Coalescence of Psychiatry Neurology and Neuropsychology From Theory to Practice. 2006 (1)

7/29/2019 Coalescence of Psychiatry Neurology and Neuropsychology From Theory to Practice. 2006 (1)

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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:

[email protected]

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

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128 Cunningham et al.Harv Rev Psychiatry

May/June 2006

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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May/June 2006

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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Harv Rev Psychiatry


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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May/June 2006

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


9/15

Harv Rev Psychiatry


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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May/June 2006

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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Harv Rev Psychiatry


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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May/June 2006

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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Harv Rev Psychiatry


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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