Exam 1 (weeks 1-3) Flashcards
Cog-Com skills
problem-solving, planning, decision-making, behavior regulation, social communication
Associated cognitive function
Attention, memory, reasoning, inferencing, abstract thinking, etc.
Associated communication function
Prosody, facial expression, social scripts, turn taking, non-literal language, etc.
Cognitive Communication
- language in use, not structure
- functional communication
- cognitive processes supporting functional communication
- neurological structure and functions supporting cognitive processes
functional communication
- communicating wants and needs
- communicating emotional state appropriately
- taking social context into account
Injuries that cause cog-com dis
- cerebrovascular accident (CVA), aka stoke
- trauma
- sudden onset, subsequent recovery
CVA (stroke)
- caused by clot or hemorrhage
- disrupt blood flow and cause cell death
- localized damage
trauma
- closed or open (through dura) head injury
- penetrating (always open) or blunt (either)
- impact and movement cause causes cell death
- swelling, bleeding, and neurochemical changes exacerbate and can have global impact
Disease that cause cog-com
- multiple possible disease processes
- micro changes lead to macro differences
- progressive deterioation
multiple possible diseases process
- multi-infarct
- protein clumps or other cell abnormalities
- lead to cell death and atrophy
Micro-changes lead to macro differences
global impact possible
causes of cog-com dis
CVA, trauma, and disease
cognitive communication profiles
- dementia
- traumatic brain injury (TBI)
right hemisphere disorder (RHD)
not a one to one correspondence
- CVA and trauma can lead to RHD or TBI
- Multiple CVA and repeated trauma can lead to dementia
Hippocampus
the main area for memory formation
damage to fornix
results in amnesia, important structure for memory formation
occipital lobe
vision- in between preoccipital notch and the parieto-occipital sulcus
parietal lobe
- somatosensory (post central )
- sensory homunculus
- pain and temperature
- integrative! (making sense of signals)
temporal lobe
- receptive language (left side only)
- memory
- hearing (auditory processing cortex)
frontal lobe
- executive function
- primary motor (precentral gyrus)
- expressive language
- Brocas area
- memory attention, decision making, impulse control
Limbic system
- emotion regulation
- memory consolidation (Papez)
basal ganglia
motor coordination/ feedback loop
cerebellum
- memory/sensory (proprioception) integration
- cognitive involvement
Meninges
- skull
- dura mater (outermost layer)
- arachnoid (blood vessel)
- subarachnoid space (present) where the cerebralspinal fluid lives
- pia mater
Apoptosis
- diminishing of neurons as we age
- neuronal “pruning” as part of the normal aging process throughout the life span
- hard to quantify (20-40% of brain cells)
- appears as widened sulci and ventricles on imaging
- not equally disrupted: (hippocampus and frontal lobe)
What abilities so we lose in normal aging?
- processing speed
- word finding abilities
- short term memory
Aging brain unique to humans?
-Atrophy of brain normal in humans
- not universal to mammals
different models of aging
- disease/disabled aging
- usual aging
- successful aging
disease/disabled aging
non-age related disease or pathology
usual aging
age-related physiological changes
- renal function
- memory/word finding
- thinning of skin
successful aging
- avoidance of age-related pathology or disease
- minimal interruption of usual function
- variable profiles ( not all cognitive abilities are affected the same)
- protective or detrimental effects of (education, physical health like cardio for cardiopulmonary, mental health, and psychological factors)
Seattle Longitudinal study
Looking at people’s cognitive functions and several sorts of standardized tests to determine their cognitive functions as they age in 7-year increments
- higher education good
- physical health (particularly cardio-pulmonary) good
- self-efficacy protective good
- depression is detrimental bad
- neurological changes not 100% predictive of cognitive function
key to Successful Aging
- physical activity
- positive mental attitude
- self-efficacy
- social engagement (high educational level and creativity)
- not 1:1 of structure and function
implications
- neuroplasticity even in old age
- mental and physical activity can alter the brain
- inconsistent cognitive profiles related to both anatomy and physiology
- mental decline is not inevitable
information processing model of memory a three-stage model
sensory input > sensory register (forgetting) > short-term memory (forgetting and rehearsal) > long term memory
retrospective memory
- declarative memory and procedural memory
declarative memory
- semantic memory: I know what a car is.
- episodic memory: I remember buying my car
procedural memory
I remember how to drive a car
1-2 seconds time frame
- sensory stage
- sense organs, primary auditory, somatosensory, and visual cortex
0-30 seconds time frames
- immediate (short-term, primary, working)
- sensory and motor association areas and prefrontal regions
30 seconds - days time frame
- recent
- medial temporal lobes (hippocampus and amygdala), diencephalon (hypothalamus and dorsal medial nuclei of thalamus)
days - years
- remote
- left and right association cortex
hippocampal damage
impaired formation of new declarative memories
damage to the diencephalon (thalamus, hypothalamus)
impaired learning and retrieval
the function of circuit of Papez
- subset of limbic system interconnections
- multiple passes through the circuit results in memory consolidation
Circuit of Papez steps
- hippocampus
- mammillary bodies
- anterior thalamic nuclei
- cingulate cortex
- entorhinal cortex (hippocampus/neocortex gateway)
- back to hippocampus
frontal lobe damage
inattention, poor short term memory (STM)
Amnesia
- deficit in consolidation
- short term memory intact
- affects episodic (explicit) memory. Implicit (procedural, habitual) not affected
- if only memory effected
- if memory, language, cognitive processes, executive function, etc affected: broader cognitive- communication disorder
anterograde amnesia
inability to form new long term memory
retrograde amnesia
recall preciously stored memories
Cognitive Reserve
- neurological changes associated with aging do not necessarily correlate with cognitive function
- bank that we have until neurological changes affect our function
neurophysiological compensation
- a person does have a deficit
- in a sentence comprehension task, older adults were able to use working memory or problem-solving areas of the brain to help with comprehension
- our brain can REROUTE to other areas if needed
Why nuns? in religious order study
- similar lifestyles/routines
- had the same environmental factors, social factors to help make the study equal
How does the religious study relate to the Seattle study?
- not always a simple 1:1 relationship between structure and function
- support the idea of successful aging
- promote idea prevention (to some degree) is possible
- in both studies, higher education, good physical health, self-efficacy, and creativity were protective. Depression and feelings of isolation were detrimental
What did the religious study find?
- detrimental to cognitive functioning: psychological stress and feeling of isolation
- protective factors: being conscientious/ having self-control, size of the social network, creativity
- depression is detrimental
- neurological changes don’t predict cognitive function psychological factors may be a better predictor
- psychological stress bad
- being conscientious (self-control), good
- feeling isolated bad
- size of social network (average 7.5) good
creativity good
psychological factors relate to cognitive function, not neurological changes
Normal aging
- apoptosis
- minimal interruption to usual function
- age-related physiological changes in renal function memory, WORDING FINDING ABILITY, and thinning of the skin
- decrease the ability of processing speed, intelligence, vocab or syntactic skills, word finding, sense of humor, long-term and short-term memory
Delirium
- sudden onset
- can come and go
- rapid deterioration
- confused mental state
- hypo-aroused
- transient rapid onset
- symptoms over lapped with dementia
Minor cognitive Impairment
- does not affect ADL’s/ independence
- gradual onset
- a significant decline from previous performance in one or more cognitive domains can be attributed to a mental disorder
- can be prodrome to dementia
- a future decline not required
- beginnings of anomia, TOT, memory
Normal Pressure Hydrocephalus
- magnetic gait
- enlarged ventricles
- affects bladder function
- treatment via shunt
- glued feet, no tremors, and bladder dysfunction
- Gradual CF pressure buildup affects gaits and functions like memory, EF, and language
- mostly 60 years +
- enlarged ventricles
- classic NPH gait pre-shunt
- similarities to Parkinson’s and Alzheimer’s
Frontotemporal dementia nuero bases
- Most likely to have a genetic origin, but has multiple causes
- Tau and TDP43 protein clumps (Pick bodies)
- Protein clumps primarily affect frontal and temporal lobes causing reduction in gyri
Frontotemporal dementia clinical presentation
- Comprise 2 to 5% of dementia cases
- Primary initial symptoms are language and behavior related, not memory
- Two subtypes with slightly different presentation:
(Pick’s disease & Primary Progressive Aphasia)
Frontotemporal dementia disease progression
- Pick’s disease
Characterized by personality changes first (changes in behavior, judgment, and empathy)
Speech, language, and memory changes follow
Onset before 65 - Primary Progressive Aphasia
Expressive and receptive language deficits appear first
Attention, memory, executive functions follow
Onset before 65
Vascular Dementia neuro bases
- Caused by series of lacunar infarcts (small strokes)
- 2 types of infarcts:
Large vessel/cortical infarcts (like stroke)
Small vessel/subcortical infarct (gradual & vague deficits) - Often goes along w/ AD
- Risk factors & medical treatment similar as for CVA
Vascular Dementia clinical presentation
- The presenting symptoms depend on where the lacunar infarct took place
- Unlike AD they often have a more intact awareness of their condition
- Defined or Gradual onset of deficits dependent upon size and location of affected vessels
- (Large Vessels) Defined onset; Identifiable areas of damage
- (Small Vessels) Gradual onset; Vague deficits; often integrative/executive functions
Step-wise deterioration and intermittent functional plateaus/improvement
**patients that will tell us they’ve had a “mini” stroke
Vascular dementia disease progression
- Small vessel/subcortical infarcts:Gradual onset of deficits (often executive functions)
- Large Vessel/cortical infarcts: defined onset, identifiable areas of damage
- Can be differentiated by deterioration and intermittent plateaus/improvement
Dementia with Lewy body nuero bases
- Caused by build-up of alpha-synuclein protein inside neurons:
Cortical Lewy bodies
Brain stem Lewy bodies (in substantia nigra)
Dementia with Lewy bodies clinical presentation
- Similar to Parkinson’s Disease in physical symptoms
Ex: tremors, stiffness, slowness of movement, festinating gait - Similar to Alzheimer’s Disease in cognitive symptoms
Dementia with Lewy bodies disease progression
- Relative progression of:
Physical and cognitive features
Fluctuating cognition
Hallucinations
Visuospatial deficits - Braak Stages of Progression
1-2: autonomic & olfactory disturbances
3-4: sleep & motor disturbances
5-6: emotional & cognitive disturbances
Alzheimer’s Disease Neuro Bases
Early onset:
Beta-amyloid overproduction (plaques)
Chromosome 21,14,1
Late onset:
Susceptibility gene and ApoE
Caused by a genetics and the environment
Alzheimer’s Disease clinical presentation
- Two or more cognitive areas are affected
- Memory is affected (new before remote)
- Decline in language context first before form
- Apraxia worsens and the perception
- Impaired ADLs
- Sundowning
- Alertness and the circadian rhythm are affected
- definitive diagnosis at autopsy (plaques and tangles)
Alzheimer’s Disease disease progression
- Decreased interest in activities
- Articulate speech becomes difficult often become mute (severe)
- Social withdrawals (don’t have memory and language to participate in
major neurocognitive disorder
- a significant decline from the previous performance level in one or more cognitive domains
- deficits not attributable to other mental disorders
- deficits sufficient to interfere with independence in activities of daily living
-primary disease to Huntington’s, Parkison’s, and Multiple Sclerosis
DSM-5 Minor (MCI, prodromal dementia) and major neurocognitive disorder (dementia)
- Complex attention (all levels and processing speeds)
- Executive function
- Learning and memory
- Language
- Perceptual-motor function
- Social cognition
- Impaired short-term memory
- Impaired long-term memory
Memory impairment not required anymore - Deficits can be in language, attention, etc.,
depending on brain areas initially affected - Insidious onset
- Not caused by delirium, schizophrenia, or
depression - Acquired
- Persistent
Warning signs of dementia normal aging
- forgetting names of people you rarely see
- briefly forgetting part of an experience
- not putting things away properly
- mood changes because of an appropriate cause
- changes in your interest
warning signs of dementia- early signs of alzheimer’s
- forgetting the names of people close to you
- forgetting a recent experience
- putting things away in strange places
- having unpredictable mood changes
- decreased interest in activities
How to distinguish a minor neurocognitive disorder from normal aging?
- rate of progression
- amount of “annoyance” without overt deficit
Delirium vs. Dementia
Delirium
- confused mental state
- changes in circadian rhythm
- sundowning
-misperceptions
- illusions
- hallucinations
- transient
- rapid onset and offset
dementia
- confused mental state
- changes in circadian rhythm
- sundowning
- misperceptions
- illusions
- hallucinations
- progressive/persistent
- insidious onset, no offset
Frontotemporal Dementia
About 2-5% of diagnosed Dementia cases
* Multiple causes, similar/distinct profiles
* Protein clumps (Tau and TDP43)
* Primarily affect frontal and temporal lobes
* More likely genetic
* Primary initial symptoms are language and
behavior changes (not memory)
Pick’s disease (previously synonymous)
Personality (Behavior, judgment, empathy, impulsivity)
changes first
* Speech (motor-speech, fluency), language (syntax,
word finding), and memory follow
* Onset before 65
Primary progressive aphasia
Onset mostly before 65
* Expressive and receptive language deficits first
* Deficits at sentence or word level
* Attention, memory, executive function deficits follow
dementia with lewy bodies
About 15% of diagnosed Dementia cases
* Caused by build-up of alpha-synuclein protein
inside neurons
* Cortical Lewy bodies
* Brain stem Lewy bodies (in substantia nigra)
* Similar to PD in physical symptoms
* Similar to AD in cognitive symptoms
* Distinguished by relative progression of physical
and cognitive features, fluctuating cognition,
hallucinations, visuospatial deficits
* Final diagnosis at autopsy (Lewy bodies)
Vascular dementia
- about 20% of diagnosed dementia cases
- not a single disease but a disease process
- caused by a series of lacunar infarct
- deficits dependent on areas of infarction
Vascular dementia risk factors same for CVA
- hypertension
- cardiovascular disease
- diabetes
- history of stroke
Alzheimer’s Disease
- about 65% of diagnosed Dementia cases
- approx five million in 2014
- anticipated approximately
- risked doubles every years post 65
Early onset of Alzheimer’s disease
- age 40- 60
- rare genetic mutation ( dominant gene, 1991)
- genetic fault in beta-amyloid overproduction
- 5% of all AD cases
- chromosomes 21, 14,1, ( trisomy 21)
- effects language and memory function
Late-onset for Alzheimer’s Disease
- age over 65
- mixture of genetic and environmental causes
“susceptibility genes,” including ApoE (shared with heart disease and high cholesterol) - ApoE, chromosome 19
- ApoE 4: Risk factor
- ApoE 2: Protective
Mild Alzheimer’s Disease
Frontal Lobes
* Trouble naming common items (language & memory)
* Less interest in things they once liked to do
* Personality changes (irritability, anger, withdrawal) Hippocampus
* Memory loss, especially with recent events
* Repetition of questions or actions
* Getting lost easily (visuo-spatial memory)
* Lose things more often than normal
Subcortical
* Depression and/or anxiety
* Sleep disturbances
- anomia
- good syntactic structure
good content with some tangential addition
- last 2-10 years
Moderate Alzheimer’s Disease
Greater ADL involvement, require supervision
* Frontal
* Difficulty dressing for the weather or occasion
* Poor judgment and insight
* Argumentative/violent
Hippocampus
* Difficulty with formulaic tasks like washing dishes
* Forget to shave or shower
Parietal/integrative, occipital
* Hallucinations and illusions
Subcortical
* Wander, often at night
- worse anomia
- neologisms
- loss of coherence and cohesion
- last 2-10 years
Severe Alzheimer’s disease
Global deficits, loss of independence
* Difficulty eating/dysphagia
* Problems with speech or no speech
* Inability to recognize loved ones
* Inability to control bowels or bladder
* Physical difficulties, including walking
- only stereotypic phrases/utterances
- no topic maintenance
- ultimately mute
- last 1-5 years
Alzheimer progression
live as long as 8-20 years
- depends when on diagnosis
More likely to be Lewy bodies when…
they score high in motor function test (not AD)
Hachinski Ischemia index
looks at different kinds of deterioration processes and historical data
- score is higher (9-18), more likely to be a vascular dementia
- score is lower (0-4) is more likely to be AD
mostly like to be lewy body when…
if there’s data of moment to moment fluctuations in cognitive functions
- if there is greater involvement of motor function
Most likely to be frontotemporal dementia when…
- if there’s greater involvement initially of personality changes
