Ataralel Pala
in Clinical Practice
Yon @. Allen
Peter Fonagy
Anthony W. BatemanChapter 4
Neurobiology
f mentalizing required understanding the neurocognitive basis of this
activity, none of us would have learned to do it. Yet we clinicians have
ample reason to become familiar with the general direction of neurobi-
ological research on mentalizing. First, neuroscience is putting some
steel reinforcement in the scientific foundation of the developmental re-
search we reviewed in the last chapter. Second, we have delineated both
heterogeneity and unity in the concept of mentalizing, and neurobio-
logical research is putting our conceptualization to the test; the brain,
through its responses to our neuroimaging probes, can inform our ways
of mentalizing it. Third, appreciating how neurobiological deficits con-
tribute to impaired mentalizing can point our attention to strategies for
clinical intervention. Finally, the neurocognitive perspective under-
scores the potential therapeutic value of psychopharmacological treat-
ment in tandem with psychosocial interventions.
‘Taking Bowlby’s (1982) lead, we begin this chapter by considering the
pivotal role of mentalizing in the evolution of attachment. Then, relying
largely on recent neuroimaging research, we devote the bulk of the chap-
13" WIN a,
tertodelineting brain regions that contribute to various componengy
sentalizing Moreconcemed with mind than brain, we organize this.
view around eritional, cognitive, and interpersonal processes to ig
fore our understanding of mentalizing, A word of caution to the ung,
tiated: with the advent of neuroimaging, the research literature petngy
to menilizing is mushrooming; the complexity of the finding
‘once the chapter with a consideration of two neurodevelopmen,
‘mentalzing disorders with genetic bases: autism and psychopathy. ng
disorder exemplify mentalzing failures associated with impaired ie
toning in bain regions that contribute to mentalizing,
Evolution
‘Aswe have already noted, Premack and Woodruff (1978) intreducg
“theory of mind” into the literature in their study of chimpanzee soc
inteligence. Individuals were construed as having a theory of mind
‘hey were capable of predicting behavior on the basis of imputing
observable mental states to conspecifics. Although Premack and Woot.
ruff presented evidence that a chimpanzee imputed unobservable in
tentions to an actor who was engaging in solving, various problens,
subsequent researchers have varied in their inclination to attribue
mentalizing to nonhuman primates; hence among researchers then:
selves, ome are more willing than others to mentalize in imputing
‘heir elationships to one another, interpret behavioral cues so stop:
dict others actions; formulate social strategies and communicate toi
‘uence others’ actions; and learn from observing the behavior of tes.
Yet Tomasllo and Call argued that Premack and Woodruft’s inital
sults have not held up to further scrutiny, concluding that “there ism
soli evidence that nonhuman primates understand the intentorlty
cor mental 5” (p. 340), notwithstanding their ability»
‘Wile not disagreeing about the lack of evidence that primates an
impute hidden mental states, Gémez (2004) argued for a broader and
‘more pluralistic conception of theory of mind that would encompass
cert mental states, that i, mental states observable in behavior, such’
‘expressing emotion, paying attention to something, or intending 0
something—an example being “who is trying to do what to whom and
Neurobiology 1s
with what final goal” (p. 236). Gémez.concluded that “Chimpanzees
primates may have some rudimentary vers
‘mentalistic schemas for making sense of the social world
ss perceive other primates’ behaviors as
they may see each other a being connecte
demonstrate incipient mentalizing and that we humans have taken a
quantum leap forward in our capacity to develop a fully representa-
tional theory of mind that enables us to impute covert as well as overt
mental states and to reason in sophisticated ways about them, not only
in regard to others but also in elation to ourselves. Accordingly, the tra-
ditional view that practical problem solving—foraging and tool mak-
ing—drove the evolution of the neocortex has been supplanted by the
view that in evolution, an escalating demand for socal intelligence has
fueled the cognitive equivalent of an arms race (Bogdan 1997; Hum-
phey 1988) Alexander, for example, proposed that our superior intl
gence evolved not for the sake of dealing with the hostile forces of nature
but rather forthe sake of competition with each other; we became our
own “principal hostile frces of nature” (Alexander 158.46).
‘Thus, while we also master folk physics and folk biology (Carey
1985), the sheer cognitive complexity of folk psychology (Godfrey Smith
2004) has provided the greatest impetus to neocortical development.
Group (and inter-group) living requires highly complex socal skills not
urpose of competition (eg, for resources or mates)
need dedicated brain apparatus to keep track of our own and othe
liances as well as the social jes within which these alliances are
embedded (Byme and Whiten 1988; de Waal 1989).Such social cognition
required increasingly sophisticated problem-solving skills of a unique
sort. Bogdan (1997) characterized these relationships skills in terms of
the capacity for interpretation—yet another term for ment
defined as “a competence that allows primates to make sense spontane-
ously and effectively of each other in terms of behavioral dispositions
‘and psychological attributes, such as character traits, emotions, feelings,
and attitudes” (p.1),16 ‘Mentallzing In Clinleal Practcg
accumulated knowledge. He identified three types of social learning
imitative learning, instructed learning, and collaborative learning, al
lives like their own, This understanding enables
themselves "in the mental shoes” of some other
person, so that they can learn not just from the other but trough the
other. (pp 5-6)
‘As we described in Chapter 3 (“Development”), Gergely and Csibra
lopment of the social brain”
1ry function of attachment goes far
ion ofthe offspring by assuring physical prox-
imity, as Bowlby (1982) originally proposed. As Fonagy (2006) notes, at-
‘ated with the exceptional dependence of the human
infant on caregiv
‘emergence of intensive
promotes brain developm
1955) We should not loses
responses, and attempt
haracterstc pattems of behavior inthe opponent. Toa lesser exten,
described their opponent a reading their own pattorns of behavior.
\olunters spoke of strategies for respons imag
ined mental states oftheir opponent, (Gallagher etal. 2002, p. 81
As the researchers hypothesized, the mentalizing condition was as
sociated with selective activation of the paracingulate cort
anterior to the most anterior part of the anterior cingulate proper
between the putative cognitive and emotional divisions” (p. 819). In
of related neuroimag-
ing studies, the authors propose that “the paracingulate cortex has @
Neurobiology a
‘game also found grea
participants played a person compared to when they played a com-
puter (McCabe etal. 2001). Yet this difference held only for those partic-
{gain for both partic h) participants who adopted
a competitive strategy, there were no differences in medial-prefrontal
cortical activation associated with playing a person versus a com-
sof game-based rules rather than employing theory-of
rolated inferences and strategies
Attachment Paradoxes
We have emphasized repeatedly that secure attachment relationships are
tivate the cortical areas associated with mentalizing (Fonagy 2006)
It is hardly surprising that seeing a photograph of one’s partner
when one is in the throes of the very early stages of int
Tove would increase activity in dopamine-rich brain a
with reward, including the ventral tegmental area and the caudate‘Mentalizing in Clinical Practice
attachment feelings we 7
ith mentalizing. Bartles and Zeki conducted two stud-
sraphs of their roma
which mothers saw pl infants (Bartles and Zeki
2004). Both studies included careful controls, such as photographs of
friends as contrasted with romantic partners and photographs of other
children with whom the mothers were acquainted as contrasted with
their own infants, These researchers found considerable overlap be-
tween romantic and maternal love in reward-related areas of act
cingulate cortex) as well as some differences. Most notably, for both
romantic and maternal love, they found overlapping patterns of deact-
is deactivation included the medial prefrontal/paracin-
the mentalizing region) as well as the amygdala,
Bartlesand Zeki (2004)
flecting a decreased need
-mentalizing in love relationshi
both romantic and maternal love activate specific regions in the reward
system and lead to suppression of activity in the neural machineries as-
sociated with the critical social assessment of other people and with
once one is closely familiar with a person (in a
need to assess the socal validity ofthat
tems necessary for doin
‘explaining in neurologic
These interesting findings point to some complexity in the relation
between attachment and mental
dependent natee of men
The findings also mesh well
»n between passionate love and
at supports robust relationship between secure a
tachment and mentalizing. We must consider the nature of the task i
volved in these studies showing deactivation of mentalizing regions:
{gazing lovingly at photographs, We might infer that a state of admiring
love precludes mentalizing, especialy in the early, infatuated stage of 8
Neurobiology
ing is relaxed while another facet is activated.
1n be blind. But we must temper our generaliza-
tions by distinguishing love from preoccupied infatuation:
Love snot, as such, irational. Like any emotion, itean be on target or of
‘warranted or unwarranted, based on the facts or wrong about the f
foolish, life-enhancing or self-destructive. Thus
appreciation of details, than ordinary perception. (Solomon 2007, p.56)
The consistent relations between secure maternal attachment and
ly and deeply;
psychotherapy in
Frazzled Mental
A useful tip in helping patients navigate conflicts in attachment rela-
tionships: mentalizing goes offline in the context of intense emotionalah ‘Mentalizing in Clinical Practice
arousal asthe fightoorflight response comes online. Arnsten (1998)
neatly captured this process in the tile of her article “The Biology of Be-
ing Frazzled."
In understanding the elation between emotional arousal and men
talizing, itis essential to go beyond a unitary concept of arousal (Rob-
bins 1997), Key neuromodulators, for example, contribute to different
forms of arousal: norepinephrine contributes to alerting, vigilance, and
controlled attentional processing in the face of stress; dopamine ener-
sizes approach behavior in response to potentially rewarding incen-
tives; and serotonin modulates arousal in the norepinephrine and
dopamine systems (Pliszka 2003). Furthermore, the effects of arousal in
t only with the extent of transmitter secre-
th the receptor subtype activated (Arnsten and Gold.
‘Amsten et al. 1999; Mayes 2000). Through dynamic
from relatively slow executive functions mediated by the
cortex to faster habitual and! instinctual behaviors m
terior cortical (eg., parietal) and subcortical structures (e.,
amygdala, hippocampus, and striatum). Concomitantly, mentalizing
_g0es offline as defensive responses (fight-flight-freeze) come online.
This capacity for rapid switching in modes of functioning in response
to threat has the presumed evolutionary value of prom
and adaptive behavioral responses to danger. Yet
sonal stress, where complex cognitive-emotion:
ferences in the threshold for swi
tor-flight) res
3F Switching can be lowered as a result of exposure to early
juma. As Mayes (2000) summarized,
ive and inhibitory effects on PEC [prefrontal cortex] and
Neurobiology 5
attentional functions may also be perma
under stressful or arousing conditions. (p,
and more apparent
emphasis added)
These neurobiological perspectives on shifting patterns of brain ac-
sa context-dependent dynamic s
ians have developed a wide range of emotion-
intended to promote adap-
ioning by keeping mentaliz~
ing online in the face of stress Allen 2001, 2005; Levels 2008)
Mentalizing Disorders
ical contributions to mentalizing impa
range of disorders; for example, Fonagy and colleagues are in the pro-
tigate neurobi contributions toimpaired ment
with borderline personality disorder.
diagnosis requires an onset prior to three years of age (American Psy=16 ‘Mentalizng in Clinical Practice
chiatric Association 2000). Much pertinent neurobiological research
encompasses a spectrum of conditions, including pervasive develop.
rental disorder as inctioning autism and Asperger syn.
drome, notwithstanding that these diagnostic distinctions are fraught
with controversy (Volkmar etal. 2004).
‘Autism exemplifies impaired mentalizing most starkly; the core def
icits in mentalizing associated with autism are listed in Table 4-2. Most
distinctive to autism is a profound lack of social engagement such th
‘mentalizing does not get off the ground (Hobson 2002, 2005), Par-
Idren subsequently diagnosed with autism retrospectively re-
six months (Berger
disturbance in social or
sponding lack of motivation for social engagement as the root problem,
that eventuates ina cascade of deficits in emotion and social cognition.
Hence parental disengagement is now seen as a consequence rather
than a cause of autism; that is, parents disengage in response to their in-
fant's inability to engage.
Berger (2006) has focused on deficits in face expression processing asa.
critical facet ofthe lack of social engagement. He notes that normal in-
fants smile in response to another's smile at one month and actively
seek eye contact by nine weeks. Infants with autism, however, fixate
less on eyes, focus more on the mouth region and, more gene:
on specific Features rather than the gestalt ofthe face—as well as show
ing less preferential interest in faces on the whole. Berger proposes that
the key dysfunction in autism resides in “the system that initiates posi
tive hedonic states to social stimuli in the main sensory domains”
though he focuses on the face, he also notes that infants with
to find pleasure not only in eye contact and smiles but also
{ntouch and the sound of the voice.
Given their lack of orientation to social stimuli, children with autism
fai to engage in join altenton (Hobson 2005). Mundy (2003) notes, how-
‘ever, that children with autism are somewhat inclined to capture others’
for instrumental purposes (e.g., pointing to some object they
th peers on into adolescence. In sum, as Hob:
thautism “do not seem to share the world wi
Neurobiology 07
TABLE 4-2. _KEY MENTALIZING DEFICITS IN AUTISM
‘+ Impaired language leaming
‘+ Poor performance in theory-o
‘+ Lack of engagement in protend play and imaginative setivities
+ Deficient se
vareness and misuse of personal pronouns ("I" vs. "You')
Extensive research on autism has focused on ment
tion; appreciating that seeing leads to knowing; distinguishing between
and mental entities; distinguishing between appearance and
‘understanding that the brain provides for a set of mental func-
te words and using.
he perspective and
largely due to the lack of en
engaged with others’ emotional states and to be moved by them (Hob-
son 2002, 2005). Hence children with autism find social
be unrewarding (Berger 2006). Consistent with this ini
tional engagement, persons with autism-spectrum disorders are deti-
facial expressions of emoti to others’ distress,
and unmoved by others’ emotions (Hobson 2002). Like
children with autism can identify what an actor is do
point-light displays, but
(Hobson 2005). As Hobson (2002)
perceivea smile asa smile but as a contorted face; he may not perceive a18 ‘Mentalizing in Clini
Practice
guestsiin the house, Reflecting
idren with autism have difficulty
h personal pronouns (eg, “I” and “you”) and are liable to refer to
selves by name. In Hobson's terms, there isa thin quality to their
self-concepts, which lack subtle emotional qualities and do not include
the significance oftheir relationships with other persons. This deficient
sense of self originates in the lack of relatedness with others, as Hobson
(2002) summarizes:
the extreme cas (and this snot true of all people with autis
not eren move ote poston of faking any atu towarde hime
(p.225:emphass in original)
As we have stated, autism has been identified as a disorder of men-
comples, perhaps is
to ten loci (Volkmar et al 2004). The search for affected brain regions
has been broad; as Volkmar and colleagues state, “At one point or an-
0 in attention and orienting
“The wide earch fr regions of brain impairment associated with au-
tism isnartowing somewhat Volkmar and colleagues (2004) noted “the
Neurobiology ne
discovery of generalized hypoactivation of an entire social processing
sm” (p. 144) which they con-
Mundy (2003)
{impairment in the
for, such as social
pernicious to the d
rrupts his/her capa
the foundation of
velopment. (P. 805)
spmental cascade in autism begins with a
al stimuli—faces, for example. As described
Berger (2006) pinpoints the lack of reward associated with social inter
action as the core problem, and he points out that this problem might
have multiple neurobiological origins:
it is hypothesi social features of autism arise when sensory
access to the affect system through a final common pathway such as
‘a sensory convergence area ofthe amygdala is dysfunctional. This can40 ‘Mentalizing in Clinical Practicg
ebecause the networks leading to the affect system, oF the af-
tem itself, orboth, are dysfunctional, Hence, ifforany
the system that initiates positive hedonic states
-main sensory domains is dysfunctional, the social
tures characterizing autism will cou. (p. 360).
riguing hypothesis regarding the early origins of
ly within our account of the development of ment
to high-but-imperfect response—>stimulus associations (eg,
their own smile).
pices aly nhc ats, hic pantie
-mely high response-stimulus contingencies.
‘While autism cannot be diagnosed reliably until two years of age by
current criteria (Volkmar etal. 2004), the developmen’
carl in infaney with the lack of orientation to social stimuli and the lack
‘of social-emotional engagement; these are the foundations of mentaliz-
ing through the developmental route of joint attention, perspective tak
ing, selfawareness, symbolizing, and representational theory of mind,
Pathological conditions often have a way of illuminating normal devel-
‘opment, and autism has brought mentalizing into bold relief by high-
lighting the devastating personal and social consequences of its ab-
sence. As we have just described, autism also provides compelling
‘converging evidence forthe contribution of key brain regions to various
facets of mentalizing-related functions—again, by the absence of normal
activation,
Psychopathy
Psychopathy exemplifies a pata but fundamental impairment of men-
1§8s Baron-Cohen (2003, 2005) construes it, mindreading with-
Neurobiology mm
charm, Cleckley ob-
him, and inevery re-
justed, happy person”
he noted extraordinary immunity from anxiety: “Even un-
‘would for the ordinary person cause
tively anything comp:
the major a
351, emphasis in original)wa Mentalizng in Clinical Pratcg
it instructively parallels autism
in reflecting stable impairment of mentalizing rooted in neurobiology
‘As Blair and colleagues (2005, 2006) state, psychopathy is a neurodevel
ther the neurobiological insults
(eg as associated with physical anomalies or birth complications) nor
lecular genetics have been characterized definitively, but psych-
ishighly heritable, and no shared environmental influence has
idies. Most pertinent for present purposes,
dysfunction has been identified in brain regions associated with men.
talizing Blair eta. 2006)
Inthe diagnostic classification system (American Psychiatric Assoc-
ation 2000), psychopathy has not been distinguished from either antiso-
cial personality disorder in adults or conduct disorder in children, None-
theless building on Cleckley’s (1976) clinical observations, Hare and
colleagues (Hare 1980; Hare et al. 1991) have developed reliable criteria
for teasing out psychopathy within the heterogeneous spectrum of ant-
social behavior. Two clusters of characteristics can be distinguished: an
interpersonataffective cluster, characterized, for example, by callous
ness and lack of remorse; and a pattern of antisocial behavior, for exam-
ple, characterized by impulsivity and an unstable lifestyle. The emo-
tional deficits can be viewed as fundamental to psychopathy, and the
antisocial pattem of behavior is “best viewed as a secondary symptom
‘or consequence of psychopathy” (Cooke etal. 2004, p. 337) —and not an
invariable consequence. Blair and colleagues (2005, 2006) reported that
the cllous-unemotional mode of relating intrinsic to psychopathy charac-
terizes about 25% of individuals inthe otherwise heterogeneous diag-
nostic categories of antisocial person
short of creating a separate diagnos
th higher rates of rec
particularas wells with a paradoxical
Jowing treatment and rehab
ig on Hare's concepts
‘etal. 2005, 2006) have developed a comprehe
standing of the in
psychopathy, pre
Neurobiology 3
distress has significant consequences
chopathic child will not be deterred,
proval, disappointment, or concern:
fe reviewed on mentalizing di
smal pattern of responding reflects not only a
1 emotion triggered by the other person's emotion, an
in order to understand another person, to predict ther behavior, and to
‘connect oF resonate with them emotionally” (Baron-Cohen 2003, p.2,
emphasis in original). In short, emp: ails being moved by
others’ emotions. Consistent with this clinial picture, psychopaths1 ‘Mentalizing In Clinical Practgg
sé emotions. Thus, without the amygdalar contribution to perception,
their mindreading lacks emotional ¢ and respor
biting aversive ment
person's potential emotional distress. In short:
them, he receives reward. (Blais 2003, p. 566)
Although psychopathicindividuals are distinctive in theirinstrumen
tal aggression, they are not immune to reactive aggression. Yet thei rae
Les to reactive aggression insofar as the ventrolateral cortex plays a sig
nificant role in inhibiting responses to stimu
previously but are no longer rewarded
area playsa critical role in response reversal iple, in adapting be
havior to changing reinforcement conting when teasing 70
longer is experienced as amusing but rather becomes hurtful). Blair and
colleagues propose that, owing fo impaired orbital/ventrolateral func
tioning, psychopaths are more likely to perseverate in unrewarding be
havior then, being unable to shit gears, they are more liable to frust-
tion nd thereby more vulnerable to reactive aggression in.
have been rewarded
‘Thus this prefrontal
Recapitulation
thinking, moving, and talking
activity inthe entre brain—a
cert. Nonetheless the teritory of
ing and thinking writ large, and there is some justification for narro-
ing our focus (sighly) tthe “social brain.”
Neurobiology ms
To summarize, on the social orienting and input side, the fusiform
face area contributes to identifying individuals, and the super
zal sulcus interprets patterns of actions such as emotional expres
the amygdala adds emotional
prefrontal region covers large and heterogeneous territory, and linking
the more specific facets of mentalizing to more narrowly defined brain
regions will be the next frontier of neuroimaging research in mental-
vvelopmental and neu
tific foundation for ou
search underscore the emotional and cognitive processes
that we are subsuming under this broad rubric. Developmental and
neurobiological research will continue to refine our understanding of
the many facets of mentalizing and their interactions. Yet, multifaceted
asitmay be, we highlight the unity in mentalizing for clinical purposes,
‘and nowhere is this unity more apparent than in the like-mindedness
ensured by our shared social brain and culture, which enables the mind
of each individual to come into being through the minds of other indi-
viduals.
Yet we have seen that optimal development of mentalizing
ties is by no means assured—even short of neurodevelopmental
ders such as autism and psychopathy. Most conspicuously, atta
‘trauma undermines the development of mentalizing capacity. But vari-
‘ous degrees of impaired mentalizing associated with a wide range of
chotherapies. As we have reviewed in the first
several decades of attachment research, recent
tic relationships. Part Il of this book
jdders a range of potential applications.we ‘Mentalizing in Clinical Practice
Key Clinical Points
# to promoting reflexive fight-or-ight responding; thresholds
for switching out of mentalizing can be lowered by early trauma,
:mentalizing has been identified in autism-spectrum disorders.
Psychopathy: Like autism, psychopathy is associated with
‘genetically based neurobiological deficits. Yet psychopathy entails
ig, namely, a callous-unemotional
‘manner of relating that can be construed as mindreading without
‘empathy: Impaired emotional responsiveness associated with
amygdala hypoactivation, coupled with impaired inhibition
associated with orbtal/ ventrolateral hy poactivation, contribute
to failures in socialization and a proclivity for instrumental
aggression.
PART I
Practicing Mentalizing