Clinical Neuropsychology for Our planpsychologyinterns.org/wp-content/uploads/HAPTC-N... · Forensic Psychology Professor by Distinction, Neuropsychology Program ... Nature of “frontal”

Clinical Neuropsychology for the Clinical Psychologist

Robert L. Denney, Psy.D., ABPPBoard Certified in Clinical Neuropsychology & Forensic Psychology

Professor by Distinction, Neuropsychology Program

The School of Professional Psychology at Forest Institute

NEW ADDRESS:

Neuropsychological Associates of Southwest Missouri

4350 S. National Avenue, Ste. B116

Springfield, MO 65810

[email protected]

Our plan

• What is a neuropsychologist?– How can I call myself one?

• Differentiating “Functional” from “Organic” conditions primer

• Neuroanatomy/neuropathology– Emphasis on TBI and validity

• Neuropsychology Screening– RBANS

Definition of Neuropsychology

• INS founded in 1967 >4500; worldwide

• NAN formed in 1975 >3300; 24 countries

• APA Div 40 formed in 1980; >4100

• Designation “Specialty” by APA in 1996.

• INS/Div 40 training guidelines (1989), replaced by

• Houston Conference on education & training (1998).

National Academy of Neuropsychology Definition of Neuropsychologist

A clinical neuropsychologist is a professional within the field of psychology with special expertise in the applied science of brain-behavior relationships.

Clinical neuropsychologists use this knowledge in the assessment, diagnosis, treatment, and/or rehabilitation of patients across the lifespan with neurological, medical, neurodevelopmental and psychiatric conditions, as well as other cognitive and learning disorders.

The clinical neuropsychologist uses psychological, neurological, cognitive, behavioral, and physiological principles, techniques and tests to evaluate patients' neurocognitive, behavioral, and emotional strengths and weaknesses and their relationship to normal and abnormal central nervous system functioning.

The clinical neuropsychologist uses this information and information provided by other medical/healthcare providers to identify and diagnose neurobehavioral disorders, and plan and implement intervention strategies.

NAN Definition of Neuropsychologist

• The clinical neuropsychologist (minimal criteria) has: 1. A doctoral degree in psychology from an accredited

university training program.

2. An internship, or its equivalent, in a clinically relevant area of professional psychology.

3. The equivalent of two (fulltime) years of experience and specialized training, at least one of which is at the post-doctoral level, in the study and practice of clinical neuropsychology and related neurosciences. These two years include supervision by a clinical neuropsychologist.

4. A license in his or her state or province to practice psychology and/or clinical neuropsychology independently, or is employed as a neuropsychologist by an exempt agency.

NAN Definition of Neuropsychologist

• At present, board certification is not required for practice in clinical neuropsychology.

• Board certification (through formal credential verification, written and oral examination, and peer review) in the specialty of clinical neuropsychology is further evidence of the above advanced training, supervision, and applied fund of knowledge in clinical neuropsychology.

Houston Conference Requirements

• 3. Foundations for the study of brain-behavior relationships– A. Functional neuroanatomy– B. Neurological and related disorders including their etiology,

pathology, course and treatment– C. Non-neurologic conditions affecting CNS functioning– D. Neuroimaging and other neurodiagnostic techniques– E. Neurochemistry of behavior (e.g., psychopharmacology)– F. Neuropsychology of behavior

• 4. Foundations for the practice of clinical neuropsychology– A. Specialized neuropsychological assessment techniques– B. Specialized neuropsychological intervention techniques– C. Research design and analysis in neuropsychology– D. Professional issues and ethics in neuropsychology– E. Practical implications of neuropsychological conditions

• # 3 is Largely obtained during doctoral work; 4 during intern/resid.

Houston Conference Requirements

• APA or CPA approved internship• Two year residency with this exit criteria:

• 1. Advanced skill in the neuropsychological evaluation, treatment and consultation to patients and professionals sufficient to practice on an independent basis;

• 2. Advanced understanding of brain-behavior relationships;• 3. Scholarly activity, e.g., submission of a study or literature

review for publication, presentation, submission of a grant proposal or outcome assessment.

• 4. A formal evaluation of competency in the exit criteria 1 through 3 shall occur in the residency program.

• 5. Eligibility for state or provincial licensure or certification for the independent practice of psychology.

• 6. Eligibility for board certification in clinical neuropsychology by the American Board of Professional Psychology.

A diagnosis not considered will be a diagnosis not given.

The task of differential diagnosis and rule outs.

Clinical traps

• Mistaking symptoms for their cause.

• Getting seduced by the “story.”

• Equating psychosis with schizophrenia.

• Relying on too little information.

Organic Brain Syndrome

• Disorientation

• Recent memory impairment

• Diminished reasoning

• Sensory indiscrimination

Presence of any hallucination--other than auditory—is presumptive evidence of an organic problem.

Alerting CluesPresumptive Clues

Alerting clues

• No history of similar symptoms.

• No readily identifiable cause.

• Age 55 or older.

• Coexistence of chronic disease.

• Use of drugs.

Presumptive clues

• Head injury.

• Change in headache pattern.

• Visual Disturbances.

• Speech deficits.

• Abnormal body movements.

• Sustained deviation in vital signs.

• Changes in consciousness.

Couple quick screening ideas

• Draw a Clock

• Copy a 3-D Cube

I am going to learn So much!

Functional Neuroanatomy

Introduction and Key Concepts

When its easy to identify brain damage.

Brain

• 100,000 miles of neural fibers– 300,000 motor

– 1.5-3 million sensory

• About 1400 grams

• Glial cells outnumber neurons 10:1

Brain

• Only about 2% of body weight but receives 20% of blood from heart.

• Requires continual cerebral perfusion.– Glucose & oxygen

• Six seconds of blood interruption causes unconsciousness.

• About five minutes to permanent damage.

Brain in situ-Falx cerebri

Right hemisphere w/o meninges or vessels

Gross Brain Structure

• Lower brain areas:– Medulla & Pons (brain stem).

– Cerebellum.

• Cerebrum– Divided into right and left hemispheres.

– Cerebral cortex (gray matter).

– Centrum semiovale (white matter).

– Limbic system and basal ganglia.

Gross Brain Structure

• Cerebrum divided into lobes:– Occipital

– Parietal

– Temporal

– Frontal

• Each has primary, secondary, and tertiary association areas.

Basic global concepts

• Old-New

• Front-Back

• Left-Right

Right cerebral hemisphere

• Prosody

• Emotion

• Music

• Environmental sounds

• Somesthesis/body image

• Geometric space

• Visual imagery

• Social, nonverbal communication

Left Hemisphere

• “Thinking”

• Language– expression

– reception

• Linear/sequential

Paul Broca 1824-1880 Broca

• Mr. Leborgne demonstrated epilepsy, right hemiplegia, and loss of speech x 20 years.

• Hospitalized for 31 years and known as “Tan.”

• Broca invited Aubertin to evaluate him, and he agreed the signs suggested left frontal.

• Six days later, he died.

Broca

• The next day, Broca presented the brain to their society with a brief statement.

Broca’s Expressive Aphasia

• Left frontal convexity

• Non-fluent/broken

• Anomia/word finding difficulty

Carl Wernicke 1833-1892

• Receptive

• Fluent but nonsense

• Possible anosognosia

• Neologisms, word salad

• Can be mistaken for schizophrenia

• Reading severely impaired

• Can write gibberish

Key Aspects of Memory

• Declarative: implies conscious awareness and the ability to report the learning.– Episodic: autobiographical; memory for

past events in one’s life.

– Semantic: knowledge and facts about the world (the origin of which is often not realized).

Other facets to memory

• Procedural: automatic behavioral sequences outside conscious awareness.

• Skills (motor): “procedural memory.”

• Priming effect: Cues (partial bits of information) prompt an accurate recall without the individual’s even being aware of, or remembering, that the information was presented before.

– Like “ch---” for “chair.”

• Classical Conditioning.

• Other: Feeling of knowing & ?

Memory TaxonomyAdapted from Squire (1987) Memory and Brain. p. 170.

Memory

DeclarativeProcedural

Episodic (working)

Semantic (reference)

SkillsPriming

Classical Conditioning

Other?

Episodic Memory Systems

• Four basic memory systems:– Medial Temporal Lobe Areas (primary)

• Hippocampal formation

• Adjacent cortex of parahippocampal gyrus

– Medial Diencephalic Areas (primary)

• Thalamic mediodorsal nucleus

• Anterior nucleus of thalamus

• Internal medullary lamina

• Mammillary bodies

– White Matter Network

– Basal Forebrain

Circuit of Papez

• Hippocampal

• Fornix

• Mammillary Bodies

• Thalamic Nuclei

• Cingulate Gyrus

• Parahippocampal areas

• From Blumenfeld (2002)

Dorsolateral view of Fornix

From Blumenfeld (2010) Neuroanatomy through clinical cases (2nd ed.)

Sinauer.

Now you are confounded…MRI Temporal Lobes - HM

Amnesia Timeline - HM

Ribot’s Law

From Blumenfeld (2010) Neuroanatomy through clinical cases. Sinauer.

Primary Mechanisms of injury (Closed Head Injury)

• Traumatic movement:

• 1. Impact contusions.– Ethmoid bone

– Sphenoid wings

• 2. Diffuse Axonal Injury.

Inferior Cranial Vault

From Blumenfeld(2010)

Neuroanatomy through clinical cases (2nd ed.)

Sinauer.

Contusion

• Severe movement creates bruising in a typical pattern.

• Results in common pattern of dysfunction as well.

• Coup-contrecoup.

Diffuse Axonal Injury (DAI)

• Inertia and centrifugal force play a role.

• Greater mass at the top moves further than the remaining portion (variable density too).

• In addition, brain stem locked into position by foramen magnum.

• Results in stretched, torn, and severed axon (“shear”).

• Rotation increases potential for damage.

Mechanisms of Injury-DAI

Stretching and tearing of axons and capillaries cause small bleeds-petechial hemorrhages.

Secondary Mechanisms of Injury

• Brain swelling– Decreases cerebral perfusion.

– Decreases blood flow-waste removal & nutrients.

• Bleeding (e.g., subdural hematoma).

• Neurotransmitter Cascade.

• Creation of toxic environment.

Bad Day at Work

Subdural Hematoma

T2 weighted MRI

Natural History - Diffuse

• Stereotypic pattern of recovery:

– 1.) Alteration of consciousness.

– 2.) Confusion and anterograde amnesia (PTA).

– 3.) Continuous memory and gradual increase in recovery/compensation

Common Residual Difficulties

• Frontal lobe syndromes:– Disinitiation syndrome (pseudodepression)

– Disinhibition syndrome (pseudopsychopathy)

• Concentration, learning, and memory.

• Executive Function Problems:– Organization

– Planning

– Self-monitoring

– Mental flexibility

Executive Functions

• Probably the single most important aspect of cognitive functioning for most people when significant Traumatic Brain Injury is involved.

• The most likely to determine social and vocational recovery.

• One of the more difficult to identify and measure.

• One of the most difficult to remediate.

Executive Functions

• Predominantly the frontal lobes which include about 30% of cortical surface.

• Numerous connections to other parts of the brain which help it to enlist and orchestrate functions from each respective area.

• Damage to various parts of the area can cause differing clinical syndromes.

Nature of “frontal” injuries

• Phineas Gage (Harlow, 1868).

• Dynamite worker who survived an explosion that blasted an iron tamping bar (about 1 meter long, 3 cm wide) up under his cheek bone and out through the top of his head.

• “…balance...between his intellectual faculties and animal propensities seems to have been destroyed.” (Cited in Blumer & Benson, 1975)

Phineas Gage

Indication: portions of both left and right frontal lobes from the medial orbital region upward to the precentral region.

H Damasio, T Grabowski, R Frank, AM Galaburda, and AR Damasio

Science 20 May 1994 264: 1102-1105

The return of Phineas Gage: Clues about the brain from the skull of a famous patient

Blumer and Benson (1975)

• Outlined two basic personality changes:

• Pseudodepression– apathy, indifference, loss of initiative, reduced

sexual interest, little overt emotion, and little or no verbal output.

• Pseudopsychopathy– immature behavior, lack of tact and restraint,

course language, promiscuous sexual behavior, increased motor activity, and general lack of social graces.

Speaking of frontal lobes… A case

46-yr.-old successful salesman sustained a compound depressed fracture of the left frontal bone in a MVA. Treatment included debridement and amputation of the left frontal pole. Recovery was slow, and 9 months post injury, he was referred for long-term custodial management. By this time, he had recovered motor function with only a minimal limp and slight hyperreflexia on the right side, had normal sensation, no evidence of aphasia, and normal memory and cognitive ability (IQ 118). Yet he remained in hospital care due to changes in personal habits.

46-year-old

Prior to injury he had been garrulous, enjoyed people, had many friends, an talked freely. He was active in community affairs, including Little League, church activities, men’s clubs, et cetera. It was stated by one acquaintance that he had true charisma, “whenever he entered a room there was a change in atmosphere, everything became more animated, happy and friendly.”

46-year-old

Following the injury, he was quiet and remote. He would speak when spoken to and made sensible replies but would then lapse into silence. He made no friends on the ward, spent most of his time sitting alone smoking. He was frequently incontinent of urine, occasional of stool. He remained unconcerned about either and was frequently found soaking wet, calmly sitting and smoking. If asked, he would matter-of-factly state that he had not been able to get to the bathroom in time, but that this didn’t bother him.

46-year-old

Because of objectionable eating habits, he always ate alone on the ward. His sleep pattern was reversed; he stayed up much of the night and slept much of the day. He did not resent being awakened or questioned. He could discuss many subjects intelligently, but was never known to initiate either a conversation or a request. He could give detailed accounts of his life prior to the accident, of the hospitals he had been in, and the doctors and treatment he had, but there was an unreality to his conversation.

46-year-old

When asked, he would deny illness, state emphatically that he could return to work at any time, and that the only reason he was not working was that he was being held in the hospital by the doctors. At no time did he request a discharge or weekend pass. He was totally unconcerned about his wife and children. Formerly a warm and loving father, he did not seem to care about his family. Eventually, the family ceased visiting because of his indifference and unconcern (Blumer & Benson, 1975, 156-157).

• Dikmen, Machamer, Winn, & Temkin (1995)– Prospective neuropsych outcome study with

436 head-injured and 121 general-trauma controls.

– Gender, age, & education matched.

– Evaluated 1 month and 1 year post.

– 92% of controls evaluated at 1 year.

– Independent Variables: GCS, # of non reactive pupils in ED, mass lesions requiring craniotomy, time to follow commands.

– Dependent Variables: Neuropsych Testing

TBI: Natural Cognitive Course

TBI: Natural Cognitive CourseAppendix B

• Further conclusions about mTBI– Research reveals that those with mTBI (defined as

minimal to no LOC, with norm mental status and imaging) will return to baseline by weeks to months post-injury.

• Five meta-analyses:– Belanger, Curtiss, Demery, Lebowitz, & Vanderploeg, 2005

– Belanger & Vanderploeg, 2005

– Carroll, Cassidy, Holm, Kraus, & Coronado, 2004

– Frencham, Fox, & Maybery, 2005

– Schretlen & Shapiro, 2003

– If mTBI is related to persistent sequelae it would be on the order of 1/8 sd (Millis & Volinsky, 2001).

– No multivariate prognostic model for variable mTBI outcome (Silverberg et al., 2015).

TBI: Natural Cognitive Course

Carroll et al. (2004)

Reviewed 428 studies related to prognosis of mTBI

120 were acceptable after critical review of their scientific merit.

Result was “best evidence synthesis on prognosis after mTBI.”

For adults, “cognitive deficits and symptoms are common in the acute stage, and the majority of studies report recovery for most within 2-12 months.”

“Where symptoms persist, compensation/litigation is a factor, but there is little consistent evidence for other predictors.”

Prognosis for Mild Traumatic Brain Injury: Results of the WHO Collaborating Centre Task

Force on Mild Traumatic Brain Injury


“The best evidence consistently suggests there are no mTBIattributable, objectively measured, cognitive deficits beyond 1–3 months’ post-injury in the majority of cases. Self-reported symptoms are common after mTBI; however there is little consistency in findings about how long such symptoms persist” (p. 101).

“On the other hand, symptoms usually resolve rapidly in athletes after a sports concussion, although it could be argued that they may under-report symptoms in order to resume play” (p. 101).






“Litigation and/or compensation have been consistently identified as prognostic of poor outcome in those cases that experience persistent symptoms and disability after mTBI, although again, no confirmatory study has been performed” (p. 102).

“No study reported that severity of the mTBI was an independent predictor of persistent post-concussion symptoms” (p. 102).




“There is an ongoing debate as to whether whiplash injuries to the head and neck can commonly result in MTBI, and our task force reviewed the available evidence. The evidence shows that mild cognitive complaints do occur after whiplash, but are not specific to MTBI and are not likely due to a brain injury per se” (p. 102).

“These same cognitive complaints are also reported in patients with chronic pain, depression, anxiety, post-traumatic stress disorder, chronic fatigue syndrome, malingering and in patients involved in personal injury litigation” (p. 102).

So, Where did the Miserable Minority Come From?

Much of the forensic private practice in neuropsychology is driven by persistent postconcussive complaints long after a mTBI.

It is frequently stated that roughly 15% of persons with mTBI have permanent impairment.

“Miserable Minority” (Ruff, Camenzuli & Mueller, 1996)

Traces to an influential Neurology paper by Alexander (1995).


Michael Alexander (1995) wrote: “At one year after injury approximately 15% of mTBI patients have not recovered” (p. 1256).

Others have cited this reference and number as common knowledge, including the CDC until 2007.

In fact, it is clinical “lore.”

Iverson (2005) wrote, “This estimate…is frankly wrong” (p.306).

So how/why did Alexander create it?


Come to find out, Alexander cited two studies to support his conclusion.

McLean, Temkin, Dikmen, & Wyler (1983)

Rutherford, Merrett, & McDonald (1979)

McLean, Temkin, Dikmen & Wyler (1983) The behavioral sequelae of head injury. Journal of Clinical Neuropsychology, 5, 361–376.

Involved mild AND moderate and severe TBI

The study followed 20 patients for only 1 month.

No 1-year follow up!


Rutherford et al. (1979) Symptoms at one year following concussion from minor head injuries. Injury, 10, 225–230.

145 consecutively admitted mTBI cases, with 1-yr f/u.

Although it was true that 19 persons (14.5%) still reported complaints at 1-year follow-up:

Only 131 were available for 1-yr f/u (13.1% of 145)

Eight (42%) were involved in lawsuits

Six (31%) showed malingering signs at 6 week assessment

Most complained of new symptoms at 1 year that were not reported at 6 weeks post-injury.

There was no control group, an omission making it difficult to draw conclusions about population base rates for symptoms.


Little dispute about “Miserable Minority.”

15% is only a myth if one equates a symptom (subjective complaint) with brain impairment (objective finding).

Complaint is not synonymous with disability.

This important distinction was addressed by WHO:

Carroll et al. (2004) PCS correlated strongest with litigation and secondary gain, but had no valid association with initial injury severity or any other neurological factor.


So called, “Postconcussion” Syndrome

ICD-10 Diagnostic Criteria for PCS

A. History of head trauma with loss of consciousness precedes symptoms onset by maximum of four weeks.

B. Symptoms in three or more of the following symptom categories:i. Headache, dizziness, malaise, fatigue, noise intolerance

ii. Irritability, depression, anxiety, emotional lability

iii. Subjective concentration, memory, or intellectual difficulties without neuropsychological evidence of marked impairment

iv. Insomnia

v. Reduced alcohol tolerance

vi. Preoccupation with above symptoms and fear of brain damage with hypochondriacal concern and adoption of sick role.

• Estimates vary widely, but 40%-60% of mTBI experience PCS up to 30 months post-injury(Szymanski & Linn, 1992).

• Problem is two fold:– Persistent complaints in absence of neurological

findings.

– Condition specificity.

Post-Concussion Syndrome

Postconcussion Syndrome: Base Rates!

Subjects Headache Dizziness Irritability Memory ConcentrationCollege Students1

36% 18% 36% 17% 42%

Chronic Pain2

Depressed3

PI Claimants (non-TBI) 4 mTBI5

College Students6

College Students7

Depressed8

80%

37%

77%

42%

67%

20%

41%

26%

49%

52%

63%

28%

33%

25%

46%

36%

63%

54%

71%

25%

40%

36%

27%

32%

44%

42%

60%

46%

60%

59%

59/28% 31/11% 77/36% 70/42% 78/47%

1Sawchyn,et al. (2000)

2Radanov et al. (1992)

3Trahan et al. (2001)

4Dunn et al. (1995)

5Ingebrigtsen et al. (1998)

6Chan (2001)

7Wang et al. (2006)

8Iverson (2006)Mild/moderate

• PCS symptoms commonly found among healthy subject w/o history of TBI (Chan, 2001; Gunstad & Suhr, 2004; Iverson, 2006; Iverson & Lange, 2003; Wang et al., 2006; Wong, Regennitter, & Barrios, 1994).

• Non-significant differences between healthy controls and TBI (Gouvier, Cubic, Jones, Brantley, & Cutlip, 1992; Gustad & Suhr, 2004).

• A recent Study by Garden & Sullivan (2010) of university and community volunteers in Australia using the British Columbia Post-Concussion Symptom Inventory.

Post-Concussion Syndrome

PCS Symptoms %

Headache 81.3

Dizziness 52.1

Nausea 53.2

Fatigue 81.3

Noise sensitivity 34.4

Irritability 78.1

Feeling sad 70.1

Nervous or tense 76.0

Temper problems 58.3

Poor concentration 73.4

Memory problems 56.3

Difficulty reading 36.5

Poor sleep 68.8

Post-Concussion SyndromePercentage of BC-PSI Symptom Endorsement: Frequency ratings for all

levels of intensity. N = 96. From Garden & Sullivan (2010)

1

1

2

3

4

5

6

• 23-year-old, married man

• Rear-ended by semi-truck on interstate

• 11th grade education.

• No psychiatric history.

• ~7 beers a night, 2 weekends a month from 18 to 20 years of age.

• Denied illicit drug use.

Case Example

• Witnesses noted apparent LOC of moments/minutes, self-extricated from car.

• EMS found him alert and walking.

• GCS = 15

• 14 cm scalp laceration & broken rib

• Life Flight to Trauma Center

• He recalls the light of the semi coming upon him.

• He describes PTA until paramedics talking to him, “they said they would pull him out” of the car (?).

• Remained in hospital 40 hours.

Case Example

• Current Complaints– Pain in chest and hip.– Can’t change a light bulb.– Buzzing in ears.– Poor sleep– Nocturnal jerk/spasm (sensation of falling/startle)– Becomes nauseous when trying to concentrate.– Doesn’t notice things in his field of vision.– Poor memory: Can’t remember things or people’s

faces.– He “will put spoon in and stir an empty cup.”– Brings wrong key out to the car.– Significant PTSD symptoms.

Case Example

• NeuropsychEvaluation at request of plaintiff 20 months later.

Case Example Case Example

Case Example

PAI

Case Example


• Axis I:– Cognitive Disorder NOS (post concussive

syndrome)

– Posttraumatic Stress Disorder, chronic

– Major Depressive Disorder, single episode, severe

– Pain Disorder associate with both psychological and factors and underlying general medical condition

– Personality change due to head trauma

• Axis II: – No diagnosis

Post hoc ergo propter hoc

Caution! Caution! Caution!

Case Example

Case Example

60 37.5 52.5 15 30 12.5

37.5% = z -1.42 p = 0.078

Case Example

80 70 60 30 40


• SIMS– NI 7 (>2)

– AF 5 (>5)

– P 1 (>1)

– LI 3 (>2)

– AM 9 (>2)

– Total 25 (>14)


• My Clinical Formulation:– From notes

– My CLINICAL FORMULATION

• Axis I:– Malingered Neurocognitive Dysfunction

– Malingered and/or exaggerated PTSD symptoms

• Axis II:– No Diagnosis

Repeatable Battery for the Assessment of Neuropsychological Status

RBANSby Chris Randolph, Ph.D., ABPP

Psychological Assessment Resources (PAR)

RBANS

• Brief individual administered test that measures:– Attention

– Language

– Visuospatial/constructional ability

– Immediate and delayed memory

• 12 subtests: 20-30 minutes

• Ages 20-89 Stratified, nationally represented N = 540 (6 groups; N=90)

• 2012 update down to 12 yrs (12-19: 3 groups; N=50)

• 4 alternate forms (+ 1 Spanish version)

RBANS

• Three-fold purpose:

– Stand-alone “core” battery for detection of dementia in the elderly.

– Neuropsychological screening battery when lengthier standardized assessments are impracticable or inappropriate

– Repeat evaluation when an alternate form is needed to protect against content practice effects.

RBANS Alternatives

• Mini-Mental Status Examination (Folstein et al., 1975)– Omnibus total score only

– Insensitive to mild dementia/cognitive compromise.

– But pretty quick.

• Saint Louis University Mental Status Examination (SLUMS) (online)

• Dementia Rating Scale-2 (PAR)– Ages 56-105

RBANS Subtests

• 12 Subtests– List Learning

– Story Memory

– Figure Copy

– Line Orientation

– Picture Naming

– Semantic Fluency

– Digit Span

– Coding

– List Recall

– List Recognition

– Story Memory

– Figure Recall

• Form A, B, C, D

• Spanish A & B

RBANS

• Immediate Memory• List Learning & Story Memory

• Visuospatial/Constructional• Figure Copy & Line Orientation

• Language• Picture Naming & Semantic Fluency

• Attention• Digit Span & Coding

• Delayed Memory• List Recall, List Recognition, Story Recall, & Figure

Recall

• Total Scale Index

RBANS

• Reliability coefficients vary from .80-.94

• Test-retest stability from .55-.88

• Validity demonstrated against standard neuropsychology tests– E.g., WAIS-III, WMS-III, Boston Naming Test,

Judgment of Line Orientation Test, & verbal fluency tests.

• The manual includes data from various neuropathological groups for comparison purposes. Revised RBANS Scoring.xls

RBANS

• Early Alzheimer’s Disease

• 73-year-old successful lawyer

• Referred by primary care physician

• Wife noted forgetfulness over last year– Misplacing things

– Frequently repeats questions

– Forgets details of conversations

• MRI normal

• Labs normal

• What would you expect regarding deficits?

RBANS

• WRAT Reading 120• WAIS-R FSIQ 114• WMS-R Verbal

Memory Index 96• BNT 48/60• RCFT Copy 34/36

• 18 months later– FSIQ 108– RBANS Total 74– BNT 40

RBANS

• Post Anoxia

• 34-year-old clinical psychologist

• Elective surgery, but respiratory arrest during recovery

• Several minutes passed before she was revived

• 3 days later consult in ICU– Alert, responsive, cooperative, good details of

early childhood and high school, but no recall for most recent 5 years.

RBANS

• Acute phase of recovery

• Language poor due to fluency.

• No signs of delirium

• Virtually no recall and chance recognition.

RBANS

• Anoxia• 6 months later:

– Visuospatial/Constructional Index– Attention Index– Language Index– All at 100 or above

• Immediate Memory Index 78• Delayed Recall Index 40• Retrograde tail reduced to weeks.• Short WAIS-R FSIQ 114• Cognitive rehab• Obtained apart-time job doing claims review for

manage behavioral health care company.

RBANS

• mTBI Early Course• 20-year old college sophomore• Serious MVA, unrestrained in back seat• LOC 30 minutes• Confused at ED• CT WNL• Released next day

– Roommate noted: irritable, losing temper, throwing things (he threatened to move out unless pt. got help).

• What would you expect?

RBANS

• C/O– Frustrated with

coursework

– Failed history test

– Trouble concentrating

– Sleepy during day

• Depression?

• Referred for NP Consultation

• What do you expect for the natural course?

RBANS

• Full NP confirmed mild deficits in attention and anterograde memory without significant compromise of most other cognitive functions.

• Academic Load was reduced for the semester w/o penalty

• Education for modifying his sleep and study habits

• Mood stabilized over several weeks

• Took catch up classes over summer

• Back to baseline by next fall

Ardolf, B. R., Denney, R. L., & Houston, C. M. (2007). Base rates of negative response bias andMalingered Neurocognitive Dysfunction among criminal defendants referred forneuropsychological evaluation. Clinical Neuropsychologist, 21, 899-916.

AACN Board of Directors (2007). American Academy of Clinical Neuropsychology (AACN) practice guidelines for neuropsychological assessment and consultation. The Clinical Neuropsychologist, 21, 209-231.

Baxter v. Temple, No.01–c–0567 (N.H. Sup. Ct. Aug. 8, 2005) (order granting motion in limine).

Belanger, H. G., Curtiss, G., Demery, J. A., Lebowitz, B. K., & Vanderploeg, R. D. (2005). Factors moderating neuropsychological outcomes following mild traumatic brain injury: A meta-analysis. Journal of the International Neuropsychological Society, 11, 215-227.

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