Transcript Title of Training Presentation

Cognition in psychopathology: can we
say one way or another whether
certain cognitive processes are
unique to a given disorder?
Dr. Tisha J. Ornstein, C.Psych
Department of Psychology
Ryerson University
Overview

Why are neuropsychologists special – particular way
of thinking, e.g., Phineas Gage; research approach

Discussion about Attention Deficit Hyperactivity
Disorder (ADHD) and relevance as related to
Traumatic Brain injury

Link between ADHD and Obsessive-Compulsive
Disorder; research endeavours to be discussed by
graduate student: Peter Egeto
Phineas Gage
●
Before the accident, Phineas Gage had been a capable and efficient
foreman who was looked on as a shrewd, smart business
man. Afterwards, he was fitful, grossly profane, impatient and obstinate.
His friends said he was, “no longer Gage.”
●
Massive damage to the frontal lobes can cause dramatic changes in
personality while keeping sensation, movement, consciousness and most
cognitive faculties intact.
Neuropsychology: As a Way of Thinking…
● Humans have evolved a range of subtle cognitive control
mechanisms to regulate more basic cognitive processes in the
service of future-oriented goals in an uncertain environment
● These mechanisms are known as executive control
● Executive control includes anticipation, goal selection, planning,
and response inhibition, among other processes.
● Executive control depends on a series of partially segregated
frontal subcortical loops (e.g., Alexander, Delong, & Strick,
1986; Lichter & Cummings, 2001).
● Perturbations of these loops and the resultant effect on
executive control are implicated in various neuropsychiatric
disorders, such as attention deficit hyperactivity disorder, and
obsessive compulsive disorder
Frontostriatal circuits and
Neurocognitive Processes
● Neurocognitive processes mediated by the circuits include
attention, the inhibition of inappropriate responses,
shifting between thoughts or actions, performance
monitoring, decision-making, planning ability, and using
working memory to help guide behavior.
● Dysregulation of frontostriatal circuits likely underlies
many of the symptoms related to the disorders of interest.
Would it not be wonderful to identify key cognitive
mechanisms associated with a disorder?
What are some implications?
Research Approach

Disorders of the frontostriatal system: Attention deficit
hyperactivity disorder, Obsessive-compulsive disorder

Other disorders that are frontal with respect to their cognitive
characteristics: Traumatic Brain injury

Understanding the nature of neuropsychological characteristics
associated with various conditions:


Consider neuropsychological test battery or neurocognitive measures
sensitive to the disorder of interest;

Comparative approach

Co-morbidities (pain, anxiety, depression)

Change and variability (early work)

Long-term follow-up (determine impact of injury on development) (future
endeavour)
Ultimate goal is to elucidate the mechanisms that underlie
abnormal behaviour
Introduction to Attention Deficit
Hyperactivity Disorder (ADHD)





Most common developmental disorder
Affects children, youth, and young adults
Costly, impairing and persistent
Phenotypically complex
Cognitive deficits
Neurocognitive Deficits

Neurocognitive deficits in ADHD, and more specifically
executive deficits, extend to adults, although the research
lags behind child/adolescent-focused studies.

DSM-5 states, “Individuals with ADHD may exhibit
cognitive problems on tests of attention, executive
function, or memory, although these tests are not
sufficiently sensitive or specific to serve as diagnostic
indices.” “No biological marker is diagnostic for ADHD.”
(p. 61).

Even so, certain neuropsychological domains have been
proposed as crucial.
Neurocognitive Tests
Barkley’s Theory of ADHD
Response
Inhibition
Working
Memory
Self-Regulation
Of Affect/
Motivation/Arousal
Internalization
Of Speech
Motor Control/
Fluency/Syntax
Reconstitution
Barkley asserts that these deficits manifest
in ADHD children through:
Ability to adapt to new information
Ability to predict what will happen
Ability to generate responses to future
info
ADHD = “nearsighted when it comes to time”
Which tests should we use? Why?
Consider:

Why is the subject being referred

What is/are the presenting issues

How old is the subject; Male or female

Any presenting difficulties, like hearing
impairment

What are the cognitive concerns presented in the
literature

Neuroanatomical substrates

Test parameters
Stop-Signal Paradigm
*
X/O
Stop Signal Delay (variable)
500 ms
TONE
Stop Signal (100 ms)
1000 ms
500 ms
• Response inhibition considered a signature deficit of ADHD; recent metaanalysis reported an effect size of .62 for SSRT in ADHD as compared to
controls (Lipszyc & Schachar, 2010), and not related to the ‘go’ response.
Caveat; even so…
● Not all children are impaired; however,
● Relatives of impaired children on the stop signal reaction time
task performed worse than relatives of non-impaired ADHD and
healthy control children; has been replicated.
● McAuley and colleagues (2014) said that certain of executive
control processes, including response inhibition, are markers of
genetic risk for ADHD. Looking to evaluate whether certain skills
are state-independent. Children were reassessed as adolescents.
● They compared ADHD children to peers and then ADHD
subgroups (persistent, remittent, and partially remittance
forms of the disorder) on average five years later. They found
that response inhibition distinguished ADHD children from
their unaffected peers, but also that the deficit persisted
regardless of the course of the disorder.
Traumatic brain injury (TBI)

Leading cause of death and disability


375 per 100,000 person years
500,000 cases / yr. to ER

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80% + are mild; 80% receive attention
7% moderate
8% severe
30,000 suffer permanent disability
Children, youth and young adults
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40% admitted
50% < 19 years; 25% < 9 years
Phenotypically complex
Cognitive deficits
Pre-injury mental illness
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15-40% have pre-injury mental illness
ADHD most common (upwards of 25% of TBI
cases)
 Aggression
 Phobia, SAD, ODD, OCD, GAD, LD
Multiple problems
Pre-injury predictors of new disorders

Mental illness

Injury severity

Number of previous head injuries

Low pre-injury adaptive functioning

SES, psychosocial adversity, family
functioning
Post-injury mental illness

Secondary ADHD (S-ADHD: ADHD develops after TBI)
Persist, inattentive


Personality change disorder
Labile, aggressive, disinhibited, apathetic, paranoid

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Oppositional defiant and conduct disorder
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Post-concussive symptoms
Headaches, dizziness, fatigue, irritability, insomnia, loss of concentration
and memory, noise and light sensitivity
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Comorbidity
–
Comorbidity predicts severity and increases health care needs.
Traumatic Brain Injury and Attention
Deficit Hyperactivity Disorder

Association between ADHD and TBI:

Those with ADHD are at a greater of
suffering a TBI due to the nature of deficits
– risk-taking behavior, impulse control
issues (cf. Adeyemo, 2014)

TBI has been shown to result in S-ADHD

Perhaps TBI and/or inhibitory control
performance shapes the expression of ADHD,
leading to an etiologically distinct form of ADHD.
SSRT

350

300

250
200
150
92
30
73
79
100
50
0
ADHD
TBI + SADHDTBI - SADHD
Controls
274 children
6–14 yrs
2 years post TBI
SSRT
400
• 6-16 yrs
• Injured at ~ 10 yrs
• 141 at 6 months
350
300
250
200
150
98
26
17
100
50
0
TBI
TBI+PADHD TBI+SADHD
SSRT
• 126 followed at 12 months
400
350
300
250
200
150
89
22
14
100
50
0
TBI
TBI+PADHD TBI+SADHD
1
0.9
0.8
Effect Size
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0
ADHD
ANX
Autism
Bipolar CD/ODD
Disorder
Disorder
NOTE: OCD; SCHZ Adults included
OCD
RD
SCHIZ
Tourette's
Obsessive-Compulsive Disorder

Estimated lifetime prevalence of 2 to 3%; approximately 600
000 Canadians will be affected by this illness in their lifetime.

Among adults, men and women are equally affected, but in
adolescents boys are more commonly affected.

The disorder begins most often in adolescence or early
adulthood; it may begin in childhood.; around one-half to onethird of adult OCD cases have their onset in childhood or
adolescence.

It is usually a chronic course that waxes and wanes.
OCD may be accompanied by depression, eating disorders, or
other anxiety disorders.

Neuropsychology
●
Few early neuropsychological studies in adults with
OCD; results were inconsistent.
●
More recent neuropsychological studies of executive
functions in adults with OCD have reported increased
difficulty with switching cognitive set, generating
strategies (i.e., executive planning), and response
inhibition; memory difficulties are said to be related to
problems with strategic learning.
Neuropsychology

Few studies have examined executive functioning in
children with OCD. Of the handful of published studies,
findings are inconsistent.

It is important to study children with OCD for many
reasons:

Executive processing plays an important role in
children’s learning and problem solving.

Can assess the underlying deficit unbiased by the
effects of treatment and the consequences of the
disorder itself.
Research Article
DEPRESSION AND ANXIETY
NEUROPSYCHOLOGICAL PERFORMANCE IN CHILDHOOD OCD:
A PRELIMINARY STUDY
Tisha J. Ornstein, Ph.D., C. Psych, Paul Arnold, M.D. F.R.C.P (C), Katharina Manassis, M.D.
F.R.C.P (C), Sandra Mendlowitz, Ph.D., C. Psych, and Russell Schachar, M.D. F.R.C.P (C)
Background: Neuropsychological deficits have often been found in studies of adults with
obsessive compulsive disorder (OCD). However, few studies have examined such impairment
in children with OCD and of those studies published, the results are mixed. Methods: In the
present study, 14 OCD children were compared to 24 healthy developing children of similar
age and intellectual ability on a series of neuropsychological tests that assess response
inhibition, abstract reasoning and problem solving, planning ability, verbal and nonverbal
fluency, working memory, attention and information processing speed, and visual and verbal
memory and learning. Results: No significant differences emerged between the children with
OCD and healthy controls for working memory, verbal fluency, attention, information
processing speed, concept formation/abstraction, and response inhibition. We observed some
deficits and a trend toward performance differences between the groups for psychomotor
speed and attention, cognitive flexibility, nonverbal fluency, planning ability, and verbal
memory and learning. Results are partially consistent with those found in adults with OCD.
Findings were not related to depressive symptoms or self-report feeling of anxiety.
Conclusions: This preliminary survey indicates that OCD children may have deficits for
cognitive flexibility and planning ability and differ from adults with OCD in not presenting
with poor response inhibition or memory deficits. Larger, multi-site studies are warranted to
help delineate the neurocognitive deficits associated with childhood OCD.
Child Literature
Tests
Findings
Beers, 1999
Digit Span, Stroop,
Null findings;
WCST, COWA, TOH,
participant with OCD
Go/No-Go, CVLT, TMT did better on some
measures
Shin, 2008
CPT, WCST, TMT-B,
RCFT
No differences on CPT,
TMT-B, RCFT
Wooley, 2008
Stop Signal Task,
Motor Stroop
No differences
Ornstein, 2010
Stop Signal, WCST,
Spatial Span, n-Back,
DKEFS ,TMT, CVLT,
RCFT
No deficits, but trends
towards deficits in
cognitive flexibility
and planning ability
Behar, 1984
Money’s Road Map
Test of Directional
sense, Maze Learning,
Rey Word Learning
List, RCFT
Deficits in mental
rotation in space &
learning mazes
Andres, 2007
RCFT, RAVLT, TMT,
WCST, COWA, Stroop
Deficits in visual
memory & visual
organization.
ADHD and OC Behaviours
Background:
 Collaboration with Sick Kids Hospital (Drs.
Schachar & Crosbie)
 Children with ADHD and OC behaviours
ADHD
: 5%
ADHD
+OCB:
11.2%
OCD:
1.2%
ADHD+
OCD:
10-33%
ADHD and OC Behaviours
Background:



ADHD & OCD: common neurobiological
abnormalities
 Cortico-striatal-thalamic pathway
 Anterior cingulate cortex activity: ↓ in ADHD,
↑ in OCD (Brem, Grünblatt, Dreschler,
Riederer & Walitza, 2014)
Inhibition impairments
 Behaviour & thought suppression
Inhibition in ADHD+OCB: Arnold et al., 2005
 Somewhat ↑ inhibition in ADHD+OCB vs ADHD
ADHD and OC Behaviours
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Measures: 3 inhibition tasks
Cognitive inhibition: Eriksen Flanker Task
(distractor suppression)
Response inhibition: Go/No-Go (response
inhibition)
‘L’

‘X’
Response inhibition: Stop Signal Task (ongoing
response inhibition)
‘X/O’
ADHD and OC Behaviours

Results:
ADHD
Task Variable (n=85)
734.9
Go/No- MCRT (165.5)
Go
253.0
MCRT SD
(105.8)
283.9
MCRT SD
Eriksen
(95.1)
Flanker MIRT SD 298.6
(140.1)
Stop
Signal
OCB ADHD+OCB Controls Post(n=10)
(n=14)
(n=68) hoc
657.6
683.54
634.6 ADHD
(165.6)
(129.0)
(121.1) > HC
178.8
231.9
188.8 ADHD
(78.9)
(149.5)
(80.7)
> HC
240.9
243.8 ADHD
241.7 (67.0)
(68.4)
(91.1)
> HC
293.8
327.3
228.5 ADHD
(314.2)
(158.9)
(125.7) > HC
All
n.s.
ADHD and OC Behaviours
Conclusions:
 ADHD slower and more variable
 General trend: ADHD > ADHD+OCB >
controls > OCB
 Processing speed vs variability?
 No differences on processing speed index
(WISC-IV coding & symbol search)
 OC symptoms: ↓ inhibition/inattention
deficits
ADHD and OC Behaviours
Future directions:
 Other inhibition measures (e.g., Stroop),
larger sample, full OCD diagnoses
 Other studies:
 EEG and neuropsychogical testing in OCD
 Error related negativity (ERN), N2
(conflict monitoring), P3 (inhibition)
Current Endeavours


Decision-making in relation to:
 Inhibition;
 Quality of life and disability
Components of decision-making – Intolerance
of uncertainty; reassurance seeking;
impulsivity; subjective reporting (Frost
Indecisiveness Scale…)

Looking at these features in OCD and
spectrum-related disorders
THANK YOU!
Acknowledgement:
Ryerson research lab, Hospital for Sick
Children, Sunnybrook Health Sciences
Centre, and US collaborators.