ncd part 2

anomia

-deficit in word finding ability
-one of most common + persistent difficulties of aphasia + cog-comm disorders
-evident at all levels of expressive language (confrontation/generative/responsive naming/convo)

anomia model

pic of object —> object recognition —> semantic system —> phonological output lexicon —> speech motor mechanisms —> spoken name

anomia exs

difficulty naming object in front of u or naming whats in a pic

alexia model

printed word —> visual analysis (perception) —> orthographic input lexicon (recognition) —> semantic store (comp) OR grapheme-phoneme conversion —> phonological output lexicon (lexical access) —> speech prod —> spoken word

global alexia

severe reading impairment

deep alexia

-reading impairment w semantic errors
-semantic paralexias: frequent subs of semantically related words (she/her)
-probs reading functor words aloud (instead/bc)
-tend to omit inflectional endings
-reads nouns better than verbs/adjs

phonological alexia

reading impairment esp w non-words

surface alexia

-phonologic errors
-no access to meaning on whole-word basis
-meaning gained by strict grapheme-to-phoneme mapping
-attempt to understand words by sounding out letters
-good w pseudowords given good phonological attack skills

allographic agraphia

difficulty converting graphemes to letter shape

apraxic agraphia

-difficulty w graphic motor programs
-impaired ability to form letters
-spells better w typewriter/aloud

deep agraphia

-spelling impairment w semantic errors (similar to deep alexia)
-best at concrete nouns (more difficulty w abstract nouns/verbs)
-extreme difficulty w functor words

global agraphia

severe spelling impairment

phonological agraphia

-spelling impairment esp non-words
-relatively good at real words
-almost total inability for pseudowords
-most difficulty w phoneme-grapheme conversion rules
-perseveration of visual contours

surface agraphia

-spelling impairment w overreliance on sublexial sound-to-letter conversion —> phonologically plausible spelling (similar to surface alexia)
-phonetic errors (sirkal/circle)
-relatively good at pseudowords

factors that affect presentation of alexia + agraphia

word frequency, imageability, phonetic complexity, personal relevance

right hemisphere role in comm

-visual perception
-basic encoding of linguistic info (single word level)
-holistic, non-linear, parallel processing
-dealing w novel input
-pragmatics

rhd impairments

attention deficits, neglect, visuoperceptual deficits, cog-comm deficits, affective + emo deficits

cog-comm disorder

-comm impairments resulting from underlying cog deficits due to neurological impairment
-difficulties in communicative competence (listening, speaking, reading, writing, convo, social interaction) that result from underlying cog impairments

rhd attention deficit: arousal + orienting

-hypoaroused
-reduced + restricted interaction w enviro
-need more intense stimuli + time to prep to attend

rhd attention deficit: vigilance + sustained attention

-may not be able to sustain attention over period of time
-failure to process crucial info

rhd attention deficit: selective attention

needs enough arousal, orienting, vigilance

rhd: neglect

-related to attentional impairments
-more long lasting + severe than in lhd
-can occur w subcortical lesions
-most commonly seen in visual modality

body neglect

-somatophrenia: inability to perceive own body parts as part of themselves
>neglected parts often show hemiparesis
-motor function may remain intact for neglected parts tho parts may stay unutilized
-motor neglect: diminished use of neglected limb despite being motorically intact

hemispatial neglect

severe cases: one may be unable to recognize existence of neglected world via vision, auditory, olfactory info

common left neglect behaviors in rhd

reading left half of printed materials + localizing sounds coming from left

rhd visuoperceptual deficits

visual attention/integration/memory, spatial orientation, topographical orientation

rhd cog-comm deficits

reduced:
-discourse comp + prod
-comm efficiency + specificity
-capacity to process alt + ambiguous meanings
-sensitivity to contextual info

types of discourse

procedural, expository, narrative, conversational

what u need to know to be successful in discourse

-awareness of gen topic
-exchange purpose
-limits of shared knowledge
-cultural rules
-means of repairing communicative breakdown

rhd discourse deficits (comp)

-gist of written + spoken narrative
-intended + implied meanings
-new info + revision of old info
-emo content

rhd discourse deficits (prod)

-ability to generate macrostructure
-reduced level of info content, specificity, flexibility

rhd prosodic deficits (comp: emo)

-discriminating mood in neutral context or w/o support
-incongruent message/prosody

rhd prosodic deficits (comp: linguistic)

-parts of speech based on stress
-auditory discrimination
-appropriate stress in sentences
-determining sentence type from prosodic info

rhd prosodic deficits (prod: emo)

-monotone
-matching prosody to emo
-increased reliance on semantic info rather than prosody

rhd prosodic deficits (prod: linguistic)

-mini use of emphatic stress
-less ability to alter fundamental frequency to describe sentence type

rhd emo deficits

-use of facial expression to show emo
-sensitivity to others expressions
-use + comp of prosody to show emo
-can have delirium, agitation, psychosis (rare)

simultagnosia

inability to visually perceive multiple details at once often bc of parietal-occipital area

cerebral achromatopsia

rare loss of color vision bc of trauma/cortical damage

neuropsychiatric disorders that may present w/ slp-concerned deficits/disorders

-anosognosia
-depression
-capgras delusion
-fregoli delusion
-visual hallucinations
-paranoid hallucinations

anasognosia

inability to recognize they have deficits

capgras delusion

belief that loved ones have been replaced by imposters who look + sound like ogs

fregoli delusion

belief that familiar person is able to take on guise of another

paranoid hallucinations

-visual + auditory
-perceived as threatening/ominous/foreboding

dorsolateral syndrome

-aka pseudodepression syndrome
-overall decrease in cog + executive functions
-apathy
-slowness
-perseveration

ventromedial syndrome

-aka pseudopsychopathic syndrome
-social impairments most noticeable
-impulsivity
-euphoria
-irritability

executive function impairment

-reduced awareness + inhibition
-difficulty setting goals + initiating action

higher-order cog impairments

-reduced control over all cog functions
-impaired memory
-concrete thinking (difficulty w generalizing concepts/actions)

cog-comm impairments

-discourse
-language comp due to reduced processing speed
-anomia
-abstract language
-social cues

psychosocial/behavioral impairment

-disinhibition
-reduced initiation
-reduced ability to learn from consequences
-perseveration
-impaired social perception

tbi severity

-determined at time of injury
-based on glascow coma scale score, loss of consciousness, post-traumatic amnesia

coma

-state of pathologic unconsciousness in which eyes stay closed + cant be aroused
-severe, diffuse bilateral cortical lesions or underlying white matter pathways
-bilateral thalamic lesion
-brainstem lesion

coma levels

persistent vegetative + minimally conscious states

persistent vegetative state

not arousable, no speech, doesnt follow commands

minimally conscious state

-minimal awareness
-often transitional state from coma to appropriate

geriatric tbi incidence

-1 in 200 americans 65-74
-1 in 50 for 75 + >

geriatric tbi etiology

falls 51% unknown 21% motor vehicle crashes 9%

geriatric tbi trend

increased over the years

geriatric tbi suicide

highest rate of suicide in all age groups 65 + >

geriatric tbi excess disability

mood, sleep disturbance, chronic pain, social support

geriatric tbi intervention methods

-functional activities
-return to community
-multi-modality cog stim
-meta-cog training

military tbi: primary blast injury

caused by blast wave itself

military tbi: secondary blast injury

caused by debri

military tbi: tertiary blast injury

caused by exposure to strong blast winds

tbi numbers

vast majority are mild

military tbi triad presentation

cog-behavioral impairments, ptsd, substance abuse
-self-perpetuating cycle

sports tbi issues to consider

-single vs multiple concussions
-concussive vs sub-concussive injuries
-recovery vs long-term impacts

is tbi a chronic disease?

yes

dementia aka major neurocognitive disorder

evidence of sig cog decline from previous level of performance in at least 1 cog domain that interferes w abilities to do iadl’s

dementia etiologies

tbi, lewy body disease, ad, huntington’s

minor neurocog disorder

-dont have severe dementia symptoms
-can include age-related memory decline
-impacts ind performance of life activities
-decline from previous level of performance per self report or slight reduction in performance on standardized cog measures

delirium

-sudden disturbance in consciousness or change in cog ability that fluctuates throughout day
-onset is result of gen med condition

ad w early onset

-< 60
-5-10% of cases
-strong genetic component

ad w late onset

-~90% of cases
-60 + >
-likely to have multiple influences (genetic link, lifestyle, enviro)

cause of comm impairment for dementia

-initial impacting cog factor: memory
-anomia
-perseveration
-lack of coherence
-impaired comp

memory + comm impairment exs

-encoding
-storage
-retrieval
-adls: routines done in avg day
-instrumental ADL (iadl): activities related to ind living

what causes comm impairment

as disease progress, can see more language probs altho not classically aphasia + further impact on ability to function ind

ad progression stage 1

no impairment + apparent memory changes

ad progression stage 2

-very mild cog decline
-changes experienced by individual but not evident on exam
-may be cog changes due to normal aging or earliest signs of ad

ad progression stage 3

-mild cog decline
-difficulty noticed by others
-detailed med interview may also show deficits
-2-4 yrs
-feelings of losing control

ad progression stage 4

-mod cog decline
-mild/early-stage ad
-evaluation will show clear deficits
-difficulty w knowledge for recent events
-less ability to handle complex adls
-reduced memory for personal history
-subdued/withdrawn in challenging sits

ad progression stage 5

-mod-severe cog decline
-mod ad
-apparent major gaps in memory + cog function
-help w most adls needed including toileting + eating
-confusion for person/place/time

ad progression stage 6

-severe cog decline
-moderately-severe/mid-stage ad
-progressive loss of mental abilities, flattened affect, mild to mod physical probs
-hyper/hypo activity, incontinence, severe comm deficits, sleep disturbance
-echolalia, dysarthria, jargon, visual agnosia

ad progression stage 7

-very severe cog decline
-severe/late-stage ad
-final
-severe physical + mental deterioration
-inability to eat, loss of voluntary movement, regression to fetal stage, respiratory problems
-full comm loss

frontotemporal dementia

-degeneration of frontal + temporal
-includes pick’s disease, progressive nonfluent aphasia, semantic dementia

pick’s disease

-personality changes
-antisocial + inappropriate behavior
-memory loss
-neuropathology: pick bodies + ballooned neurons

huntington’s disease

-subcortical
-progressive terminal illness w distinctive involuntary erratic body movements
-can cause changes in personality, cog, language, emo
-neuropathology: prod of mutant huntington protein

huntington’s stage 1 + 2

-motor symptoms of chorea
-emo probs
-difficulty concentrating
-memory probs

huntington stages 2-4

-chorea + hyperkinesias that interfere w speech prod
-training on aac for future loss of verbal + written expression

huntington stage 5

nonambulatory, bradykinesia, incoordination, high aspiration risk

vascular dementia

-mixed dementia caused by small ischemic strokes in cortex/subcortex/both
-memory loss, aphasia, apraxia of speech, difficulties w executive functioning
-hyperactive reflexes + weakness
-acute onset followed by stepwise progression of degeneration

vascular dementia neuropathology

-cortical multi-infarct dementia caused by many usually small infarcts to various brain areas
-lacunar state caused by multiple subcortical thrombotic ischemic strokes in brain stem, bg, other subcortical

lewy body disease

motor speech disorder

disorder resulting from neurologic impairments affecting motor programming or neuromuscular execution of speech (includes dysarthria + apraxia)

dysarthria

-neurologic
-changes in strength/speed/range/steadiness/tone/accuracy of movements required from all systems involved in speech prod
-respiratory, phonatory, articulatory, prosody

apraxia

-neurologic
-impaired capacity to plan/program sensorimotor commands needed to make speech
-left hemisphere

flaccid dysarthria

-lower motor neurons
-weakness
-hypotonia
-hyporeflexia
-atrophy
-fasciculations
-fibrillations

spastic dysarthria

-bilateral upper motor neurons
-spasticity
-strained vocals
-slow + less motion range
-limited pitch range

ataxic dysarthria

-cerebellum
-incoordination
-can manifest in any/all speech systems
-articulation + prosody
-over/undershooting targets
-imprecise
-variable phase length

hypokinetic dysarthria

-bg
-rigidity
-may manifest in any speech system
-most proof in voiced, articulation, prosody
-slow individual movements
-fast + small repetitive movements
-less motion range
-limited pitch variability

hyperkinetic dysarthria

-bg
-abnormal movement
-involuntary movement
-can occur at rest, during voluntary movements, or static postures
-not usual during sleep
-worse w anxiety or high emotions
-doesnt indicate speech of movement, only extra movements
-highly variable