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![Page 1: Cognitive and Neuropsychiatric Effects of Stroke Thomas Sugalski, Ph.D. Psychology Associates of Bethlehem March 7, 2015 De Sales University.](https://reader035.fdocuments.in/reader035/viewer/2022062712/56649c9a5503460f94957f95/html5/thumbnails/1.jpg)
Cognitive and Neuropsychiatric Effects
of Stroke
Thomas Sugalski, Ph.D.
Psychology Associates of Bethlehem
March 7, 2015
De Sales University
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Vascular Cognitive Impairment- Introduction -
Heterogeneous group of cognitive disorders
Share vascular cause
No “typical” patient
Symptoms range from mild to severely disabling
Executive dysfunction or classical AD phenotype
Presentation depends
Location, extent of cerebrovascular disease
Severity of co-existing neurogenerative pathology
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History of TerminologyUnderstanding of how syndrome has evolved
“Senile dementia”, “hardening of arteries”
Multi-infarct dementia
Used interchangeably with Vascular Dementia VaD
VaD superseded by VCIRecognize dementias with mixed neurodegenerative (AD) and vascular features
Step away from “Alzheimerization of dementia”
• Recognizing that memory impairment may not be one of cognitive domains affected
• Vascular Cognitive Impairment, No Dementia - VCIND
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Clinical Subtypes of Vascular Cognitive Impairment
Subtype DescriptionVascular Dementia (VaD)
Disorders in the original VaD construct (post-stroke dementia, multi-infarct dementia, subcortical dementia syndromes)
Mixed dementia (Alzheimer disease/VaD)
Cognitive impairment associated with a mixed vascular and neurodegenerative cause (most often AD)
Vascular cognitive impairment, no dementia (VCIND)
Cognitive impairment of presumed vascular cause whose symptoms are not associated with significant functional impairment
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Epidemiology
Cognitive impairment with vascular etiology common1/3rd those with dementia show vascular pathology at autopsy
2nd most common form of impairment after ADPrevalence - 1.5% over age 70 to 39% over 65
Incidence -VaD ranges from 6 to 12 cases/1000 over age 70
VCI affect increasing number of patientsPopulation aging
Increasing prevalence cardiovascular disease
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Conceptual Neuropathological Subtypes of VCI
Large Vessel Disease
Small Vessel Disease
Non-infarct Ischemic Changes
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Conceptual Neuropathological Subtypes
Large Vessel Disease
Post-stroke dementia clinical archetype for VCI caused by large vessel disease
Prevalence dementia after stroke 14-32%3 months 20%
5 years 33%
Post stroke dementia has shown inconsistent relationship:Smoking
DM
HTN
Hyperlipidemia ? Number of risk factors More robust predictor
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Neuropathological SubtypesLarge Vessel Disease
Dementia can occurSingle strategic infarct Multiple strokes/varying size and locations
• Angular gyrus Caudate Basal Ganglia
• Hippocampus Globis Pallidus Basal Forebrain
• Thalamus
Post-stroke dementia more commonOlder age
Low educational attainment
Pre-existing cognitive impairment
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Neuropathological Subtypes
Small Vessel Disease – Most common cause VCILeukoaraiosis
Subcortical infarcts
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Neuropathological Subtypes
Leukoaraiosis (Small Vessel Disease)Describes diffuse, punctate, or confluent white matter abnormalities
MRI (hyperintensity of white matter), CT (hypodense)
Occurs with infarcts, leukodystrophies, metastases, inflammatory condition
Detected in most older adults
No distinct cognitive profile
White matter changes associated with
• Increased risk of stroke
• Dementia
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Neuropathological Subtypes
Leukoaraiosis (continued)Small amounts of white matter abnormalities
• Memory/language impairment some patients
Large amounts
• Cognitive impairment • Motor deficits
• Personality change • Urinary incontinence
• Gait disturbance
In deep white matter
• Executive impairment
• Slowed processing speed
• Working memory
• Visuo-spatial abnormalities
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Neuropathological Subtypes
Sub-cortical Ischemic Vascular Disease (SIVD)Occurs through… Within…
Small vessel infarct • Cerebral white matter
Ischemia • Basal Ganglia
Incomplete ischemia • Brainstem
• Prefrontal subcortical circuit
Thalamo-cortical circuit
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Neuropathological Subtypes
Pattern lesions associated with clinical syndromePre-frontal subcortical circuit (pre-frontal cortex, caudate, pallidum, and thalamus) or Thalamo-cortical circuit
“subcortical syndrome” “dysexecutive” syndrome
• Deficits in ability to plan, organize, initiate, and shift between tasks
Three distinct frontal lobe syndromesDorsolateral (executive functions and impaired recall)
Orbitofrontal (behavior, emotional changes)
Anterior cingulate (ebulia, akinetic mutism)
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Neuropathological Subtypes
Non-infarct Pathology in VCINot all lesions are infarcts
Neuropathological abnormalities
• Amyloid proteins aggregating in vessel walls and cortical arteries, aterioles, capillaries, veins
Cognitive profiles similar to SIVD
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When to Look for VCI?
Becoming more common in aging population
Cognitive screening
Over age 65
Vascular risk factors• HTN• DM• Hyperlipidemia• Evidence white matter disease
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Common Neuropsychological Symptoms
Executive DysfunctionCentral functions that control other abilities
• Plan
• Organize
• Decision making
Problems most detectable in non-routine situations
Classes of executive disorders
• Behavioral
• Cognitive
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Common Neuropsychological Symptoms
Behavioral DisturbancesGlobal hypoactivity with abulia, and apathy, and aspontaneity
Global hyperactivity with distractibility, impulsivity, disinhibition
Perseveration, stereotyped behavior
Syndrome of environmental dependency (imitation and utilization behavior)
Disturbances of emotion, social behavior
Anosognosia
Confabulation and reduplicative paramnesia
Disorders of sexual behavior, hyperorality
} Highly Suggestive
}Supportive Features
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Common Neuropsychological Symptoms
Cognitive Disturbances Response initiation
Response suppression
Focused attention
Rule deduction, shifting set
Problem solving, planning
Information generation
Sustained and divided attention
Working memory
Processes of Retrieval
“Theory of Mind”
}Highly Suggestive
}Supportive Deficits
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Memory Deficits
Memory disorders after stroke common
Can occur following strokes to all cerebral arterial territories
ACA
MCA
PCA
Deep Branches
Hemiparesis, aphasia typically overshadows memory complaints
Over 50% of all stroke survivors complain of memory difficulties
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Memory Deficits
Memory is not a unitary capacityEpisodic memory – remembering personal experiences
Semantic memory – storage, retrieval of general knowledge, facts
Procedural memory – learn activities, skills that will then be performed automatically
Working memory
– governs ability to pay attention, concentrate
– holding information, manipulating information
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Distribution of Functions
Although brain is symmetrical organ, there is a lateralized distribution of functions
Left-Hemisphere
Organization of functions discreet
Sequential/analytic processing style• Extract/process perceptual detail• Temporal resolution of events (rapidly
changing speech sounds)
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(L) Hemisphere Dominant for Verbal Abilities
Oral and written language
Production and comprehension of phonology/syntax
Motor planning
Gesture communication
Number processing
Calculation
Verbal memory (semantic memory)
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(L) Hemispheric Cognitive Syndromes
(L) hemispheric vascular lesions
Aphasia
Reading/writing disorders
Learned skill - buccofacial, limb apraxia
Depression
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Distribution of Functions
Right Hemisphere
Functions distributed in large scale networks
Has a more “configurational” processing style• Integrate across inputs• Process global percepts (faces, voices, music)• Comprehension of metaphoric/emotional
components of language• Better ability to handle new information
(LH) superior in automatized processes (reading, writing)
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(R) Hemisphere Specializes in Visuospatial Abilities
and other “non-verbal” (or difficult to verbalize) abilities
Capacity to orient
Engage and shift attention
Processing and recognition of complex visual patterns
Visual learning
Typographic memory
Music
Emotions
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(R) Hemispheric Cognitive Syndromes
(R) hemispheric vascular lesions
Unilateral spatial inattention or neglect
Transient mutism, abulia, akinesia
Alien hand syndrome
Production/comprehension emotional speech
Delusional misidentification syndrome
Agitation, anxiety, emotional incontinence, mania
Hallucinations, apathy, anasognosia
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Emotional Distress Accompanying Stroke
More than 100 years, recognition emotional disorders accompany stroke
Causes viewed from two perspectives
Pathological changes produced by brain injury
Psychological responses to impairment
Neuropsychiatric symptoms Depression - Apathy
Mania - Disturbances of prosody
Anxiety - Irritability
Psychosis - Pathological laughing & crying
Catastrophic Reaction
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How Do We Classify Depression?
Is depression a continuum or are there distinct formsResearchers distinguished between major depression and minor depression
When viewed in this mannerDuring acute stroke period patients with
• Minor depression posterior lesions of (L) hemisphere
• Major depression anterior (L) hemisphere lesions
Depression related cognitive impairment associated with major but not minor depression
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What is Prevalence of Post Stroke Depression?
Most common/severe emotional disorderMajor depression can last average of almost 12 months
Few last three years or more
Minor depressionFew months to 24 months
Can develop into major depression
Risk developing post-stroke depression last for at least 2 years
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Differences Between Post Stroke Depression and Primary Mood Disorder?
Phenomenology of MDD w/stroke appears similar to that found in patients with primary mood disorder
Post Stroke DepressionProvoked by injury to strategic areas of brain
By social, psychological factors
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Is There a Remission of Depressive Symptoms?
Two consistent findings:Majority post stroke major depression over by 12 months
Remissions occur without treatment
Primary depressions (patients with no lesions), natural course of approximately 9 months
Group of post stroke depressionsDo not remit within one year
Become chronic major depressions
Possible pre-morbid vulnerabilityFamily history of mood disorder
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What is the Time of Onset?
Depression may develop
During acute post stroke period
Several months
Years following stroke
Some acute, some delayed depressions related to lesion location
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Depression and Lesion Location
During first two months
Frequency of MD 2x as great following:• (L) Frontal or (L) Basal Ganglia Stroke, compared
• (R) Anterior Lesions or (L) Parietal/Occipital Lesions
Over 6 months
Severity of depression symptoms correlate with proximity of lesion to L-frontal pole
Frontal-Basal Ganglia-Thalamic circuits mediate post stroke depression
Areas of brain injury related to depression disorders
Basal Ganglia, compared with thalamic stroke
MCA compared to infarcts of posterior circulation (i.e. vertebral-basilar arteries supplying brainstem, cerebellum, thalamus, posterior hemisphere)
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Depression and Lesion Location (cont’)
What about R-Hemisphere stroke?Depression associated with family history of psychiatric disorder
Anterior, posterior lesion locations
Insular CortexDepression not associated
Tiredness, amotivational states
Greater frequency depression/anxiety withLateral pre-frontal lesions vs. medial frontal lesions
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Depression and Physical Impairment
Many investigations of this relationshipMotor impairment most common presenting symptom
• Acute hemispheric stroke Motor impairment = 70/80% Sensory Loss = 35% Visual Loss = 25%
Severity of depression in first few months after stroke associated with impaired recovery in ADL’s at 1-2 year follow-up.
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Depression and Social Functioning
Patients with,Poor social support develop depression
Depression deteriorate in social functioning
Focus of concern change over timeAcute
• Impaired relationship with closest other• Limited social activities prior stroke
3 to 6 months• Fears of economic security• Limited social activities
1 to 2 years• Fear of loss of job satisfaction
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Suicidal Thoughts and StrokeAmong stroke patients
SI relatively frequent, completed suicide rare
About 10% of patients with stroke develop suicidal thoughts
Strongest association with suicidal thoughts is existence of MD
Typically go away when no longer depressed
Factors playing role in development of suicidal planSocial isolation
Younger age
Prior alcohol abuse history
Cognitive/social impairment
Prior stroke
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Causes of Post Stroke Depression
Should be considered in light of clinical findings
Cognitive impairment associated with major, not minor depression
Following the left, but not right hemisphere stroke
Associated with (L) frontal, (L) basal ganglia lesions
MD associated with proximity lesion to frontal pole
Minor depression with posterior lesions of (L) hemisphere
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Causes of Post Stoke Depression
Major debate in literaturePsychological response to impairment/loss
Neurophysiological response to brain injury
Etiology of PSD, like all depressive disorders, unknownSerotonin depletion
• Metabolites of serotonin decreased in spinal fluid of depressed stroke patients
• Serotonin receptors decreased in (L) temporal cortex
Cortical-thalamic circuits are disrupted
• Ischemic injury
• Altered serontonergic modulation
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Causes of Post Stroke Depression
Recent workIschemic injury increased production proinflammatory cytokines activates or inhibits enzymes decreased production of serotonin
Disruption of certain frontal-thalamic circuits decreased perception of emotional stimuli, perhaps by serotonergic dysfunction
• i.e. inability to experience happy emotional feelings depression
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Post Stroke ManiaSymptoms
Elevated mood
Decreased sleep
Increased talk
Increased activity
Grandiosity
Risk FactorsFamily history mood disorder
Right hemisphere lesions• Orbitofrontal cortex• Basotemporal cortex• Basal ganglia• Thalamus
Lithium remains first line of treatment
About 1% higher frequency in TBI
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Post Stroke Anxiety Disorders
Frequency of experiencing anxiety with acute stroke is 21%
50% will have Major Depression
33% will have Minor Depression
CorrelatesPrior history alcohol abuse
Right hemisphere cortical lesions
Greater impairment ADL’s/social functioning
Natural courseAcutely after stroke = 1.5 months
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Psychosis Following Stroke
Variety of presentationsNo insight about the non-reality of hallucination/delusion
Retain awareness of reality in spite of existence of hallucinations (Peduncular Hallucinosis)
Associated with (R) hemisphere lesions
Often affecting parietal temporo-occipital junctionSome subcortical, mostly cortical lesions
Seizures
Subcortical brain atrophy
Small vessel disease
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Anosognosia and Denial
1. Anosognosia – failure of awareness of one’s own deficits/diseases
2. Denial – failure to acknowledge illness/deficits
– reported among patients with/without brain injury
Patient has brain injury
• Nature of brain injury creates cognitive/sensory impairments deficits in awareness of impairment
No brain injury
• Unawareness psychological response
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Anosognosia and Denial
3. Indifference Reaction – do not deny the existence of impairment , but their unconcern seems clearly inappropriate to severity to illness
4. Alien Hand Syndrome – inability to recognize that one’s hand, usually the left, is their own
Try to throw hand out of bed
Strike it with the right hand
Button shirt with (R) hand, (L) hand follows, undoing work of (R) hand
Usually (R) hemisphere has sustained injury
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Anosognosia and Denial
Attempts to ExplainPsychological etiologies
• Denial is a psychological defense mechanism
• Which attenuates the emotional impact of a catastrophic reaction
Confusional state
Insufficient sensory feedback to brain that limb is weak
• Or, proprioceptive system is impaired
• Consequently, they do not sense an absence of motor activity
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Anosognosia and Denial
Attempts to Explain (cont’)Hemispatial neglect
• If patient neglects their (L) visual field
• May be unaware there is no movement in their (L) arm
Disconnection syndrome
• With areas in (R) hemisphere disconnected from language centers in (L) hemisphere
• Leading to language-mediated unawareness of impairment
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Anosognosia and Denial
Today…Not associated with prior history of psychiatric disorder
Higher frequency of (R) hemisphere lesions
Dysfunction in pathways extending from
• (R) parietal/temporal lobe basal ganglia thalamus orbitofrontal cortex
• Could impede integration of sensory input
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Catastrophic ReactionSudden onset – anxiety, tears, aggressive behaviors, swearing, compensatory boasting
A response to the inability of person to cope
Emotional outbursts last only a few seconds
Usually associated with stressor
Prevalence estimates ranged from 4% to 19%
Clinical correlatesImpairment severity
Post stroke MD
Basal ganglia lesions
Reaction can be very disruptive families
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Apathy
A lack of feeling or emotion, or lack of interest or concern
27% of patients
Associated with lesions of many brain regionsThalamus
Frontal
Sub-cortical
Cortical – basal ganglia – thalamic circuits implicatedSame circuit suspected in depression
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Pathological Laughing, Crying
Outbursts of emotion which are out of proportion to the underlying feelings of happiness and sadness
Occurs in approximately 15% patients during acute post stroke period
20% during first year
Socially DebilitatingMay occur as frequently as 100 times a day
Last from few seconds to several minutes
Embarrassing for patient
Fears of uncontrollable emotion social phobia, withdrawal
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Pathological Laughing, Crying
Most frequent clinical correlate:Depression
Clinical pathological correlates:Unilateral lesions of basal ganglia
Frontal or temporal cortex
Lesions of brain stem
Periventricular structures
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Disturbance of ProsodyMelodic line of speech produced by variations of pitch, rhythm, and stress of pronunciation
Two types:Comprehension of affective prosody – recognizing emotional intonation in a person’s affective expression
Expressive affective prosody – showing facial expression consistent with their own mood
Comprehension of prosodyAssociated with (R) temporoparietal, (R) basal ganglia lesions
Patients unable to comprehend emotional intonations appear able to recognize their own inner emotional state
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Irritability and AggressionCommon disorder associated with several conditions:
Stroke
Dementia
TBI
Huntington's disease
Clinical correlates with strokeGreater cognitive impairment
Greater frequency of depressive symptoms
Higher frequency of major depression
Generalized anxiety
Lesions closer to frontal pole