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PERSPECTIVES
Coalescence of Psychiatry, Neurology, and
Neuropsychology: From Theory to Practice
Miles G. Cunningham, MD, PhD, Martin Goldstein, MD, David Katz, PhD, Sarah Quimby ONeil, MD,Anthony Joseph, MD, and Bruce Price, MD
In a climate of renewed interest in the synergy between neurology and psychiatry, practitioners areincreasinglyrecognizing the importance of exchange and collaboration between thesetwo disciplines.However, there are few working models of interdisciplinary teams that freely share expertise in realtime, while providing clinical and academic training to future physicians who specialize in the centralnervous system. Over the past 11 years, the McLean Hospital Neuropsychiatry and BehavioralNeurology service has provided proof-of-principle for such collaboration, demonstrating that ateam comprising psychiatrists, neurologists, and neuropsychologists can function effectively as aunit while maintaining the autonomy of these three disciplines and also synthesizing their combinedknowledge. In addition to delivering enhanced patient care and promoting medical research, thisclinical service has provided enriched cross-specialty training for fellows, residents, and medicalstudents. The practical functioning of the team is described, and case vignettes are presented toillustrate the teams collaborative synergism in practice. (HARV REV PSYCHIATRY 2006;14:127140.)
Keywords: collaboration, cross-training, multidisciplinary, neurology, neuropsychiatry, psychiatry
From the Departments of Psychiatry (Drs. Cunningham, Quimby
ONeil, and Joseph) and Neurology (Dr. Price), Harvard Medi-
cal School; McLean Hospital, Belmont, MA (Drs. Cunningham,
Quimby ONeil, Joseph, and Price); Department of Neurology, Mount
Sinai School of Medicine (Dr. Goldstein); Department of Psychol-
ogy, University of British Columbia, Vancouver (Dr. Katz); Depart-
ment of Neurology, Massachusetts General Hospital, Boston, MA
(Dr. Price).
Supported, in part, by the Sidney R. Baer Foundation.
Original manuscript received 4 September 2005, accepted for pub-
lication subject to revision 25 October 2005; revised manuscript re-
ceived 6 January 2006.
Correspondence: Miles G. Cunningham, MD, PhD, MRC 333,
McLean Hospital, 115 Mill St., Belmont, MA 02478. Email:
c 2006 President and Fellows of Harvard College
DOI: 10.1080/10673220600748536
RENEWED INTEREST, REDISCOVERY
One hundred ninety years ago, Benjamin Rush, considered
the father of American psychiatry, in a letter to John Adams,
wrote: The [diseases of the mind] have hitherto been en-
veloped in mystery . . . I have endeavored to bring them down
to the level of all other diseases of the human body, and to
show that the mind and body are moved by the same causes
and subject to the same laws.1
Modern neurologists- and psychiatrists-in-training inter-
ested in behavioral neurology and neuropsychiatry haveseen themselves as venturing onto new ground, on the
cutting edge, and yet as being in the minority of main-
stream neurologic and psychiatric training. In fact, how-
ever, their conceptualization of mind, brain, and behavior
was shared by the forefathers of neurology and psychia-
try, including Freud, Kraepelin, Charcot, Alzheimer, Breuer,
and many others.2 Sigmund Freud, the founder of psycho-
analysis, was trained as a neurologist. Alois Alzheimer,
best known for describing the dementing neurologic disor-
der subsequently named after him, was a psychiatrist. A
127
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128 Cunningham et al.Harv Rev Psychiatry
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century ago, however, while some recognized that mind and
brain were inseparable, most diseases of the brain could not
be visualized, measured, or readily treated. Now, advances
in neuroscience have illuminated anatomical, cellular, and
molecular substrates of mental illness. Once again, we rec-
ognize that the mind and brain are inseparable. The patho-
physiologic bases of many mental illnesses are beginning to
be empirically identified,38 and many can be characterized
microscopically. 911 Moreover, mechanisms of recovery with
pharmacologic and psychotherapeutic treatment are being
defined.1214
As reviewed by Price, Coyle, and Adams,15 as well as
by Martin,16 historically there was much less conceptual
and practical separation between neurology and psychia-
try. Practitioners were trained in both; they were neu-
ropsychiatrists committed to the study of the biologic sub-
strates of psychiatric disease. Ironically, by the middle of the
twentieth century, the penetrance of psychoanalysisthe
brainchild of one of the most prominent neuropsychiatrists,
Sigmund Freudresulted in his followers virtually aban-
doning efforts to explain cognition and behavior in bi-
ological terms. A rift developed between neurology and
some elements of psychological psychiatry, separated by
a false void. That void, in fact, was an artifact of in-
adequate scientific sophistication and consequent miss-
ing knowledge, and it was maintained and perhaps
widened by frank resistance to neural models of behavior.17
While neurology essentially detached itself from men-
tal phenomena, psychiatry progressively adopted psycho-
logical conceptualization and methodology. In the midstof the divide, writing in Brain in 1946, A. S. Paterson
observed:18
Freud, faced with the barrenness of contemporary
neurology and physiology in accounting for mans
emotional and instinctive behaviour, canalized and
developed the popular explanation of behaviour in
terms of vital principles . . . [T]he psychogenic the-
ory was elaborated in isolation from other considera-
tions, and unfortunately became, in the eyes of some
of its adherents, entirely self-sufficient . . . [T]here
has been . . . a tendency for [neurology and psychia-
try] to pursue separate paths, to be not a little suspi-cious of each other and to maintain in isolation their
own traditional concepts . . . In the face of the fick-
leness of emotional reactions and personality traits
compared with the relative uniformity and consis-
tency of the perceptual process, it is small wonder
that the clinical neurologist has devoted little time
to the study of the former . . . The psychiatrist, on
the other hand, has made some sense of the prob-
lems presented by human behaviour in the emotional
sphere.
EGO STRENGTH
The mind/brain dichotomy that ensued was not just intel-
lectually debated, but passionately defended, by each fields
respective practitioners. Those traditionally trained in neu-
rology and psychiatry, as tends to happen to those being
inducted into any specialized discipline, seemed to embrace
explicit and implicit teachings as if those teachings were a
part of their identity. Joseph Martin, a neurologist and neu-
roscientist by training and dean of the Faculty of Medicine
at Harvard Medical School, remarked:16
To take full advantage of the enormous opportunities
for elucidating the causes of neuropsychiatric disor-
ders and seeking effective treatments for them, bold,
revolutionary planning and experimentation will be
required. Progress will also depend on overcomingso-
cial and psychological obstacles, including ingrained,dualistic concepts of brain and mind, rigid educa-
tionaltraditions, and protective instincts with regard
to professional turf.
It seems we have now come full circle in conceptualizing
the mind/brain paradigm. With techniques such as immuno-
histochemistry, in situ hybridization, microdialysis, DNA
microarray analysis, and progressively more sophisticated
structural and functional imaging techniques, we are armed
with powerful tools to investigate previously subtle cellular
and molecular pathoetiology of diseases of the mind. But are
psychiatrists prepared to acknowledge the neurology of psy-
chiatry? Are neurologists prepared to acknowledge the psy-
chiatry of neurology? More importantly, are the respective
physicians prepared to collaborate to provide appropriate
care for the (frequent) patient manifesting both psychiatric
and neurologic symptoms?
THE NEUROSCIENCE OF PSYCHIATRY:INEVITABLE BIOLOGY
Mental illness has been conceptualized as organic if ge-
netic, biochemical, cellular, histologic, or gross structural
changes can be identified, and functional if such changes
cannot be appreciated; that is, when the function of a cogni-tive, emotional, or perceptual process is disorderedwithout a
clear biologic cause. As psychiatric disease becomes increas-
ingly understood in a biologic context, the terms organic
and functionalwhile still in use to describe symptoms
and syndromesare beginning to lose their significance. We
are approaching the point of being able to measure differ-
ences between the psychiatrically disordered and the nor-
mal brain. For example, schizophrenia and bipolar disease
are associated with decreases in inhibitory interneurons in
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Volume 14, Number 3 Cunningham et al. 129
specific brain regions.9,11,19 While imaging studies remain
inconclusive, single photon emission computerized tomog-
raphy analysis has shown that patients with intractable
unipolar depression have decreased blood flow in the cau-
date, cingulate gyrus, and the frontal and anterior temporal
cortices.20 Moreover, positron emission tomography (PET)
studies have demonstrated reduced 5-HT1A binding poten-
tial in limbic and neocortical regions of depressed patients.21
PET has shown activation of subcortical nuclei, limbic and
paralimbic structures, and regions of auditory cortex during
auditory hallucinations in schizophrenics.22 In fact, there
is now also evidence for neurophysiologic correlations for
personality or characterologic disorders. Volumetric struc-
tural MRI studies of patients with borderline personality
disorder have found a tendency toward reduced hippocam-
pal and amygdala volumes.23 And a functional MRI study
has demonstrated in these patients increased activation ofthe amygdala and select prefrontal cortex regions compared
to normal control subjects when presented with visual stim-
uli having emotional valence.24 Furthermore, violent offend-
ers have been shown to have hypoperfusion of the head of
the caudate nuclei and hippocampi.25
A debate that has paralleled the dichotomy of neurol-
ogy and psychiatry is that of nature versus nurture. This
conceptual framework has lost its significance, as they are
inextricably bound. It can be argued that nature is nur-
ture and that nurture is natureas illustrated by a series
of studies demonstrating proliferation of granule neurons
within the dentate gyrus of mice exposed to an enriched
environment.26,27
This environment provided animals morediversity in their living space, interaction with other ani-
mals, opportunity for increased physical activity, and expo-
sure to colorful, complex objects. In more anthropomorphic
terms, the animals were provided with new perceptions, new
experiences, and new perspectives.
The capacity of experience, learning, and cognitive pro-
cessing to alter brain anatomy, physiology, and function
was demonstrated in a landmark study by Baxter and
colleagues.12 Patients diagnosed with obsessive-compulsive
disorder were treated with either cognitive-behavioral ther-
apy (CBT) or pharmacotherapy. The responders in each
group demonstrated attenuation of glucose metabolic rate
within the right caudate nucleus as measured by PET. Thesefindingsare consistent with conceptualization of psychother-
apy as a biological intervention, whereby gene expression
and neural connectivity are altered through the therapeutic
process,17 be it psychoanalysis, insight-guided therapy, CBT,
or other approaches. In an editorial for the first volume of
Molecular Psychiatry, Joseph Coyle (professor of psychiatry
and neuroscience at Harvard Medical School) commented,28
Genes, especially as they affect brain function, are not ex-
pressed in a vacuum but rather in the rich personal context
of individual experience. And genomics promises a new con-
trol over the complex simultaneous equation of Nature and
Nurture that shapes brain and behavior.
As the substrates of mental illness continue to be ac-
tively explored and discovered, our understanding of the
biology of mind is rapidly progressing. Consequently, this
new knowledge will fundamentally alter how we concep-
tualize mental illness, practice medicine, and train future
practitioners.
THE PSYCHIATRY OF NEUROLOGY: INEVITABLEBEHAVIOR
The unfortunate and arbitrary divide between the disci-
plines of neurology and psychiatry can be further illustrated
by findings of a study by Koponen and colleagues,29 who
evaluated the occurrence of psychiatric disorders in patients
with traumatic brain injury. Criteria for evaluation were
that trauma was of sufficient severity to have caused neu-
rologic symptoms lasting at least one week and also, at a
minimum, loss of consciousness for at least one minute, post-
traumatic amnesia for at least 30 minutes, or neuroradio-
logical findings suggesting traumatic brain injury. Over a
30-year observation period, approximately 50% of patients
developed symptomatology consistent with an Axis I disor-
der, and 25% developed symptomatology consistent with a
personality disorder. Another recent report30 highlighted the
cognitive, personality, and mood disorders seen in patients
with degenerative cerebellar syndromes and Huntingtons
disease. Over 75% in both patient populations manifestedpsychiatric symptoms, in contrast to a much lower rate in
a group of comparison subjects who were not neurologically
impaired. These and numerous other studies3133 demon-
strate that reducing complex brain disorders into simplistic
categories and restricting pathophysiologic characterization
to a singlediscipline is no longer tenable. Manypatientswith
neurologic disease suffer fromserious mood, cognitive, or be-
havioral changesthat may be pathophysiologically related to
the same disease process causing their neurologic manifes-
tations; yet, because of artificial clinical demarcations, these
patients may remain underdiagnosed and undertreated.
Grounded in the principles, language, and scientific rigor
of anatomy, physiology, and pathology that characterizethe terminology and constructs of modern medicine, neu-
rology has commanded full membership in the family of
medical specialties. In contrast, since psychiatry has not
been amenable to traditional medical-scientific methodology
and has adopted, instead, unconventional approaches to its
unique array of diseases, it has not enjoyed the positive re-
gard that such membership normally bestows. In point of
fact, in the not-so-distant past, many teachers of psychiatry
discouraged new thinking and devalued scientific inquiry.17
The result has been what may be perceivedas an inadequacy
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130 Cunningham et al.Harv Rev Psychiatry
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in psychiatric training and patient care. The consequences
for neurology are equally unfortunate. That is, while neu-
rology attempts to diagnose and treat disorders in a context
that is scientifically grounded, dysfunction of the mind of-
ten complicates the presentation of neurologic disease with
the ambiguity and subjectivity of emotional discord. Some
neurologists choose not to attend to a patients affective and
behavioral components, perhaps seeing these symptoms as
irrelevant to the biology and successful treatment of the dis-
ease. However, clinical manifestations that are defining ele-
ments of certain disordersand that are thus often essential
to their diagnosiscan span the neurologic-psychiatric dis-
ease spectrum. Examples include auras and other affective,
thought, and perceptual phenomena associated with com-
plex partial seizure disorders; hallucinations seen early in
the course of Lewy body disease; and prodromal depression
seen with Alzheimers and Parkinsons disease. Table 1 lists
examples of psychiatric conditions associated with neuro-
logic diseases.
TABLE 1. Psychiatric Conditions and Associated Neurologic Diseases
Psychiatric condition Associated neurologic diseases Relevant neuroanatomy
Depression Stroke, Parkinsons disease, Huntingtons disease, epilepsy,
traumatic brain injury, multiple sclerosis, Alzheimers
disease, HIV, vascular dementia
Usually left hemisphere lesions: frontal and
temporal lobes, basal ganglia
Mania/hypomania Stroke, Parkinsons disease, Huntingtons disease, Fahrs
disease, traumatic brain injury, multiple sclerosis,
epilepsy, frontotemporal dementias, syphilitic
encephalitis
Usually right hemisphere lesions:
orbitofrontal cortex, caudate nuclei,
thalamus, basotemporal area
Anxiety Stroke, epilepsy, Parkinsons disease, migraine, m ultiple
sclerosis, encephalitis, posttraumatic/concussive
syndromes
Limbic lesions, esp. right-sided
Mood lability Seizure disorders, pseudobulbar palsy, Angelmans
syndrome
Lesions of orbitofrontal cortex, basal ganglia
dysfunction
Delusions Epilepsy (esp. TLE), degenerative and vascular dementias,
Huntingtons disease, posttraumatic encephalopathy,
Creutzfeldt-Jakob disease, multiple sclerosis, B12
deficiency, temporal lobe tumors/strokes, mental
retardation
Limbic system dysfunction (esp. subcortical
structures), temporal lobe dysfunction
Visual hallucinations/
illusions
Migraine, TLE, narcolepsy, neurodegenerative diseases,
Lewy body disease, drug intoxication or withdrawal,
Tay-Sachs disease
Lesions of eyes, optic nerves,
geniculo-calcarine projections, occipital or
temporal cortex
Auditory
hallucinations
TLE, stroke, tumor Auditory association cortex, paralimbic
cortex, hippocampus, striatum, thalamus
OCD/repetitive
behavior
Picks disease, Huntingtons disease, Alzeheimers disease,
Tourettes syndrome, Sydenhams chorea, progressive
supranuclear palsy, CO poisoning, Mn toxicity
Frontotemporal lobe degeneration, lesions of
caudate, globus pallidus
Dissociative disorders TLE, migraine, postconcussive states, encephalitis,
toxic-metabolic disorders
Temporal and parietal lobe dysfunction,
notably the angular gyrus
Personality change Basal ganglia disorders, vascular dementia, Huntingtons
disease, Alzheimers disease, TLE, B12 deficiency
Lesions of medial frontal, orbitofrontal, and
temporal lobes
Source: Adapted from Cummings and Trimble (1995)34 and Price (1999).35
TLE, temporal lobe epilepsy.
COALESCENCE IN THEORY
Thought leaders in neurology, psychiatry, and neuroscience
have encouraged a rapprochement of disciplines and have
called for a revision in medical education that crosses tradi-
tional boundaries.1517,36 Kandel17 has outlined an intellec-
tual framework designed to align, within modern biology, the
current psychiatric thinking and the training of future prac-
titioners within modern biology. This framework is based on
three principles: (1) the functions of mind reflect functions of
brain, (2) genes and their products underlie neural connec-
tivity patterns and their function, including mental illness,
and (3) experience, behavior, and other variables that affect
learning alter gene expression, neural connectivity, and, in
turn, perception, affect, and behavioral patterns.
Leon Eisenberg, professor of psychiatry (emeritus) at
Harvard Medical School, has asked: Is it time to integrate
neurology and psychiatry?37 He proposes that residency
programs be restructured, incorporating training within
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each specialty that will help build sophistication in the other.
He also proposes that medical students be exposed early to
a consolidation, or coalescence, of brain medicine and sci-
ence through a combined neuroscience/neurology/psychiatry
track. Jack Gorman, editor of CNS Spectrums and pres-
ident and psychiatrist in chief at McLean Hospital, also
intrepidly champions collaboration among psychiatry, neu-
rology, and neuropsychology.3840 George Murray, emeritus
director of the consultative-liaison psychiatry service at
Massachusetts General Hospitalusing seizure disorders
to emphasize his pointobserves that if you know tempo-
ral lobe epilepsy, you know how contemporary psychiatry
should be [approached].41 Murray argues, too, that psychi-
atrists shouldbecome more knowledgeable in neuroanatomy
and imaging techniques since neuroimaging is becoming an
important diagnostic tool in psychiatric diseaseyet most
psychiatrists, including trainees, arenot trained in the inter-
pretation of brain images. Similarly, Donald Schomer, pro-
fessor of neurology at Harvard Medical School, argues that
there should be more psychiatry for neurologists in the for-
mative years of training.41 Despite these and other experts
opinions, the American Board of Psychiatry and Neurology
has only recently recognized even the most minimal need
for psychiatry rotations within neurology residency pro-
grams, and, in parallel, the board has progressively reduced
medicine-rotation requirements for psychiatry residencies.
Interestingly, despite the persisting wall between the two
disciplines, on Part IB of the boards written examinations,
approximately 30% of questions pertain to the other dis-
cipline, while many of the remaining 100 questions over-lap the two disciplines. Even so, as a specialty, psychiatry
stands alone in not requiring the study of the functional
anatomy and physiology of the organ from which its diseases
arise.
While leaders in neurology and in psychiatry have openly
expressed their support for a rapprochement, there are
few clinical models for effectively converting theory into
practice. Even within larger teaching hospitals, doctors-in-
training rarely have the opportunity to simultaneously ad-
dress patients neurologic and psychiatric signs and symp-
toms under the supervision of experts in the respective
disciplines. Likewise, practitioners in these fields rarely
have a forum available in which to share their experi-ences and knowledge, thereby enriching their own clinical
judgment. However, with forward-thinking leadership, con-
tinued progress in medical neuroscience, the progressive
effacement of the boundaries between disciplines, and in-
creasing demands by students for a more integrated curricu-
lum, there will surely come a time when collaborative pro-
grams and teams are more practical. They could also become
more cost-effective through potentially greater efficiencies
in diagnostic assessment, treatment formulation, and plan
implementation.
The model presented here for a collaborative initiative
between psychiatry and neurology is drawn from the ongo-
ing program at McLean Hospital. Another potential model,
not discussed in this article, is the one used by the Geriatric
Treatment Center of the Colorado Mental Health Institute
at Pueblo, which treats patients with psychiatric disorders,
behavioral syndromes that result from neurologic disease,
or a combination thereof.42
These changes within neurology and psychiatry should
also be seen within a larger perspective as representing the
ongoing evolution of medical education. In 1910, the Flexner
Report43 concluded that for medical education to flourish
from one generation to the next, it [has] . . . to reconfigure it-
self in response to changing scientific, social, and economic
circumstances. Almost 100 years later, medicine continues
to react to these ever changing forces to ensure that a physi-
cians education and training keep pace with an ever ex-
panding base of medical knowledge, coupled with changes in
venues and in the manner that care is provided to patients.
For these reasons, Harvard Medical School and other insti-
tutions are in the midst of a major curriculum evaluation
and reform, with a particular focus on the third and fourth
years of medical school. Residency and fellowship training
programs have been similarly affected, as alternative ap-
proaches to training are being explored.
COALESCENCE IN PRACTICE
Founded in 1811, McLean Hospital was the first psychiatrichospital established in New England and the third in the
United States. Considered the worlds birthplace of hospital-
based laboratory research in psychobiology,44 the hospitals
neuroscience research program is larger than that of any
other private psychiatric hospital in the United States and
also of any other department or affiliated institution of Har-
vard University. Moreover, with a current inpatient census
of 170 beds, the hospitals psychiatric teaching facility is the
largest at Harvard Medical School. And with its diversity
in both patient population and psychiatric/neuropsychiatric
diseases, the hospital offers an ideal setting for research
and training. Reflecting McLeans reputation as the setting
for the beginnings of conjoint medicine,45 we constructed amultidisciplinary team whose members work together syn-
ergistically; the interchange of perspectives and knowledge
makes each team member more effective. Thisapproachgen-
erates a comprehensive, insightful formulation for patients
with comorbid neurologic and psychiatric diseaseone that
is superior to what either discipline would produce on its
own.
Neuropsychology, an integral component of the service,
is itself a working model for the coalescence of neuro-
logic and psychiatric principles. The field evolved as an
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interdisciplinary approach synthesizing information from
diverse, but interrelated, areasfunctional neuroanatomy,
ethnology, cognitive psychology, and comparative neuro-
physiology, as well as clinical neurology and psychiatry. It
provides expertise in performing standardized and normed
tests that quantitatively measure cognitive domains (e.g.,
attention, language, memory, and visuospatial function),
myriad executive functions (e.g., decision making, error
monitoring, behavioral-motor control, socio-emotional regu-
lation, working memory), and affective modulation of behav-
ior (e.g., motivation, approach/withdrawal). Neuropsycholo-
gists also perform psychodiagnostic testing, a standardized
mixture of qualitative and quantitative evaluations of
thought content, affect, and personality. Remarkably, de-
spite neuropsychologys broad relevance to both psychia-
try and neurology, it has remained a relatively uneven
presence across academic neurology and psychiatry depart-
ments. It has nonetheless experienced a significant renais-
sance in connection with the emergence of new research
methodologies such as functional neuroimaging; neuropsy-
chologys indisputable utility has been catalyzing the fields
transition from lesion-based traditions. Moreover, the in-
creased recognition of both the profound cognitive conse-
quences of primary psychiatric disorders (e.g., the work-
ing memory and language deficits of schizophrenia that are
neglected by the limited criteria sets of DSM-IV) and the
profound affective consequences of primary neurologic dis-
orders (such as those associated with stroke or epilepsy)
positions neuropsychology as an important clinical and re-
search discipline for contemporary psychiatry and neurol-ogy. Even with regard to non-CNS-related interventions
(e.g., coronary artery bypass surgery), the attention now
given to their cognitive and behavioral consequences is re-
quiring sophisticated neuropsychological studies. The field
of neuropsychology thuscontinuesto increase in importance,
for it provides a bridge between psychiatry and neurol-
ogy, promoting an interdisciplinary formulation of complex
cases.
McLean Hospitals Neuropsychiatry and Behavioral Neu-
rology (NBN) consult service began in 1994 as an academic
forum bringing together neurologists, psychiatrists, and
neuropsychologists to formulate diagnoses and treatment
plans for clinically challenging inpatients. The NBN servicewas inspired by a prior model, the Beth Israel Behavioral
Neurology Program, as pioneered by Norman Geschwind,
under whom the founder of the NBN service trained. Collab-
orations such as these serve many functions. They disman-
tle perceived barriers between the disciplines. They promote
the free interchange of knowledge and techniques between
the disciplines, through which all of the specialists gain new
clinical insights and tools. This collaborative setting also
provides for rich cross-training for medical students, res-
idents, and fellows, and offers enhanced service to patients
and their treatment teams through coordinated insights and
recommendations for difficult clinical problems.
The model we describe below has been adjusted and pol-
ished over a number of years. Throughout this period, how-
ever, our ongoing assumption has been that medical educa-
tion, developments in neuroscience, and the delivery of high
quality care to patients must continue to develop synergis-
tically and in parallel.
The structure of the McLean NBN consult service is
based on a multitiered system of collegial interaction among
attendings, fellows, residents, and medical students. Se-
nior staff neurologists, psychiatrists, and neuropsycholo-
gists participate as clinician-mentors. A two-year fellowship
in neuropsychology, funded by clinical income, was initiated
in 1995. A privately funded one- or two-year fellowship in
behavioral neurology and neuropsychiatry was started in
1999one of the first fellowships of this kind available any-
where. Residents from psychiatry training programs within
the Harvard Medical School system rotate through the NBN
service for oneor two months to satisfy their two-month neu-
rology requirement as set by the Residency Review Com-
mittee for Psychiatry and Neurology. Neurology residents
electively rotate for one-month intervals. Harvard medical
students participate one day per week during their psychi-
atry rotation at McLean Hospital. Fellows, residents, and
medical students are also encouraged to participate in clini-
cal and basic science investigationespecially in connection
with the ongoing research of the NBN services core team
members. Moreover, during their NBN rotations, residents
are asked to produceat least onecase study suitable for pub-lication in the NBN online periodical or in a peer-reviewed
journal. We have also made these opportunities available
to doctors-in-training visiting from other U.S. programs, as
well as from abroad.
The NBN consult service meets for two to three hours
twice weekly to round on patients who are presented primar-
ily by residents, but also by fellows and occasionally medi-
cal students. During each session, two to four patients are
presented in detail, including: history; psychiatric evalua-
tion; and mental status, physical, and neurologic examina-
tions. Each patient then meets with the entire team, which
enables the members to observe and interact with the pa-
tient and apply their expertise. This meeting also allowspatients to express specific concerns regarding their psychi-
atric experiences and physical symptoms. For each patient,
the team provides a focused neurologic exam that takes into
account the results of all relevant diagnostic investigations
(e.g., EEG, imaging studies, and other laboratory findings).
Many of these patients have also been given neuropsycho-
logical testing, which further promotes the teams compre-
hensive synthesisof the case. Diagnosis and treatment plans
are then formulated and reported to the patients treatment
team on the hospital ward. The text box lists conditions
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Volume 14, Number 3 Cunningham et al. 133
involving brain-cognition-behavior relationships for which
NBN consults are frequently requested.
Conditions for Which the NBN Service Is Commonly
ConsultedDelirium/confusional statesNeurodegenerative diseasesFirst-break psychosis
Atypical intractable psychiatric syndromesTraumatic brain injuryCerebrovascular disease/strokesTemporal lobe epilepsy/spells
Abnormal laboratory studies (MRI, EEG, etc.)Movement disordersChronic pain syndromes
Viral, metabolic, toxic, hypoxic encephalopathiesSomatoform disordersDevelopmental syndromesMultiple sclerosisBrain tumors
The multidisciplinary product of these evaluations allows
relevant aspects of neurology, psychiatry, and psychology to
be addressed in the same patient at the same time. Illustra-
tive cases include the following:
Vignette 1
A 25-year-old right-handed man with a prior diagnosis of
Aspergers syndrome, psychosis NOS, and seizure disorder
was admitted to McLean Hospital for depression and psy-
chotic symptoms. The patient began to decompensate upon
the recent death of a loved one, to whom he was strongly
attached emotionally. He became severely depressed withsuicidal ideation and began experiencing auditory halluci-
nations. The NBN service was asked to assess for neurologic
causes of his psychotic behaviors.
The patient had a history of a developmental disorder and
psychotic behavior diagnosed at age 6. Atage 16he was diag-
nosed with a seizure disorder (partial complex) after being
admitted to the hospital for psychosis. A thorough history
revealed that the patients psychotic symptoms appeared to
correlate positively with seizure activity. His seizures had
been well controlled with divalproex for a number of years.
However, he continued to demonstrate flat affect, slowed
speech, and apparent thought-blocking, with long response
latencies. Nine months prior to his current admission, di-valproex was replaced with topiramate (since the patient re-
mained seizure free and had gained a considerable amount
of weight on divalproex). The psychiatric history of the pa-
tients family was remarkable for his mothers depression
and his fathers history of psychotic episodes. His educa-
tional history was notable for receiving special education
during high school but nevertheless graduating. Other than
the aforementioned seizure disorder, his medical history was
remarkable only for a benign heart murmur. He had no sub-
stance abuse history.
The patient presented to the team in an apparent altered
state of consciousness. His verbal responses were delayed,
appearing abulic, and he ritualistically stared into the dis-
tance, often with three to ten beats of eyelid flutter, accom-
panied by covering of his eyes with his hands. His speech
was hypophonic, slowed, and devoid of prosody. His stated
mood was sad, confused, and scared, and his affect was
severely blunted. He endorsed difficulty sleeping, anhedo-
nia, depleted energy, poor appetite, and difficulty concen-
trating, and he reportedly was unable to carry out activities
of daily living. His thought processing was tangential, and
he responded to questions or followed simple instructions
only after some latency. He endorsed auditory hallucina-
tions of voices that said Dont do it, and reported bifrontal
headaches concurrent with these hallucinations. He was un-
able to provide an interpretation for his auditory hallucina-
tions. His insight was poor, stating the reason for his admis-
sion to be restlessness.
Physical exam was notable for truncal obesity with de-
creased muscle mass in arms and legs bilaterally. A 2/6 sys-
tolic ejection murmur was corroborated. The elemental neu-
rologic exam was normal except for bilateral slowness in
rapid alternating movement with sluggish fine motor move-
ment, and a slowed, unstable gate, with difficulty in tan-
dem walking. Laboratory values were all within normal lim-
its. Medications (all by mouth) at the time of the consult
were: topiramate, 75 mg daily; fluoxetine, 20 mg daily; clon-
azepam, 1 mg twice daily; risperidone, 2 mg at bedtime;
and benztropine, 1 mg twice daily. A routine sleep-wake
EEG was read as normal. However, based on the patientshallucinations and thought disorder, appearance of possible
stereotopies, and distant history of epileptiform activity co-
incident with psychotic symptoms, the NBN service ordered
48-hour EEG telemetry. An MRI with contrast was also ob-
tained with thin slices through the hypothalamus and pi-
tuitary in order to rule out lesions that could be associated
with Cushingoid signs and symptoms. The MRI and cortisol
and magnesium levels were normal. During the two-day am-
bulatory EEG recording, there occurred approximately 700
automated interictal epileptiform detections, most of which
showed either 1 to 3 second bursts of bifrontal 1315 Hz ac-
tivity or right-greater-than-left independent or occasionally
synchronous temporal sharp waves and spikes (Figure 1).No definite ictal patterns were detected.
Since unequivocal seizure behavior was not witnessed,
and telemetry EEG recordings did not detect definite ictal
patterns, epileptiform activity as the antecedent cause for
the patients psychotic states remained speculative. How-
ever, the patient had a number of risk factors for develop-
ment of psychosis associated with epilepsy: early onset of
a seizure disorder, a positive family history for psychosis,
and borderline intellectual functioning.46 Based on psychi-
atric evaluation, neurologic observation, and a thorough
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134 Cunningham et al.Harv Rev Psychiatry
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FIGURE 1. Abnormal telemetry EEG tracing with bifrontal polyspike bursts and bitemporal sharp waves in this 25-year-old man with
stereotypies and psychosis.
neuropsychiatric history, interictal psychosis remained adistinct possibility as a contributor to the patients presen-
tation.
The team recommended discontinuing topiramate and
placing the patient on extended-release divalproex in or-
der to minimize side effects (particularly weight gain) and
eliminate the possibility of topiramate neurotoxitya rec-
ommendation that took into account that the patient had
a history of successful control of seizures with the stan-
dard formulation of divalproex. The NBN team also recom-
mended neuropsychological testing to better quantify cogni-
tive strengths and weaknesses, and to better characterize
psychiatric signs. Upon discharge five days later, the pa-
tients psychotic symptoms had disappeared. The patientcontinued to exhibitpeculiar mannerisms, including delayed
verbal responses and occasional eyelid fluttering, but with
decreased frequency. The patient also remained somewhat
anhedonic and melancholicwhich was likely associated
with a superimposed grief reaction or a persisting mood
disorder.
This case illustrates the teams proactive approach re-
sulting in the discovery of persisting abnormal EEG activity.
Although these readings were considered epileptiform in na-
ture, the patient did not meet criteria for a seizure disorder.
Had an ambulatory EEG not been ordered, epileptiform ac-tivity contributing to the patients psychiatric symptoms
may not have been suspected in light of the patients routine
EEG, which has been normal. The patient would likely have
received only psychotropic medications targeting his psy-
chiatric symptoms and would not have been administered
the antiseizure agent, which quickly resulted in marked im-
provement. In addition, the team consolidated the patients
history, psychiatric symptoms, and electroencephalographic
findings while incorporating psychopharmacological exper-
tise into a formulation and treatment plan that provided eti-
ologic insight and guidance to the patients treatment team.
Vignette 2
A 41-year-old single woman was admitted to McLean Hospi-
tal with new onset of auditory and visual hallucinations. The
NBN service was asked to rule out a neurologic cause for her
psychosis. After terminating a long-standing and volatile
relationship, the patient found herself homeless and un-
employed. As a result, her mood deteriorated, and she ex-
perienced suicidal ideation in addition to her auditory and
visual hallucinations. Her auditory hallucinations included
a threatening voice that was derogatory and commanding
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Volume 14, Number 3 Cunningham et al. 135
her to kill herself. Her visual hallucinationscomprised shad-
ows taking the form of animal or human figures; they were
usually perceived in her peripheral vision (never within
her central fields) and disappeared upon attempts to look
directly at the shadows. The patient described occasional
episodes of binge drinking but did not endorse other recre-
ational drug use. She had experienced two events with po-
tential for being complicated by traumatic brain injury: first,
in childhood, with loss of consciousness for an unknown pe-
riod of time, and later, as a teenager, when involved in a
motor vehicle accident, also losing consciousness for an in-
determinate period. Neither event required hospitalization.
On review of systems she noted intermittent left arm tin-
gling and a recent episode of vertigo lasting several days
before spontaneously resolving. In addition, she complained
of intermittent difficulty in walking and described her gate
as feeling as though she were drunk. These episodes were
not associated with alcohol or drug use. Her psychiatric his-
tory was remarkable for a standing diagnosis of depression
with a significant anxiety component. She had attempted
suicideonce by cutting both wrists transversely. Medical his-
tory was remarkable for lower extremity cellulitis, lower ex-
tremity venous-stasis dermatitis, and chronic neck and low
back pain. Her family medical history was remarkable for
FIGURE 2. Axial T2 FLAIR MRI demonstrating bihemispheric subcortical white matter hyperintensities (arrows).
her father and one of her sisters with depression, another
sister with an anxiety disorder, and her mother dying of a
cerebral hemorrhage. Her medications at the time of the
consult were: trazodone, 50 mg each morning and 300 mg
at bedtime; clonazepam, 2 mg twice daily; fluoxetine, 80 mg
daily; penicillin for cellulitis; acetaminophen as needed for
back pain; and rofecoxib as needed for joint pain.
Thorough physical and neurologic exams were unreveal-
ing. On mental status exam, she endorsed neurovegetative
symptoms of depression, including suicidal ideation, and au-
ditory hallucinations as described above. She displayed in-
sight into her situation and understood that the voices were
hallucinations. Her language, memory, and executive func-
tion were intact. Her comportment was contextually appro-
priate. With a compelling history and curious temporal vari-
ability of neurologic signs, our team requested an MRI of the
brain (Figure 2).
Axial T2 FLAIR MRI revealed multiple focal subcortical
white matter hyperintensities. Although differential diagno-
sis for lesion etiology was broad (e.g., ischemia, metastatic
disease), a demyelinating process (e.g., multiple sclerosis
[MS]), was suggested by the overall clinical context, includ-
ing the patients report of periods of vertigo, ataxia, and
parasthesias. The patients depressive syndrome47 and her
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auditory hallucinations were also considered possible man-
ifestations of early MS. The NBN team alerted the patients
treatment team to this possibility and recommended a lum-
bar puncture to survey for abnormal cells, myelin basic pro-
tein, and oligoclonal bands. In the event that MS was diag-
nosed, administration of an interferon agent was suggested
as a possible intervention for her cognitive and behavioral
symptoms. In addition, the NBN service recommended re-
peating an MRI with contrast in one month to assess any
progression of the patients lesions. The service also rec-
ommended an EEG to rule out seizure foci as a source of
symptoms, and suggested reevaluation of the patients high
dosages of fluoxetine and trazodone as possible contributors
to her symptoms (e.g., parasthesias, vertigo, anxiety symp-
toms), particularly since inhibition of CYP 2D6 by fluoxe-
tine interferes with the metabolism of the active metabolite
of trazodone, mCPP, which could potentially result in unto-
ward side effects.
This patients psychiatric symptoms had overshadowed
her neurologic signs for an unknown period of time. Even soft
neurologic signs, however, are broughtto the forefront by the
NBN teams methodology, which in this case prompted stud-
ies that revealed pathology that may have played a signifi-
cant contributory role in the patientspsychiatric symptoms.
In the context of severe psychosocial stress and a depressive
syndrome, the patients neurologic signs could easily have
been overlooked or considered a form of somatization. But
the NBN consult led to the discovery of anatomic findings
consistent with a highly morbid, yet treatable, neurologic
disorder.
Vignette 3
A 53-year-old woman with a diagnostic history of complex
partial seizure disorder complicated by comorbid anxiety-
associated, psychogenic seizures self-admitted to McLean
Hospital with severe anxiety in the context of marital dis-
cord. She described worsening of her seizure disorder (now
averaging three seizures a week) and reported that intense
anxiety preceded each seizure. She explained that repeated
intrusive thoughts about an imminent seizure attack re-
sulted in an anxious state, which then seemed to culminatein an actual seizure. During these 5- to 15-minute events,
she would experience tunnel and blurred vision, and she
would place her hands to her head and often engage in loud
nonverbal utterances. She would frequently find herself in
another area of her house after the event. Postictally, she de-
scribed herself as being very lethargic. Her seizure disorder,
which started when she was two years of age, had been well
controlled by medication until puberty. Since her teens, how-
ever, these paroxysmal episodes have been more difficult to
manage.
Eight years prior, the patient underwent an epilepsy
presurgical evaluation (which included a neuropsychological
evaluation and surface EEG monitoring), which confirmed
complex partial seizures with secondary generalization. The
neuropsychological evaluation at that time suggested com-
promise of the dominant hemisphere and frontotemporal
lobe systems, perhaps consistent with a seizure disorder. The
patient displayed impairment on tests involving aspects of
attention, inhibition, psychomotor speed, and verbal and vi-
sual memory. It was suggested that episodic stress and anxi-
ety increased the patients susceptibility to seizures. Prior to
her evaluation by the NBN service, the patient had under-
gone CBT, which she reported was effective in controlling
her anxiety. Coincidentally, her seizure disorder improved
dramatically for about six months. However, due to a recent
increase in life stressors, including severe marital difficul-
ties, she was unable to use her cognitive-behavioral tech-
niques effectively, and she reported losing control of her
seizure disorder. The patient reported no substance abuse
history. Her family psychiatric history was noncontributory,
and her family medical history was remarkable for epilepsy
in several paternal family members.
At the time of her NBN consult, a new neuropsychological
evaluation revealed deficits in cognitive function associated
with the frontal region of the dominant hemisphere. These
deficits included inhibition of verbal responses and verbal
fluency, as well as secondary deficits (e.g., verbal learning,
memory) related to the mesial temporal region of the dom-
inant hemisphere. It was evident from the specificity and
lateralization of these findings that some of her cognitivedeficits were consistent with an epileptiform disorder. Nev-
ertheless, her high anxiety level, poor coping skills, and re-
ported ability to control some of her seizures by applying
cognitive-behavioral techniques were strongly suggestive of
a complex emotional contributor to the manifestation of her
seizures.
The teams assessment was that, although there ap-
peared to be a significant psychological component, the
patient likely suffered from a genuine complex partial
seizure disorder that was refractory. The extent to which
her seizures were emotionally driven nevertheless remained
unclear. The NBN service recommended a comprehensive
epilepsy workup, which led to a surgical evaluation, inwhich a deep electrode EEG study revealed bilateral foci
in the temporal lobes. Instead of proceeding with a surgi-
cal treatment, however, we initiated a trial of vagal nerve
stimulation (VNS, now also FDA approved for depression),
which was found to reduce her seizure frequency by ap-
proximately 30%. Based on results from neuropsycholog-
ical testing and psychiatric interview, CBT was resumed
in order to help her control the anxious states that ap-
peared to be associated with her seizures. Further, indi-
vidual psychotherapy was begun in order to address her
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poor coping skills, anxiety, and stressful marital situation.
This patient requested continued care by an NBN team
member, and within four monthswith continued dival-
proex (1500 mg at bedtime) and VNSseizure frequency
decreased to 12 events per week. In addition, her depres-
sion resolved, and significant improvement in her anxiety
was noted.
When contemplating this patient, it becomes evidentthat
the boundary between the patients psychogenic seizures
(psychiatric/functional component) and her documented
complex partial seizures (neurologic/organic component) is
indistinct. Psychosocial stressors appear to have played a
role in triggering both types of events, and both psychi-
atric (e.g., CBT) and neurologic (e.g., antiseizure medica-
tions and VNS) interventions were effective in reducing
seizure episodes. Neuropsychological testing was helpful in
mapping brain areas that were likely involved, as well as in
providing insight as to the patients cognitive capability and
type of therapy most suitable in the context of her specific
neuropsychological impairment.
DISCUSSION
A continental drift has occurred between neurology and
psychiatrytwo bodies of knowledge that, although hav-
ing distinct virtues and resources, actually originated from
the same land mass. Perhaps it was first necessary to drift
apart in order to develop a certain sophistication in each
field. For example, had psychological psychiatry not beenexplored, the effective modes of intervention still in use
today might not have been formulated. But the costs
polarization and indoctrinationwere significant. Never-
theless, with the continuing maturation of neuroscience, it is
clear that there is a neurology of psychiatry and also a psy-
chiatry of neurologywith the consequence that the bound-
aries between these two disciplines are becoming more and
more difficult to delineate.
A proposed restructuring of neurology and psychiatry
training would include both more formalized instruction in
related foundation sciences and cross-training in behavioral
and neurologic medicine.15 In many residency programs,
cross-training is currently deficient. Psychiatry training pro-grams do not typically emphasize the importance of the
many neurologic diseases that can manifest with psychiatric
symptoms; few programs require their residents to become
proficient in conducting a thorough neurologic exam, read-
ing neuroimaging studies, or interpreting EEGs; and the
value of appropriate neuropsychological testing and its in-
terpretation seems marginalized. Likewise, most neurology
programs do not require proficiency in diagnostic psychi-
atric evaluation, psychopharmacology, psychosocial consid-
erations and intervention, and neuropsychological testing.
The construction of a subspecialty in Behavioral Neurology
and Neuropsychiatrythrough the combined efforts of the
American Neuropsychiatric Association and the Society for
Behavioral and Cognitive Neurology, under the auspices of
the United Council for Neurologic Subspecialtiesis a de-
cisive step toward eliminating the shortcomings of training
in the respective fields.
Here, we do not propose that the fields of neurology and
psychiatry merge, and we do not advocate that psychiatry
should increasingly focus on biology to the exclusion of psy-
chologically based techniques. Rather, we propose that a cer-
tain coalescence of disciplines is necessary in order to pro-
vide comprehensive care for the complex neuropsychiatric
patient. Residents and medical students alike are becoming
mindful of this unmet need and are increasingly express-
ing interest for more integrated training in neurology and
psychiatry. In Table 2, we propose areas of extended train-
ing that could reasonably and appropriately complement the
knowledge base of modern practitioners of medicine of the
central nervous system.
The proposed means of supplementing psychiatry and
neurology training, while raising the bar of mastery for
trainees in these disciplines, nevertheless remain realis-
tic. Moreover, they align with both the core curriculum
for fellowship training and the fund of knowledge required
for board certification in Behavioral Neurology and Neu-
ropsychiatry. Wepredict that neurologists and psychiatrists
clinical repertoires will need to expand in response to, and
parallel with, emerging neuroscience. For sufficient grasp of
the relevant pathophysiology, psychiatrists will need to betrained in emerging principles of behavioral neuroanatomy
underlying the affective- and thought-disorder phenomenol-
ogy that they already study, and neurologists will need to
be trained in the psychiatric phenomenology now recog-
nized as attributable to normal and abnormal neuroanatom-
ical function. Emerging neuroscience will, in effect, require
cross-training such as that embodied in McLean Hospitals
NBN service.
In this article we have described a multidisciplinary team
whose members, for more than a decade, have worked to-
gether to provide comprehensive evaluations of patients
with comorbid neurologic and psychiatric disease. The clerk-
ship that has spun out of the NBN service has implementedwhat has been described, in theory, by Eisenberg, Kandel,
Martin, Price, and othersproof that an integrated clinical
experience is both feasible and valuable. Such clerkships
are essential in developing a framework for education de-
signed to train practitioners comprehensively in neurology,
psychiatry, and neuropsychology, while also recognizing the
expertise and focus that each field independently offers. We
offer this model for further discussion and development, and
with the hope that it will also help expedite similar attempts
in other settings.
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TABLE 2. Proposed Areas of Extended Training for Modern CNS Physicians
Psychiatry Neurology
Disorders Seizure disorders, e.g., TLENeurodegenerative disorders, e.g., AD, FTLD, HD, LBD, PD
Movement disorders
Amyotrophic lateral sclerosis
Multiple sclerosis
Traumatic brain injury
Headache
Hydrocephalus
Neoplastic disorders
Cerebrovascular disorders
Delirium and confusional states
Toxic exposures
CNS infections, e.g., HIV, neurosyphilis, Lyme, herpes,
prion disease, viral encephalitides
Cognitive disorders, e.g., aphasias, memory disorders
Somatoform disordersMalingering and factitious disorders
Formal thought disorders
Mood disorders
Anxiety disorders
Impulse control disorders
Attention-deficit disorders
Developmental disorders, e.g., PDD, autism,
mental retardation, Aspergers
syndrome
Personality disorders
Toxic exposures
Addiction and substance abuse
Skills/fund of
knowledge
EEG interpretation
Psychodiagnostics
Neurocognitive/mental status exam
Functional neuroanatomy
Neuropsychological testing
Neurodevelopment
Neurorehabilitation
Cognitive neuroscience
Neuroimaging (MRI, CT, PET/SPECT)
Neurologic exam, including the fundoscopic exam
Psychopharmacology
Psychodiagnostics
Neurocognitive/mental status exam
Functional neuroanatomy
Neuropsychological testing
Neurodevelopment
Neurorehabilitation
Cognitive neuroscience
Geriatric care
Genetics/epidemiology of psychiatric diseases
Electroconvulsive therapy
AD, Alzheimers disease; FTLD, frontotemporal lobar dementia; HD, Huntingtons disease; LBD, Lewy body disease; NVLD, nonverbal
learning disorder, PD, Parkinsons disease; PDD, pervasive developmental disorder; TLE, temporal lobe epilepsy=
partial complex seizures.
In addition to the aforementioned benefits, we see the
strengths of our model as including the purposeful slowing
down of patient volume in favor of in-depth examinations
of a more limited number of complex patients. (To compen-
sate, other consultants will deal with simpler cases and, by
design, maintain a rapid response time.) Our model empha-
sizes case-based teaching with an interdisciplinary team
approach; the involvement of senior faculty who directly
observe, and are accountable for, students and residents;
and trainee exposure to the critical thinking, problem solv-
ing, and lifelong learning required for the effective practiceof mind/brain medicine. The proposed model offers cross-
training in neurology, neuropsychology, and psychiatry for
our residents, medical students, and fellows in Neuropsy-
chiatry and Behavioral Neurology, as well as for established
practitionerswho are drawn to this model. The patients seen
by the NBN team receive simultaneous evaluations across
disciplines with real-time communication and formulations,
as opposed to separate evaluations by individual special-
ists that may be separated temporally by days, weeks, or
months. This approach holds promise as being more cost-
effective and time-efficient since diagnosis and treatment
can be improved and expedited. A case in point is presented
in the first vignette. Prior to his NBN consult, the patient
underwent several months of evaluations by numerous spe-
cialists without a unified synthesis of his symptoms and di-
agnostic test results. By contrast, the NBN team consoli-
dated existing data with current evaluations and diagnostic
data into a working diagnosis and treatment plan within
the time constraints of a single hospitalization (i.e., five
days).The limitations to our model are primarily fiscal. In
the absence of proof that our integrated, multidisciplinary
team approach ultimately increases efficiency, this approach
will be perceived as economically inefficient. Furthermore,
there is little incentive for faculty to involve themselves
in such labor-intensive teaching endeavors. We need to
establish better mechanisms for supporting and reward-
ing senior clinical facultyincluding protected time, pro-
motional merit, and financial opportunities with equitable
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Volume 14, Number 3 Cunningham et al. 139
compensation. As we move forward, we should formulate an
even clearer definition of our curriculum, with overarching
goals that emphasize outcomes, cognitive rehabilitation, and
neuropsychology. We realize, too, that this model may not be
easily generalized. We offer it for itsheuristic value and hope
that it may be subject to further evaluation, revision, and
innovation.
We live in exciting times. We are gaining theability to un-
derstand thebiology of a memory, of a thought, of an emotion.
This knowledge will surely improve our ability to treat pro-
found and debilitating dysfunctions of the central nervous
system. It could invigorate the exploration of mind,48 posi-
tioning psychotherapy as potentially one of the most elegant
forms of noninvasive neurosurgery, through which neural
circuits could be modified and reconstructed. Yet even as we
face a future with its ever expanding arsenal of technology,
we must also, as Dean Joseph Martin asks, proceed with
humility.16 Indeed, the lack of humility, the seduction of ar-
rogance, and defiant ego defense have been our enemies, and
stood in our way, for decades. By recognizing areas in need of
improvement, by encouraging creative, open thinking, and
by promoting innovative training and committed leadership,
we will be further empowered in our ability to heal.
An earlier version of this manuscript was previously presented at
the FebruaryMarch 2005 meeting of the American Neuropsychia-
try Association in Bal Harbour, Florida.
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