMcLean. Anderson used T2-relaxometry methods, a new MRI-based
functional imaging technique we developed. For the first time,
we can monitor regional cerebral blood flow at rest without the
use of radioactive tracers or contrast dyes.
When
the brain is resting, the neuronal activity of a region closely
matches the amount of blood that area receives to sustain this
activity. Anderson found a striking correlation between the activity
in the cerebellar vermis and the degree of limbic irritability
indicated by my TLE-related question checklist in both healthy
young adult controls and young adults with a history of repeated
sexual abuse.
At
any level of limbic symptomatology, however, the amount of blood
flow in the vermis was markedly decreased in the individuals with
a history of trauma. Low blood flow points to a functional impairment
in the activity of the cerebellar vermis. On average, abused patients
had higher checklist scores presumably because their vermis could
not activate sufficiently to quell higher levels of limbic irritability.
Together
these findings suggest an intriguing model that explains one way
in which borderline personality disorder can emerge. Reduced integration
between the right and left hemispheres and a smaller corpus callosum
may predispose these patients to shift abruptly from left- to
right-dominated states with very different emotional perceptions
and memories. Such polarized hemispheric dominance could cause
a person to see friends, family and co-workers in an overly positive
way in one state and in a resoundingly negative way in another--which
is the hallmark of this disorder. Moreover, limbic electrical
irritability can produce symptoms of aggression, exasperation
and anxiety. Abnormal EEG activity in the temporal lobe is also
often seen in people with a greatly increased risk for suicide
and self-destructive behavior.
Adaptive Detriment
Our team initiated this research with the hypothesis
that early stress was a toxic agent that interfered with the normal,
smoothly orchestrated progression of brain development, leading
to enduring psychiatric problems. Frank W. Putnam of Children's
Hospital MedicalCenter of Cincinnati and Bruce D. Perry of the
Alberta Mental Health Board in Canada have now articulated the
same hypothesis. I have come to question and reevaluate our starting
premise, however. Human brains evolved to be molded by experience,
and early difficulties were routine during our ancestral development.
Is it plausible that the developing brain never evolved to cope
with exposure to maltreatment and so is damaged in a nonadaptive
manner? This seems most unlikely. The logical alternative is that
exposure to early stress generates molecular and neurobiological
effects that alter neural development in an adaptive way that
prepares the adult brain to survive and reproduce in a dangerous
world.
What
traits or capacities might be beneficial for survival in the harsh
conditions of earlier times? Some of the more obvious are the
potential to mobilize an intense fight-or-flight response, to
react aggressively to challenge without undue hesitation, to be
at heightened alert for danger and to produce robust stress responses
that facilitate recovery from injury. In this sense, we can reframe
the brain changes we observed as adaptations to an adverse environment.
Although
this adaptive state helps to take the affected individual safely
through the reproductive years (and is even likely to enhancesexual
promiscuity), which are critical for evolutionary success, it
comes at a high price. McEwen has recently theorized that overactivation
of stress response systems, a reaction that may be necessary for
short-term survival, increases the risk for obesity, type II diabetes
and hypertension; leads to a host of psychiatric problems, including
a heightened risk of suicide; and accelerates the aging and degeneration
of brain structures, including the hippocampus.
We
hypothesize that adequate nurturing and the absence of intense
early stress permits our brains to develop in a manner that is
less aggressive and more emotionally stable, social, empathic
and hemispherically integrated. We believe that this process enhances
the ability of social animals to build more complex interpersonal
structures and enables humans to better realize their creative
potential.
Society
reaps what it sows in the way it nurtures its children. Stress
sculpts the brain to exhibit various antisocial, though adaptive,
behaviors. Whether it comes in the form of physical, emotional
or sexual trauma or through exposure to warfare, famine or pestilence,
stress can set off a ripple of hormonal changes that permanently
wire a child's brain to cope with a malevolent world. Through
this chain of events, violence and abuse pass from generation
to generation as well as from one society to the next. Our stark
conclusion is that we see the need to do much more to ensure that
child abuse does not happen in the first place, because once these
key brain alterations occur, there may be no going back.
MORE TO EXPLORE
Developmental Traumatology, Part 2: Brain Development.
M.D. De Bellis, M.S. Keshavan, D.B. Clark, B.J. Casey, J.N. Giedd,
A.M. Boring, K. Frustaci and N.D. Ryan in Biological Psychiatry,
Vol. 45, No. 10, pages 1271-1284; May 15,1999.
Wounds That Time Won't Heal: The Neurobiology of Child Abuse.
Martin H. Teicher in Cerebrum [Dana Press], Vol. 2, No. 4, pages
50-67; Fall 2000.
McLean Hospital: www.mcleanhospital.org/
By
Martin H. Teicher
MARTIN H. TEICHER is an associate
professor of psychiatry at Harvard Medical School, director of
the Developmental Biopsychiatry Research Program at McLean Hospital
in Belmont, Mass., and chief of the Developmental Psychopharmacology
Laboratory at the Mailman Research Center at McLean.
Teicher, M. H. (2002). Scars that Won’t Heal: The Neurobiology
of Child Abuse. Scientific American, 286(3), 68-75.
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Source: Scientific American, Mar2002, Vol. 286 Issue 3,p68, 68-75.