See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/237622208

Best Practice Guidelines for COGNITIVE REHABILITATION FOR PEOPLE WITH

SERIOUS MENTAL ILLNESS

Article

CITATIONS READS

2 124

2 authors, including:

Jason Peer
U.S. Department of Veterans Affairs
22 PUBLICATIONS   943 CITATIONS   

SEE PROFILE

All content following this page was uploaded by Jason Peer on 08 April 2015.

The user has requested enhancement of the downloaded file.

 Best Practice Guidelines for
COGNITIVE REHABILITATION FOR PEOPLE WITH SERIOUS
MENTAL ILLNESS

Developed by Myla Browne, Jason Peer and Will Spaulding

University of Nebraska - Lincoln

Developed for
Behavioral Health Recovery Management Project
An Initiative of Fayette Companies, Peoria, IL;
Chestnut Health Systems, Bloomington, IL;
and the University of Chicago Center for Psychiatric Rehabilitation
The project is funded by the Illinois Department of Human Services’
Office of Alcoholism and Substance Abuse.

Authors:
Myla Browne, M.A. is a graduate student in clinical psychology at the University of
Nebraska-Lincoln. The focus of her research and clinical work is in the area of the
rehabilitation of the severely and persistently mentally ill. She has participated in
research on the innovative cognitive rehabilitation technique of shaping procedures
integrated with modular skills training to increase attention spans and has co-authored a
book chapter entitiled "Cognitive-Behavioural Therapies in Psychiatric Rehabilitation".

Jason Peer, M.A. is a graduate student in clinical psychology at the University of

Nebraska-Lincoln. His research and clinical interests are in the area of the rehabilitation
of persons with severe and persistent mental illness. Specific research interests include
investigating how neurocognitive and social cognitive variables impact response to
rehabilitation interventions and how these variables may interact with clinical variables in
this population.

Will Spaulding, Ph.D. is professor of psychology, University of Nebraska - Lincoln, and

a consulting psychologist with the Community Transition Program, Lincoln Regional
Center. His interests include the clinical and experimental psychopathology of severe
and disabling mental illness, psychiatric rehabilitation, cognitive and neurocognitive
assessment and treatment, mental health policy and service provision for severe mental
illness.

1
 Theoretical Rationale for Cognitive Rehabilitation

There is little doubt that neurocognitive recovery occurs in people with severe
mental illness. At least since the 1970's specific interventions, ranging from practice on
laboratory tasks to comprehensive rehabilitation approaches, have shown that specific
aspects of performance can improve (Corrigan & Storzbach, 1993; Spaulding, Storms,
Goodrich, & Sullivan, 1986; Storzbach & Corrigan, 1996). Much of this improvement
may be attributable to recovery from acute psychosis, and this part of the recovery
process is increasingly subjected to systematic analysis (Olbrich, Kirsch, Pfeiffer, &
Mussgay, 2001; Spaulding, Fleming et al., 1999). However, in many individuals
significant cognitive impairment persists after other indications of acute psychosis are
resolved. Some of these post-acute impairments respond to psychosocial interventions
directed at the neurocognitive level of functioning. As of this writing there are 3 large
scale controlled clinical trials (Bell, Bryson, Greig, Corcoran, & Wexler, 2001; Hogarty
& Flesher, 1999; Spaulding, Reed, Sullivan, Richardson, & Weiler, 1999) showing that
interventions that explicitly target neurocognitive functioning contribute uniquely and
importantly to rehabilitation progress. The pressing research question is no longer
"whether" but "when" and "for whom."
The term 'cognition' can refer to any and all of the brain's information processing
activity, from the most elemental sensory processes to the most complex levels of
thought. Cognition thus spans a broad continuum of levels of organization. If it were
possible to divide this continuum in half, with the more molecular levels of cognition in
one half and the more molar levels in another, the more molecular category would be
neurocognition. The prefix neuro- is added to indicate a closer, more isomorphic
relationship between specific neurological structures and processes and the specific types
of cognitive activity they support.1 For example, the cognitive process of visual feature
detection, which allows us to perceive the boundaries of objects in our visual field, is a
relatively molecular process closely associated with specific neurons in the retina, optic
tract and various brain structures. Manipulation of spatial relations is a more molar
cognitive process, by which we use visual feature information to track and manipulate
objects in space. This involves a greater number of neurons distributed more widely
across the brain, but it still falls within the neurocognitive continuum. Other processes
generally included in the neurocognitive continuum include simple problem solving,
memory storage and retrieval, concept formation, organization and execution of
behavioral responses, and elemental language processes. These involve widely
distributed, but still identifiable, neurological structures and processes. Complex
language and problem solving, abstract reasoning, formation of beliefs, attitudes and
complex habits, generally fall outside the neurocognitive continuum, and for present
purposes are categorized as social cognition.

1
In psychology, isomorphic relationships are generally one-to-one correspondences between the function
of a particular brain structure and a particular behavior or type of behavior.

2
 Neurocognitive Impairments in Serious Mental Illness

Abnormalities are found in schizophrenia at all levels of the cognitive system and
in all phases in the course of the disorder. Cognitive impairments are thought to play a
number of roles in schizophrenia’s etiology and expression (Cromwell & Spaulding,
1978; Nuechterlein & Dawson, 1984; Nuechterlein & Asarnow, 1989). Green and
Nuechterlein (1999) state that schizophrenia is now seen by many clinicians as essentially
neurocognitive in nature due to findings that deficits in such areas as attention and verbal
learning have been found to be related to the etiology of the disorder as well as to
functional outcome. It is therefore an appealing hypothesis that remediation of such
impairments might lead to improvements in personal and social functioning. Many
classical treatment approaches in psychiatry have attempted to address cognitive
impairments in schizophrenia, but systematic specification of procedures and evaluation
of outcome began in the cognitive-behavioral era.
Present day research is gradually overcoming the historical barriers to
understanding the discrete nature of neurocognitive impairments in mental illness, but the
picture is far from complete. The next few years will probably see substantial progress,
and perhaps revision of current organizational schemes. For the time being, however,
there is reasonable consensus in the neuropsychological and psychopathological
communities about a few relevant principles:
1. Global neurocognitive impairment is ubiquitous in mental illness, but covers the
complete range of severity across individuals;
2. Impairments in executive functioning, which include concept manipulation,
response planning and organization and working memory, are also ubiquitous,
and are somewhat independent of global impairments;
3. Impairments in verbal and nonverbal memory are also common, and somewhat
independent of global impairment;
4. Many people with disabling mental illness have individually unique constellations
of neurocognitive abnormalities, including various combinations of impairments
in executive, memory, sensorimotor, perceptual and other functions.

A Three Factor Model of Neurocognitive Impairment

The episodic and qualitative dimensions of neurocognitive impairment can be

integrated into a 3-factor model that is heuristically useful for clinical assessment and
rehabilitation planning (Spaulding et al., 1994). It is important to remember that factors
are sources of variance, and not types or categories. In the present context, a 3-factor
model describes ways that individuals are different from each other, within the population
of people with severe mental illness. An individual may occupy any point along the
quantitative dimensions that the factors define.

Pervasive Impairment Factor: The first factor of neurocognitive impairment is pervasive,

meaning a broad range of specific processes spanning the molar-molecular continuum are
affected. In this sense, the first factor is somewhat like the concept of intelligence, in that
it reflects a person's overall adaptability and behavioral functioning. Unlike intelligence,
however, first factor impairment is not equally distributed across all neurocognitive

3
processes.2 Some appear to be more affected than others. Research does not yet allow
confident conclusions about what areas are most affected by first factor impairment, but
executive processes appear to be especially vulnerable. Impairments in concept
formation, planning, complex problem solving and working memory appear to be
especially common. This is reflected in neuropsychological test findings, and it is also
consistent with neurodevelopmental models of etiology that emphasize malformation of
limbic-frontal activation pathways. Executive processes involve many brain areas and
mechanisms, but limbic and frontal cortex are especially heavily involved.
The first factor is by definition a treatment refractory factor. Science and
technology do not currently provide the means to correct structural problems in brain
development. Even deficits in acquired abilities may not be treatable if acquisition is
constrained to developmental windows. If an impairment improves, then it is not a first
factor impairment. However, first factor impairment can certainly get worse over time,
as in the Kraepelinian view of schizophrenia. Whether by accumulation of impairments
associated with acute psychosis, or some other progressive neurophysiological factor,
some individuals' first factor impairment may worsen over time despite all efforts to
prevent it.

Episode-Linked Impairment Factor: The second factor in the 3-factor model is an

episodic factor. Baseline neurocognitive impairment worsens, and new impairments
appear, during acute psychosis. Thus, an alternative term for second factor impairment is
episode-linked impairment. Presumably, episode-linked impairments reflect a cascade of
events originating with neurophysiological dysregulation. There is considerable
individual variation in how neurocognition changes over the course of an episode. High
levels of first factor impairment may obscure the second factor, because detection of the
second factor requires relatively good test performance at some point in time. There is
some evidence that the executive domain is differentially affected by the second factor, at
least in individuals with little first factor impairment. As previously discussed, some
processes at the molecular end of the neurocognitive spectrum appear to be distinctly
invulnerable to acute psychosis.

Post-Acute Recovery Factor: The third factor in the 3-factor model is a post-acute
recovery factor. Its existence is supported by the clinical observation that some
individuals require more time than others to regain baseline functioning in the wake of a
psychotic episode. It is further evidenced in the finding that people sometimes
experience slow but significant improvement in personal and social functioning over
protracted periods of neurophysiological stability, suggesting this improvement is made
possible (at least in part) by improved neurocognitive functioning. The most important
evidence for a post-acute recovery factor in neurocognition comes from studies of direct
treatment of neurocognitive impairment, using environmental or psychological
interventions. A number of interventions, ranging from a highly structured therapeutic

2
Intelligence is equally distributed by design; i.e. psychometric definitions of intelligence assume that the
average level of performance within any particular subdomain is "normal" for that domain. This is
arbitrary in a sense, but to the degree that a subdomain of intelligence corresponds to specific
neurocognitive processes, it provides a standard by which the relative severity of impairments in
neurocognitive processes can be quantitatively characterized.

4
milieu to training and practice on laboratory tasks, appear to bring about improvements in
neurocognitive functioning, especially in the executive domain. Improvement on
laboratory tasks can be explained away as the result of ordinary learning, but more
generalized changes, or changes in response to a therapeutic milieu, are more feasibly
explained as acceleration of a natural recovery process that for some individuals is so
slow as to be indiscernible.

Mechanisms of Post-Acute Recovery

At least three mechanisms have been proposed to explain how post-acute
recovery could be influenced by environmental manipulations or psychological
interventions. The first is a conventional learning process, wherein the affected
individual learns "microskills" that help compensate for deficits in other areas. For
example, to compensate for deficits in sustained attention and vigilance, a person might
learn to take frequent breaks, use self-talk as a cue to pay attention, and avoid situations
where attentional deficits are especially detrimental.3 The second mechanism involves a
behavioral response organization process thought to be supported by dopaminergic
neuronal subsystems in the limbic system, basal ganglia and primitive frontal cortex.
This mechanism monitors the environment and organizes the person's behavioral
repertoire to most efficiently meet environmental demands. The mechanism is
temporarily disabled in the dopaminergic firestorm of an acute psychotic episode. After
the episode is neurophysiologically resolved, experience with the environment over time
is required to reorganize the behavioral repertoire. The structure of a therapeutic milieu
or a psychological intervention condenses the environmental factors that reorganize the
repertoire, and so behavioral functioning shows more rapid improvement. The third
explanatory mechanism is neuroendocrine. A loss of the activating effects of the stress
hormone cortisol appears to be associated with chronic mental illness. Cortisol acts
directly upon cortical neurons to mediate cognitive activity. The predictable routines of a
therapeutic milieu may help reestablish cortisol rhythms and enhance cortical activation.

Assessment of Neurocognitve Impairment

The 3-factor model elucidates the important questions to be raised about

neurocognition in the context of rehabilitation:

1. Is the person's current functioning and recovery potential limited by second factor
neurocognitive impairment, i.e. impairment that would be reduced or eliminated
by resolution of a psychotic episode?
2. Is the person's current functioning and recovery potential limited by third factor
neurocognitive impairment, i.e. impairment residual to psychosis that would be
reduced or eliminated by a structured milieu and/or psychological interventions?
3. Is the person's current functioning and recovery potential limited by first factor
neurocognitive impairment, i.e. baseline impairment that will not respond to any

3
This is arguably not really a model of post-acute recovery, as one could learn compensatory skills any
time, not just in the post-acute phase. On the other hand, baseline deficits tend to appear in the wake of
acute episodes, so the post-acute phase would be the period in which the preponderance of such learning
would take place.

5
 available treatment, and if so what must be done to minimize the impact of the
impairment?

Assessment and intervention at the neurocognitive level are organized by these questions.

The rehabilitation team's hypotheses about the acute, post-acute or baseline status
of a recovering person's neurocognitive impairments have straightforward implications
for intervention. Baseline impairments, being refractory to all known technologies for
improvement, require compensatory strategies and environmental prosthetics. The
permanence of baseline impairments gives special importance to the particular pattern of
the person's neurocognitive strengths and weaknesses, and so they must be articulated in
detail. Acute and post-acute impairments demand trials of corrective interventions.
Treatment of acute neurocognitive impairment is essentially treatment of acute psychosis.
Post-acute impairments can be addressed with combinations of therapeutic milieu and
specialized individual- and group-format therapies.

Assessment of Pervasive Impairment

Instruments for comprehensive assessment of intellectual functioning, e.g. the

WAIS III, are useful for assessing the severity of first factor impairment. Overall
summative test scores such as a WAIS IQ provide useful information about the rate at
which a person can acquire new skills, a central concern in rehabilitation. Similarly, a
WAIS IQ contributes to formulation of general expectations about the nature of a
person's functioning after maximal recovery. The pattern of WAIS subtest scores also
provides a picture of the individual's relative strengths and weaknesses. In this particular
sense, pervasive baseline neurocognitive impairment, as measured by IQ tests, is
comparable to the concept of intelligence. However, IQ's and subtest patterns do not
provide sufficient measurement of executive dysfunction and related impairments
associated with hypofrontality. Assessment of baseline impairment should therefore
routinely include additional instruments to measure frontocortical functioning. There is
no generally accepted battery for this purpose, especially for assessment of severe mental
illness. New instruments are currently being developed at a rapid pace, so practically any
recommendation in this regard may be quickly dated. Generally speaking, however, a
reasonably complete battery for assessment of frontal functioning should at least include
measures of concept formation and manipulation, working memory, inhibitory
functioning and simple problem solving. Neuropsychological instruments often used to
assess hypofrontality in mental illness include the Wisconsin Card Sorting Task, verbal
fluency tasks (thought to measure inhibitory functions), Trailmaking, Halstead Categories
and backward digit span (thought to measure working memory). The next few years will
probably see development of instruments and batteries specialized for measuring baseline
hypofrontality in severe mental illness.
Indications of additional, discrete neurocognitive impairments in the residual
phase may necessitate further assessment. Such indications may include a history of head
trauma, significant variability across WAIS subtests and/or measures of hypofrontality,
behavior indicative of memory failure, or difficulties in behavioral performance that are
not accounted for by low IQ or executive dysfunction. At this point, assessment becomes

6
indistinguishable from traditional neuropsychological assessment, the primary purpose
being to develop a complete profile of the recovering person's neurocognitive strengths
and weaknesses. The consulting services of a traditional neuropsychologist should be
available to the rehabilitation team, as the assessment of individual constellations of
impairments, and their functional implications, requires skills different from those usually
required of rehabilitation professionals.
Theoretically, first factor cognitive impairment is not subject to change, so its
assessment is not directly relevant to evaluating rehabilitation progress. Nevertheless,
progress must be continually interpreted in light of what is known about baseline
impairment. A rate of progress slower than that predicted by baseline impairment may
indicate that other, undetected factors are creating barriers. A rate of progress faster than
that predicted by baseline impairment may indicate that the impairment wasn't really
baseline, which in turn suggests that the recovering person was not in a fully stable
residual state when assessed. This may mean the person is experiencing undetected
fluctuations, possibly undetected psychotic episodes. This would be corroborated by a
change in test performance during ostensibly stable periods. Little is known about the
prospects for long-term improvement in cognitive functioning in mental illness, so
nothing can be taken for granted in this regard. Periodic reassessment of baseline
neurocognitive functioning is necessary to prevent mistaking slowly improving
impairments for permanent ones.

Assessment of Episode-Linked Impairment

The purpose of second factor assessment, determining the consequences of

episode-linked impairment for other aspects of rehabilitation, is essential to efficiency
and timely progress. Episode-linked impairment may severely compromise response to
an array of rehabilitation modalities, especially those involving acquisition of new skills.
It may be a waste of time and resources, and a needless stress on the recovering person,
to attempt some rehabilitation activities while episode-linked impairments are active. At
the same time, many individuals do not experience severe changes in neurocognition
during acute psychosis. Some rehabilitation activities are amenable to modification in
order to compensate for neurocognitive impairments, and this may be a better option than
postponement for some individuals. The severity and nature of episode-linked
impairment must be individually assessed to determine its immediate implications for
rehabilitation.
The episode-linked neurocognitive impairments most likely to interfere with
rehabilitation interventions are gross disruption of continuous attention and vigilance.
The behavioral consequences are readily observable when the impairments are especially
severe; people are unable to attend to even simple tasks or function in skill training
groups. As resolution of the episode progresses, it may be more difficult to determine
how much behavioral performance is being compromised by these impairments.
Abatement of extreme agitation and anxiety may make a person appear more able to
attend, when in fact attentional impairment continues to be severe. Simple laboratory
measures such as the Continuous Performance Task (CPT) provide quantitative
measurement of continuous attention and vigilance, and are probably not greatly affected
by practice. Repeated use of such measures is thus a useful adjunct to the traditional

7
means of evaluating resolution of psychosis, such as behavioral observation and
structured interviews.

Assessment of Post-Acute Impairment

Little is known about the nature of post-acute neurocognitive impairment. All

indications are that it is qualitatively similar to episode-linked impairment, and indeed
may be produced by the same etiological processes. Treatments directed at
neurocognitive impairment appear to exert their most definitive effects in the executive
domain. Therefore, the transition from post-acute to residual is generally characterized
by a differential improvement in executive cognition, relative to other domains. The
WCST, Halstead Categories and tests of verbal learning have proven sensitive indicators
of third factor neurocognitive recovery.

Neurocognitive Interventions

In the first large scale controlled trial of neurocognitive intervention (Spaulding,

Reed et al, 1999) it was clear that the intervention produced better progress in social
functioning, compared to intensive, comprehensive rehabilitation without the
neurocognitive intervention. However, all the participants in the study showed
substantial improvement in their neurocognitive functioning, whether they received the
explicitly neurocognitive treatment or not. In fact, the degree of improvement was
substantially greater than the additional improvement added by the neurocognitive
intervention. This was unexpected, as previous studies had shown little or no
neurocognitive improvement associated with conventional treatment or rehabilitation.
The only feasible explanation was that the extraordinarily intensive rehabilitation
program produced nonspecific neurocognitive benefits that less intensive programs do
not produce. A complete model of neurocognitive treatment effects thus needs to explain
the nonspecific benefits of comprehensive rehabilitation, in addition to the specific
benefits of explicitly neurocognitive treatment.
Neurocognitive interventions include specific procedures for activating and
exercising the executive microskills associated with performance microskills relevant to
rehabilitation. The nonspecific treatment effects of the intensive rehabilitation milieu
accrue from its demand for and reinforcement of the executive microskills associated
with performing activities of routine daily functioning, (e.g. self-care, being at the right
place at the right time, responding to other people).
The model of neurocognitive failure and recovery in mental illness described
above generates some general principles for constructing a treatment strategy:
1. Recovery of executive and memory functions, which mediates subsequent
recovery of personal and social functioning, is enhanced by an environment rich
in salient reinforcing events, with clear and consistent relationships between
individual behaviors and their environmental antecedents and consequences, and
where behavior associated with appropriate attention to routine environmental
demands is heavily and differentially reinforced.

8
 2. Recovery of the neurocognitive abilities that support basic social and
interpersonal functioning is enhanced by an environment that provides frequent
opportunities and support for appropriate social behavior, with consistent and
perceptible reinforcement of effective and/or appropriate behavior and minimal
inadvertent reinforcement of ineffective or inappropriate behavior. The relatively
nonspecific effects of an orderly, consistent, prosocial and contingency-rich
environment are further enhanced by specific interventions that explicitly invoke
the neurocognitive microskills that underlie performance of social and
interpersonal skills.
3. The relatively nonspecific effects of an orderly, consistent, prosocial and
contingency-rich environment are further enhanced by specific interventions that
explicitly invoke the neurocognitive microskills that underlie performance of
social and interpersonal skills.
4. For both specific and nonspecific interventions, the ability to identify specific
situations requiring specific microskills, and to allocate resources to perform
those microskills, are as important as performance of the microskills themselves.
Exercising the ability to recognize various task demands, and to modify one's
cognition (i.e. activation of microskills) in response to changing demands, is as
important as exercising the ability to perform a particular skill.
5. Although executive and memory functioning mediate subsequent recovery, they
are not strict prerequisites. Identifying situational demands, allocating capacity
and activating the appropriate microskills are complex cognitive activities, some
of which are highly specific to particular situations and skills. As recovery
progresses, restoration of advanced executive functions may require intact
performance functions. This requires a cyclic rather than linear approach to
neurocognitive intervention. Exercise of fundamental microskills should be
preceded by exercise in detecting relevant situational demands, but treatment
should then address detection of more complex situations and demands, followed
by exercise of more complex skill performance, and so on.

Neurocognitive interventions can be understood to be of two types, those that

address post-acute impairments and those that address residual impairments. In the sense
that residual impairments are by definition not amenable to change, interventions for
residual impairments are generally prosthetic in nature. That is, they are designed to
compensate for the functional disabilities that the neurocognitive impairment produces,
rather than change the neurocognitive impairment itself. Interventions for post-acute
impairments are designed to facilitate recovery from the neurocognitive disorganization
that accompanies acute psychosis.

Interventions for Post-Acute Impairment

Nonspecific intervention for neurocognitive impairment in the later post-acute
phase is basically an extension of intervention in the earlier phase. Maximum
neurocognitive benefit is expected from comprehensive rehabilitation at the highest
intensity the recovering person can comfortably tolerate. Specific interventions enhance
the nonspecific benefits of intensive rehabilitation, and should be provided whenever
possible. For heuristic purposes, specific neurocognitive interventions can be categorized

9
as dyadic vs. group in format. The optimal format, or combination of formats, is
expected to be jointly determined by the needs and preferences of the individual
recipient, and the resources and capabilities of the mental health service system.
All specific interventions for neurocognitive impairment have in common some
procedure(s) for isolating hypothetical neurocognitive abilities ("microskills" in the terms
of this discussion) and "exercising" those abilities by engaging the recovering person in
activities designed to invoke their use.

Dyadic therapy techniques: The literature provides procedural descriptions of specific

techniques easily adapted to a dyadic psychotherapy-like format (e.g. Spaulding et al,
1986; Reed, Sullivan, Penn, Stuve, & Spaulding, 1992; Corrigan & Storzbach, 1996;
Medalia et al 1998; vanderGaag et al., 1994, Wykes, et al 1999; vanderGaag, 1992). In
this approach, exercises are constructed in an ad hoc manner, derived from the results of
laboratory testing, direct observation and functional assessment. Progress toward short-
term treatment goals is typically assessed with laboratory tasks adapted to measure the
specific impairments targeted for treatment. Generalization of treatment effects and
progress toward longer-term goals are assessed through measurement of changes in
performance of ecologically significant skills and abilities hypothesized to be affected by
the targeted cognitive impairments. For example, when performance in a work setting is
hypothesized to be compromised by distractibility and deficits in continuous attention,
improvement on laboratory measures of attention and vigilance is expected following
neurocognitive treatment, followed in turn by improvement on in vivo measures of work
performance. Multiple-baseline quasi-experimental designs capable of detecting the
separate effects of medication, neurocognitive treatment and other interventions are
generally well suited to this purpose.
Individualized neurocognitive treatment is usually provided by including the
specific exercises in a broader, dyadic rehabilitation counseling and psychotherapy
context. The exercises are accompanied by collaborative formulation of relevant
treatment and rehabilitation goals, discussion of the role of the abilities addressed by the
exercises in naturalistic settings, assignment and review of "homework" (in vivo
applications of the exercises), and review and evaluation of overall rehabilitation
progress. For example, "better interactions with people" may be identified as a treatment
goal. Functional and laboratory assessment may indicate that the problem derives from
social skill deficits, to which distractibility, poor interpersonal problem solving and a
rigid, stereotypic way of analyzing complex social situations all contribute (the
assessment would also indicate that these do not derive from a transient, acute psychotic
state). Exercises demanding focused attention, resistance to distraction, and conceptual
flexibility would be included in dyadic sessions, accompanied by interpersonal problem
solving and social skills training in group formats. In addition to the neurocognitive
exercises, the dyadic sessions include review of performance data in therapy and in vivo
situations, discussion of the role of neurocognitive factors in ongoing experiences
relevant to social competence and comfort, review of objective measures of social
performance, and appraisal of overall progress toward the goal.
In addition to a dyadic psychotherapy-like setting, individualized neurocognitive
exercises can be integrated with occupational and recreational therapy, work, and other

10
rehabilitative activities. The optimal setting varies with individual needs and
rehabilitation goals.

Group Formats: At least two comprehensive, systematic approaches to treatment of

neurocognitive impairments in schizophrenia have evolved over the past two decades,
Integrated Psychological Therapy (IPT; Brenner et al., 1994) and Cognitive Enhancement
Therapy (CET; Hogarty & Flesher, 1999a, 1999b). They share the strategy of
identifying, isolating and exercising specific cognitive abilities typically impaired in
chronic schizophrenia. They use somewhat similar procedures, including a diversity of
specific exercises, formatted as group activities, targeting specific abilities. Both
combine a primary focus on cognitive processes, i.e. emphasis on strengthening
information processing, with didactic provision of factual information, the content of
cognition, pertinent to personal and social functioning. Both are highly manualized, and
the IPT manual is commercially available (Brenner et al, 1994). There have been no
studies of therapist skills or qualifications required for effective provision of these
modalities. However, considerable clinical judgment is required to determine when to
persist with a particular exercise, when to provide special assistance to group members,
and when to move on. It is probable that considerable experience with
neuropsychological assessment, functional assessment and group skill training is
necessary.
There is arguably a theoretical difference between the two approaches. IPT was
developed from classical ideas in experimental psychopathology that predate
contemporary interest in distinctively social cognition. CET also draws heavily from
experimental psychopathology and neuropsychology, but in addition is heavily
influenced by developmental theories of social cognition. This theoretical difference
implies two different types of treatment effect mechanisms. In IPT, treatment effects are
thought to accrue in a stepwise fashion. Molecular cognitive processes are exercised
first, so that later those strengthened molecular processes can enhance acquisition of
more molar abilities. Therefore, the rehabilitation process progresses from process-
focused therapy to more conventional social skills and interpersonal problem solving
training.
CET is less linear and stepwise. It draws heavily on the theory that a crucial
problem in schizophrenia is deficient apprehension of the "gist" of social problems and
situations. "Gistful" social cognition is not a gradual compilation of information from
more molecular processes, e.g. the gradual synthesis of "the big picture" from
informational elements, but a rapid and conceptual apprehension. "The big picture" is
inferred from a relatively small amount of information about a situation, when that
information correlates with specific social schemata (declarative relationships, social
roles, procedural scripts, etc) stored in memory and acquired in the course of
development. The CET approach is guided by the hypothesis (among others) that
impairment of processes for identifying and using the "gist" of social situations and
interactions is a key limiting factor in schizophrenic social performance.
Both IPT and CET have been shown to be effective in enhancing social
competence and performance, in controlled outcome studies (Spaulding et al,199b;
Hogarty & Flesher, 1999b). So far, there is insufficient data to conclude whether the
mechanisms of their respective treatment effects are as different as their respective

11
theoretical premises. Indeed, the actual procedural differences between the two
approaches have yet to be systematically assessed.4 The subject samples in the two
studies were quite different (the IPT participants were severely disabled and involuntarily
institutionalized, while the CET participants were less severely disabled voluntary
outpatients), and any differences in outcome or treatment effect mechanisms are
potentially attributable to that. In addition to sheer severity of impairment, the two
samples could have been at different points in the continuum from "acute" to "post-acute"
to "residual." Systematic comparative studies of the two approaches, across a range of
subpopulations, will be necessary to sort this out.
The original developers of IPT recommend providing this modality separately to
recipients with higher and lower overall cognitive functioning. The therapy procedures
do not differ, but the rate of progress through the modality is expected to be slower with
lower-functioning groups. Comprehensive neuropsychological assessment is not
required for group assignment, but a reliable overall evaluation of baseline cognitive and
neurocognitive functioning, taking into account episodic psychosis, is necessary. Such
assessment capability should be in the repertoire of any program or agency that serves
people with severe and disabling psychiatric disorders.
The IPT subprograms proceed as a sequence of structured group activities, each
demanding various combinations of cognitive abilities and operations. The therapist
introduces each activity, guides the participation of the participants, and evaluates their
responses. The therapist is given some flexibility to repeat specific activities when
patients have difficulties which further practice may overcome. All the activities are
designed to include social interaction between patients, and the therapist selectively
facilitates social interaction relevant to completion of an activity. The Cognitive
Differentiation subprogram includes activities designed to exercise concept manipulation
and related operations. A representative activity is a sorting task that engages the group
in alternative strategies for sorting objects of different color, size and shape. The Social
Perception subprogram includes activities designed to exercise the processing of social
information. A representative activity involves systematic examination and description
of pictures of individuals involved in social situations. The Verbal Communication
subprogram is designed to exercise the cognitive substrates of verbal interaction,
including attention and short term memory. A representative activity engages
participants in carefully listening to each others' verbal statements, then repeating
verbatim, then paraphrasing. Across all the subprograms, the activities are graduated in
complexity and amount of required social interaction.
To manage group dynamics, the therapist follows a set of interaction rules. These
include maintaining a friendly but matter-of-fact social atmosphere, never telling patients
they are wrong or factually incorrect, but rather eliciting group feedback and discussion,
empathetically reflecting emotional expressions when they occur, clarifying
participants’verbalizations, and encouraging participation by all group members. Bizarre
behavior may be met with a brief reflection of its affective component (e.g. "Mr. Smith, it
appears you find this topic distressing"), but is otherwise ignored. Disruptive behavior is
met with a request to desist, and if it continues the person is excused from the session.

4
As noted previously, research on IPT arguably militates for revision of its assumptions about the linear,
hierarchical nature of its treatment effects. There may be even less difference between the CET theoretical
model and updated version of the IPT model.

12
When participant populations include individuals who are involuntary recipients of
treatment, or who otherwise have difficulty engaging in treatment, a contingency
management system may be a necessary adjunct to IPT (Spaulding et al, in press).

Implementation of Treatment and Dosage Considerations: In lieu of reliable tracking

measures, neurocognitive intervention must be conducted on the basis of dosages and
time frames reported in outcome research. The Spaulding et al (1999) study provided
three hours per week of the cognitive subprograms of IPT, for six months. For a severely
disabled recipient population, this dosage and time frame should probably be considered
the minimum required for a fair trial. A shorter or less intensive trial period may be
justifiable for less severely impaired recipients. Regardless of the time and dose of
specific interventions, neurocognitive impairment should be considered truly residual
only after sufficient exposure to intensive rehabilitation. As with the specific
interventions, 6 months is a minimal trial period.

Attentional Training Remediation Methods: Another suggested method of targeting

neurocognitive deficits in treatment is to work on the remediation of basic information
processing difficulties before beginning traditional skills training in order to remove these
obstacles to effective learning (Thompson & Breakey, 1997). According to information-
processing theory, more molar cognitive processes, such as planning and problem
solving, are dependent on the effective functioning of more molecular functions, such as
attention. Therefore, some theorists believe (e.g., Goldberg, 1994) that attentional
training is essential in order to facilitate the effective functioning of other cognitive
processes. A number of behavioral methods have been employed for increasing
attentional functioning as well as reaction time with some success. Monetary
contingencies have been found to increase attention span, although these effects have
only been found for the stimulus that has been specifically reinforced. For example, if a
participant was continually reinforced for paying attention to a computer for fifteen
minutes for a number of sessions, he or she would most likely not exhibit the same
attention span when engaged in a different task. However, one of the widely regarded
theories of cognitive functioning, the limited capacity model, states that reinforcing
contingencies that improve attention should also globally expand one’s overall capacity
for information and generalize to higher level processes that are affected by attention
span, including encoding and memory (Storzbach & Corrigan, 1996). A method that was
developed to increase the attention spans of brain-injured patients, Attention Process
Training (APT; Sohlberg & Mateer, 1987), has been found to be extensively beneficial in
a small sample of patients with schizophrenia. This comprehensive treatment addresses
all areas of attending, including sustained, selective, alternating, and divided attention in
a series of graduated stages of difficulty and complexity. Two participants who were
administered these treatments demonstrated improvements in a wide range of areas,
including auditory and visual memory and conversation skills (Goldberg, 1994). More
extensive, controlled research is needed in order to further demonstrate the efficacy of
this method.

Executive Functioning Remediation Methods: Wykes et al. (1999) conducted a study

utilizing a treatment procedure aimed at remediation of executive functioning

13
 deficits which is in line with this model. This treatment employs the use of
errorless learning, immediate feedback, and non-didactic training using very
simple tasks in three domains of executive functioning: cognitive flexibility,
memory, and planning. These researchers found that both groups (experimental
and control utilizing intensive occupational rehabilitation to control for
nonspecific therapist contact effects) achieved some gains in cognitive
functioning and symptom levels, although those of the experimental group were
superior. The cognitive remediation group also showed improvements in self-
esteem, and some generalization of cognitive processes was achieved (Wykes et
al., 1999). The fact that the improvements made on the very simple treatment
tasks generalized to the different tasks used to measure outcome points to the
possibility of remediating impaired cognitive processes rather than simply
improving performance on specific tasks through practice and repetition.
Heinssen and Victor (1994) also developed a treatment modality to increase
participants’ vocational functioning through cognitive remediation. In this
procedure, graduated steps working towards a final task were developed in order
to ensure success while enhancing the cognitive processes that would facilitate
appropriate task behavior. For example, in order to teach participants how to
water plants, an explanation of the task and the skills sequence to be followed is
given. Next, a sorting task is implemented, where patients sort plants into wet
and dry categories. This type of gradual progression continues until the patients
are watering the plants effectively on their own. Environmental manipulations
were also used to decrease distractions and compensate for impaired memory and
executive functioning. An unusual aspect of this treatment is that cognitive-
behavioral therapy methods were utilized in order to address any maladaptive
expectations or beliefs that the patients might have in order to avoid the negative
impact of these cognitions on performance. This type of treatment was also
shown to be very effective in the areas of job interest, work activity and
behavioral performance (Heinssen & Victor, 1994).

Prosthetic Interventions to Address Residual Impairments and to Maximize

Rehabilitation Effectiveness.
The literature on traumatic brain injury and other neuropathological conditions is
rich in strategies for compensating for the neurocognitive consequences of those
conditions. Living environments can be designed to compensate for memory
impairments by locating key prompts (e.g. written signs) at key locations to support key
activities. Individuals can be trained to make special use of personal calendars and date
books. All such interventions are potentially useful for people with disabling mental
illness, whose residual neurocognitive impairments are primarily in the memory domain.

Prosthetic Methods for Skills Training and General Rehabilitation: Cognitive deficits in
schizophrenia have also been found to be related to poorer performance in skills training
(Mueser et al., 1991; Kern et al., 1992; Bowen et al., 1993; Corrigan et al., 1994).
Specifically, deficits in the areas of verbal learning have been found to be predictive of
general knowledge and behavioral skill acquisition, while attention and verbal memory
mediate learning of skills (Thompson & Breakey, 1997). One response to this has been

14
to develop “cognitively sensitive” methods of skills training. This includes orienting the
skills trainer or therapist to be alert for attention and short-term memory problems,
minimizing distraction in the training setting, employing overlearning and repetition, and
carefully pacing the training procedures. Another method that has been posited regarding
adapting traditional rehabilitative methods to accommodate cognitive deficits is
categorization. It has been found that people with schizophrenia tend to be able to
remember verbal and visual information more effectively when it is organized into
meaningful categories or when items are placed on a continuum. These types of
remediational methods serve as prostheses by which the automaticity of demanding
cognitive processes is increased (Storzbach & Corrigan, 1996). Environmental methods
have been used effectively for decreasing distractions and for helping to overcome
memory impairments. Methods such as clearing unnecessary clutter out of group rooms,
using posters to visually present information while teaching, and having patients’
schedules, ward rules and other necessary information posted in various places could all
enhance functioning and response to treatment. Heinssen (1996) also stated that the
effectiveness of rehabilitation can be increased through environmental manipulations that
would facilitate patients’ attention, concentration and memory. Demands of
rehabilitation can be adjusted based on individuals’ cognitive deficits so as to avoid
cognitive overload, while environmental manipulations would facilitate integration of
information and limit distractions. In order to keep arousal levels low, which may be
prone to excitation during learning of novel or difficult information, the therapist should
keep voice tones calm, low and regular, and should also encourage motivation and effort
through ongoing emotional support (Heinssen, 1996).

Shaping Approaches to Attentional Remediation in Skills Training: Regarding the

shaping of attending behaviors, Silverstein and colleagues (Silverstein et al., 1998;
Silverstein et al., 1999) have tested this method both before initiating typical
rehabilitation modalities and during social skills training. In one study, it was found that
severely attentionally impaired subjects were able to increase their attention spans from
less than five to 45 minutes in a skills training class (Silverstein et al., 1998). It has also
been found that shaping procedures to increase attention spans employed during a
modular social skills training program, the Basic Conversation Skills Module of the
UCLA Social and Independent Skills series (Liberman & Corrigan, 1993), can be
effective for increasing the attention spans of participants while they are learning
appropriate conversation skills (Silverstein et al., 1999). These shaping procedures could
also be used during other types of activities, including work and other skills training
modalities, to facilitate improved attention. However, large-scale controlled studies of
this type of intervention are needed, as the current information is based only on a few
small pilot studies.

Prosthetic Methods for Executive Function Deficits: Specialized neuropsychological

interventions have been developed for people with specific impairments in the executive
domain. Such impairments are ubiquitous in people with frontal head injury, as caused
by hitting the dashboard in a car accident. Because of the predominance of executive
impairment in severe mental illness, there has been special interest in these techniques in
rehabilitation. An approach to compensating for severe frontal/executive impairment,

15
specialized for disabling mental illness, has been developed by Velligan and her
colleagues (Velligan et al., 2000). The approach uses the distinction between
disinhibitory impairment and attentional impairment to design individualized
compensatory strategies. For example, severe disinhibitory problems are hypothesized to
be instrumental in the problem of wearing inappropriate clothing, often observed in
people with severe mental illness. The mechanism for this is hypothesized to be a failure
to inhibit dressing behaviors when confronted with a varied wardrobe. A person who
can't inhibit dressing behavior puts on whatever clothing they encounter, regardless of
what they might have already put on. The solution is to package each day's clothing in a
separate unit, so that the person has only to open the package and put on whatever it
contains. So far research has suggested that this approach can be useful, for behavioral
problems ranging from inappropriate dressing to nonadherence to a medication regimen.
However, the research has not systematically separated post-acute from residual
neurocognitive impairments, nor compared the results with interventions intended to
resolve post-acute impairments. Further research will doubtless clarify the relationship
between post-acute and truly residual impairments as they respond to this approach. For
the time being, great caution is indicated so that prosthetic solutions such as these are not
used where a rehabilitative approach to post-acute impairment would establish more
normal behavioral functioning. Fortunately, therapeutic and prosthetic interventions are
not inherently incompatible, and can be applied in complementary ways (Goldberg,
1994), as long as the individual’s functioning is continually reassessed and adjustments
are made in response to functional recovery.

Contingency management: Another traditional modality for severe mental illness,

contingency management, also can serve as a prosthetic, as well as therapeutic,
intervention. As the immediacy hypothesis indicates, people with neurocognitive
impairments that prevent normal functioning in a natural environment can function in a
therapeutic milieu where stimulus-response relationships are made more proximal,
immediate and concrete. To the degree that those neurocognitive impairments are truly
residual, a contingency management intervention may serve to sustain more normal
functioning. Although contingency management is usually associated with rehabilitation
in relatively restrictive settings, especially institutions, newer approaches are adaptable to
more naturalistic settings and circumstances. Under these circumstances, formalized
contingencies can be part of a "cognitive exoskeleton" that compensates for an
individual's inability to respond to the most distant or abstract circumstances that
normally motivate functional behavior (Heinssen, 1996).

Higher Order Cognitive Interventions for Serious Mental Illness

Social problem solving insufficiency is directly addressed by the problem solving
approach in CBT (D'Zurilla, 1988). This is one of the oldest and most established of the
modern cognitive-behavioral therapy approaches. A number of specific modalities and
manuals have been produced over the several decades of its development. Problem
solving therapy is usually done in a group format, although it works well in a dyadic
format as well. In the widely disseminated skill training modules produced by the UCLA
Center for Rehabilitation of Schizophrenia (see Kuehnel, Liberman, Storzbach, & Rose,

16
1990) the problem solving approach has been thoroughly integrated with behavioral
social skills training.

Symptom-linked attribution problems. Delusions that interfere with personal and social
functioning, that persist despite resolution of acute psychosis, and that are not resolved by
education and skill training in management of one’s mental illness, are appropriate
targets for specialized sociocognitive interventions. Delusional behavior was often a
target of early behavior modification efforts (Liberman, Teigen, Patterson, & Baker,
1973; Nydegger, 1972; Patterson & Teigen, 1973; Wincze, Leitenberg, & Agras, 1972).
These met with some success, although it remained unclear whether there was actual
sociocognitive recovery or simply a change in overt behavior. The last several years
have seen considerable research on use of CBT specially adapted to address delusions
and other attribution problems associated with severe mental illness (Alford & Correia,
1994; Alford, Fleece, & Rothblum, 1982; Bentall & Kinderman, 1998; Chadwick,
Birchwood, & Trower, 1996; Haddock et al., 1998; Kinderman, 2001; Kingdon &
Turkington, 1994; Kingdon & Turkingtron, 1991). These generally involved a
combination of psychoeducation, interpersonal support and validation, and disputational
interventions. Disputational interventions involve question-and-answer interactions
designed to induce the recovering person to consider the factual basis of the delusion, to
reflect on other possible explanations of real events involved in the delusion, to test the
validity of the delusion by gathering more information, and to examine the consequences
of accepting a delusional belief. This approach is generally similar to traditional
individual psychotherapy approaches based on the psychodynamic concept of reality
testing. In addition, CBT approaches are currently being developed that make use of
cognitive dissonance and related concepts from attribution theory, in order to reverse the
interpersonal and intrapersonal processes that sustain the delusion. These techniques
show promise, but so far there is insufficient data to confidently conclude that
sociocognitive interventions contribute uniquely to resolution of problematic delusional
beliefs.

In conclusion, sophisticated and well-researched technologies are now available

to address cognitive impairments in people with serious mental illness. These
interventions are available for a variety of impairments that are associated with different
factors of the disorder. Rehabilitation practitioners can utilize these interventions both to
directly address impairments as well as to maximize rehabilitation effectiveness. A
careful assessment and clinical understanding of the individual, the nature of their
disorder and the impairments experienced in the various factors outlined above is crucial
to the effectiveness of the interventions and rehabilitation efforts in general.

17
 References

Alford, B., & Correia, C. (1994). Cognitive therapy of schizohrenia: Theory and
empirical status. Behavior Therapy, 25, 17-33.
Alford, H., Fleece, L., & Rothblum, E. (1982). Hallucinatory-delusional
verbalizations: Modification in a chronic schizophrenic by self-control and cognitive
restructuring. Behavior Modification, 6, 412-435.
Bell, M., Bryson, G., Greig, T., Corcoran, C., & Wexler, B. (2001).
Neurocognitive enhancement therapy with work therapy: Effects on neurocognitive test
performance. Archives of General Psychiatry, 58, 763-768.
Bentall, R., & Kinderman, P. (1998). Psychological processes and delusional
beliefs: Implications for the treatment of paranoid states. In T. Wykes & N. Tarrier & S.
Lewis (Eds.), Outcome and innovation in psychological treatment of schizophrenia (pp.
117-144). London: Wiley.
Bowen, L., Wallace, C.J., Nuechterlein, K.H., & Lutzker, J. (1993). Relationship
of attentional deficits to learning instrumental and problem-solving skills. Unpublished
manuscript.
Brenner, H., Roder, V., Hodel, B., Kienzle, N., Reed, D., & Liberman, R. (1994).
Integrated psychological therapy for schizophrenic patients. Toronto: Hogrefe & Huber.
Chadwick, P., Birchwood, M., & Trower, P. (1996). Cognitive therapy for
delusions, voices and paranoia. New York: John Wiley & Sons.
Corrigan, P., & Storzbach, D. (1993). The ecological validity of cognitive
rehabilitation for schizophrenia. Journal of cognitive rehabilitation, 11, 14-21.
Corrigan, P.W., Wallace, C.J., Schade, M.L., & Green, M.F. (1994). Cognitive
dysfunctions and psychosocial skill learning in schizophrenia. Behavior Therapy, 25, 5-
15.
Cromwell, R. L., & Spaulding, W. (1978). How schizophrenics handle
information. In W. E. Fann & I. Karacan & A. D. Pokorny & R. L. Williams (Eds.), The
phenomenology and treatment of schizophrenia (pp. 127-162). New York: Spectrum.
D'Zurilla, T. J. (1988). Problem-Solving Therapies. In K. S. Dobson (Ed.),
Handbook of cognitive-behavioral therapies (pp. 85-135). New York: Guilford.
Goldberg, J. (1994). Cognitive retraining in a community psychiatric
rehabilitation program. In W. Spaulding (Ed.), Cognitive technology in psychiatric
rehabilitation (pp. 67-86). Lincoln, NE: University of Nebraska Press.
Green, M., & Nuechterlein, K. (1999). Should schizophrenia be treated as a
neurocognitive disorder? Schizophrenia Bulletin, 25, 309-319.
Haddock, G., Tarrier, N., Spaulding, W., Yusupoff, L., Kinney, C., & McCarthy,
E. (1998). Individual cognitive-behavior therapy in the treatment of hallucinations and
delusions: A review. Clinical Psychology Review., 18(7), 821-838.
Heinssen, R. (1996). The cognitive exoskeleton: Environmental interventions in
cognitive rehabilitation. In P. Corrigan & S. Yudofsky (Eds.), Cognitive rehabilitation of
neuropsychiatric disorders. Washington DC: American Psychiatric Press.
Heinssen, R., & Victor, B. (1994). Cognitive-behavioral treatments for
schizophrenia: Evolving rehabilitation techniques. In W. Spaulding (Ed.), Cognitive
technology in psychiatric rehabilitation (pp. 159-182). Lincoln, NE: University of
Nebraska Press.

18
 Hogarty, G., & Flesher, S. (1999a). A developmental theory for cognitive
enhancement therapy of schizophrenia. Schizophrenia Bulletin, 25(4), 677-692.
Hogarty, G., & Flesher, S. (1999b). Practice principles of Cognitive Enhancement
Therapy for schizophrenia. Schizophrenia Bulletin, 25(4), 693-708.
Kern, R.S., Green, M.F., & Satz, P. (1992). Neuropsychological predictors of
skills training for chronic psychiatric patients. Psychiatry Research, 43, 223-230.
Kinderman, P. (2001). Changing causal attributions. In P. Corrigan & D. Penn
(Eds.), Social cognition and schizophrenia (pp. 195-215). Washington DC: American
Psychological Association.
Kingdon, D., & Turkington, D. (1991). The use of cognitive behavior therapy
with a normalizing rationale in schizophrenia: Preliminary report. Journal of Nervous
and Mental Disease, 179(4), 207-211.
Kingdon, D., & Turkington, D. (1994). Cognitive-behavioral therapy of
schizophrenia. New York: Guilford.
Kuehnel, T. G., Liberman, R. P., Storzbach, D., & Rose, G. (1990). Resource
book for psychiatric rehabilitation (2nd ed.). Baltimore: Williams & Wilkins.
Liberman, R.P., & Corrigan, P.W. (1993). Designing new psychosocial
treatments for schizophrenia. Psychiatry, 56, 238-249.
Liberman, R. P., Teigen, J., Patterson, R., & Baker, V. (1973). Reducing
delusional speech in chronic paranoid schizophrenics. Journal of Applied Behavior
Analysis, 6, 57-64.
Medalia, A., Aluma, M., Tyron, W., & Merriam, A. (1998). Effectiveness of
attention training in schizophrenia. Schizophrenia Bulletin, 24(1), 147-152.
Mueser, K.T., Bellack, A.S., Douglas, M.S., & Wade, J. (1991). Predictions of
social skill acquisition in schizophrenia and major affective disorder patients from
memory and symptomatology. Psychiatry Research, 37, 381-396.
Nuechterlein, K.H., & Asarnow, R.F. (1989). Cognition and perception. In H.I.
Kaplan, & B.J. Sadock (Eds.), Comprehensive textbook of psychiatry, 5th ed. (pp. 241-
256). Baltimore: Williams & Wilkins.
Nuechterlein, K. H., & Dawson, M. E. (1984). Information processing and
attentional functioning in the developmental course of schizophrenic disorders.
Schizophrenia Bulletin, 10, 106-203.
Nydegger, R. (1972). The elimination of hallucinatory and delusional behavior by
verbal conditioning and assertive training: A case study. Journal of Behavior Therapy
and Experimental Psychiatry, 3, 225-227.
Olbrich, R., Kirsch, P., Pfeiffer, H., & Mussgay, L. (2001). Patterns of recovery
of autonomic dysfunctions and neurocognitive deficits in schizohrenics after actue
psychotic episodes. Journal of Abnormal Psychology, 110, 142-150.
Patterson, R. L., & Teigen, J. R. (1973). Conditioning and post-hospital
generalization of non-delusional responses in a chronic psychotic patient. Journal of
Applied Behavior Analysis, 6, 65-70.
Reed, D., Sullivan, M., Penn, D., Stuve, P., & Spaulding, W. (1992). Assessment
and treatment of cognitive impairments. In R. P. Liberman (Ed.), Effective psychiatric
rehabilitation (Vol. 53, pp. 7-20). San Francisco: Jossey-Bass.

19
 Silverstein, S.M., Pierce, D.L., Saytes, M., Hems, L., Shenkel, L., & Streaker, N.
(1998). Behavioral treatment of attentional dysfunction in chronic, treatment-refractory
schizophrenia. Psychiatric Quarterly, 69, 95-105.
Silverstein, S.M., Valone, C., Jewell, T.C., Corry, R., Nghiem, K., Saytes, M., &
Potrude, S. (1999). Integrating shaping and skills training techniques in the treatment of
chronic, treatment-refractory individuals with schizophrenia. Psychiatric Rehabilitation
Skills, 3, 41-58.
Sohlberg, MM , Mateer, CA: Effectiveness of an attention training program.
Journal of Clinical and Experimental Neuropsychology 2: 117-130, 1987
Spaulding, W., Fleming, S., D., R., Reed, D., Sullivan, M., Storzbach, D., & Lam,
M. (1999a). Cognitive functioning in schizophrenia: Implications for psychiatric
rehabilitation. Schizophrenia Bulletin, 25(2), 275-289.
Spaulding, W. D., Reed, D., Sullivan, M., Richardson, C., & Weiler, M. (1999b).
Effects of cognitive treatment in psychiatric rehabilitation. Schizophrenia Bulletin, 25(4),
657-676.
Spaulding, W. D., Storms, L., Goodrich, V., & Sullivan, M. (1986). Applications
of experimental psychopathology in psychiatric rehabilitation. Schizophrenia Bulletin,
12(4), 560-577.
Spaulding, W., Sullivan, M., Weiler, M., Reed, D., Richardson, C., & Storzbach,
D. (1994). Changing cognitive functioning in rehabilitation of schizophrenia. Acta
Psychiatrica Scandinavica, 90(Supplementum no. 384), 116-124.
Storzbach, D.M., & Corrigan, P.W. (1996). Cognitive rehabilitation for
schizophrenia. In P.W. Corrigan & S.C. Yudofsky (Eds.), Cognitive rehabilitation for
neuropsychiatric disorders. Washington, DC: American Psychiatric Press.
Thompson, J.W., & Breakey, W.Z. (Eds.). (1997). Mentally ill and homeless:
Special programs for special needs. Amsterdam, Netherlands: Harwood Academic
Publishers.
vanderGaag, M. (1992). The results of cognitive training in schizophrenic
patients. Delft, Netherlands: Eburon.
vanderGaag, M., Woonings, F., vandenBosch, R., Appelo, M., Sloof, C., &
Louwerens, J. (1994). Cognitive training of schizophrenic patients: A behavioral
approach based on experimental psychopathology. In W. Spaulding (Ed.), Cognitive
technology in psychiatric rehabilitation (pp. 139-158). Lincoln, NE: University of
Nebraska Press.
Vellligan, D., Bow-Thomas, L., Huntzinger, C., Ritch, J., Ledbetter, N., Prihoda,
t., & Miller, A. (2000). Randomized controlled trial of the use of compensating strategies
to enhance adaptive functioning in outpatients with schizohrenia. American Journal of
Psychiatry, 157, 1317-1323.
Wincze, J. P., Leitenberg, H., & Agras, W. S. (1972). The effects of token
reinforcement and feedback on delusional verbal behavior of chronic paranoid
schizophrenics. Journal of Applied Behavior Analysis, 5, 247-262.
Wykes, T., Reeder, C., Corner, J., Williams, C., & Everitt, B. (1999). The effects
of neurocognitive remediation on executive processing in patients with schizophrenia.
Schizophrenia Bulletin, 25, 291-308.

20
 Additional Resources

General Information Web Sites:

http://www.psychosocial.com/psr/assessment_treatment.html Journal article about

current treatment approaches for Serious Mental Illness.

http://www.iop.kcl.ac.uk/main/Mhealth/CogRemed/ Information about cognitive

remediation from the Institute of Psychiatry and the South London and Maudsley NHS
Trust.

http://www.ncrrn.org/ Information from the Northeast Cognitive Rehabilitation Research

Network

http://www.neuropsychologycentral.com/ General information about neuropsychology

Web Sites with Information about Assessment and Treatment Materials:

http://www.neuropsychworks.com/ Information about computer based cognitive

assessment tools.

http://www.npi.ucla.edu/irc/index.html Information from the UCLA Center for Research

on Treatment and Rehabilitation of Psychosis. Includes information on obtaining
rehabilitation skills training materials.

Several neurocognitive rehabilitation interventions have utilized a computer based

component (i.e., Bell et al. 2001). Listed below are some Web sites with commercially
available cognitive training rehabilitation computer programs.

http://www.neuroscience.cnter.com/ (includes information about CogRehab software)

http://www.braintrain-online.com/ (includes information about “Captain’s Log”

software)

For a product list of assistive technologies that includes cognitive training software see
the Center for Rehabilitation Technology Web site. The link below connects to their
training archives page which includes a downloadable Adobe pdf product list under the
September 13 2000 “Cognitive Disabilities in the Workplace” training session.
http://www.techconnections.org/training/Archives.html

21
 Books:
Brenner, H., Roder, V., Hodel, B., Kienzle, N., Reed, D., & Liberman, R. (1994).
Integrated psychological therapy for schizophrenic patients. Toronto: Hogrefe & Huber.
Corrigan, P.W., & Yudofsky, S.C. (Eds.). (1996). Cognitive rehabilitation for
neuropsychiatric disorders. Washington, DC: American Psychiatric Press.
Harvey, D.D., & Sharma, T. (2002). Understanding and treating cognition in
schizophrenia: A clinician’s handbook. Boston: Boston Medical Publishers, Inc.
Kuehnel, T.G. (1990). Resource book for psychiatric rehabilitation: Elements of
service for the mentally ill. Baltimore: Williams & Wilkins.
Sharma, T., & Harvey, D.D. (Eds.). (2000). Cognition in schizophrenia:
Impairments, importance, and treatment strategies. Oxford, UK: Oxford University
Press.
Sohlberg, M.M., & Mateer, C.A. (Eds.). (2001). Cognitive rehabilitation. New
York: Guilford Publications, Inc.
Spaulding, W.D. (Ed.). (1994). Cognitive technology in psychiatric
rehabilitation. Lincoln, NE: University of Nebraska Press.
Stuss, D.T., Robertson, I.H., & Winocur, G. (Eds.). (1999). Cognitive
neurorehabilitation. Cambridge, UK: Cambridge University Press.

Assessment/ Monitoring Tools:

Controlled Oral Word Association Test (COWA): Benton, A.L., & Hamsher, K.
(1976). Multilingual Aphasia Examination. Iowa City: University of Iowa.
Booklet Category Test- Psychological Assessment Resources, Inc.
Devis Kaplan Executive Function System (D-K EFS)- The Psychological
Corporation, A Harcourt Assessment Company
Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)-
The Psychological Corporation, Harcourt Brace & Co.
Wechsler Adult Intelligence Scale- 3 (WAIS-III)- The Psychological Corporation,
Harcourt Brace & Co.
Wechsler Memory Scale- 3 (WMS-III)- The Psychological Corporation, Harcourt
Brace & Co.
Wisconsin Card Sort Test (WCST)- Psychological Assessment Resources, Inc.

The above instruments can be used in combination as a comprehensive battery to assess

cognitive functioning, with the primary emphases being in the areas of verbal memory
and executive functioning, both of which appear to be the most pertinent to severe mental
illness.

22

View publication stats