Neurophysiological Consequences of Neurological Conditions

function of neuroimaging

detecting gross changes in structure (tumors) or function (seizures)

services of neuropsychology

diagnosis of disorders, assess cognitive impairments, generate recommendations for treatment

types of neuropsychology treatment

psychotherapy, behavioral intervention, cognitive rehabilitation

neurocognitive disorders

delirium, major neurocognitive disorder, mild neurocognitive disorder

delirium criteria

disturbance in attention and awareness, rapid development, fluctuates throughout the day, disorientation

symptoms of delirium

waxing/waning attention, distractibility, confusion, disordered perception, hypo/hyperkinetic behavior

assessment of delirium

screen for problems with attention, disorganized thinking, altered consciousness, executive dysfunction

risk factors of delirium

recent surgery, UTI, organ failure, constipation, chronic fatigue, dehydration, poor nutrition, dementia

treatment of delirium

treat underlying cause (hydration, nutrition, medication), minimize distractions, address sensory issues, sleep

delirium tremens (alcohol withdrawal delirium)

complication of alcohol withdrawal marked with confusion, disorientation, hallucinations, hyperactivity, tremors typically 1-3 days after the last drink

treatment of delirium tremens

calm well-lit environment, electrolytes, benzos

difference between major and mild neurocognitive disorder

major cognitive deficits interfere with independence in ADLs

function of Montreal Cognitive Assessment (MoCA)

screen to detect mild cognitive impairment or dementia

cognitive functions assessed by the MoCA

memory, executive function, attention, language, visuospatial skills

cutoff score for the MoCA

23/60

domains of neurocognitive function

perceptual motor function, language, learning/memory, social cognition, complex attention, executive function

crystallized cognitive abilities

information acquired through education, experience, socialization

fluid cognitive abilities

ability to reason and solve new problems

crystallized and fluid intelligence with aging

crystallized stays the same or gets better, fluid intelligence gets worse

how to assess crystallized abilities

word pronunciation, picture vocabulary, word definitions

crystallized vs fluid intelligence after neurological injury

affects fluid more and crystallized abilities remain stable

types of fluid cognitive abilities

attention, processing, working memory, visuospatial, praxis, language, learning

definition of attention

process where individuals receive and process incoming information

brain areas involved in attention

frontal lobe, right hemisphere, subcortical structures

common disorders that cause attention impairments

ADHD, TBI, stroke, delirium

definition of processing speed

how quickly your brain takes in, interprets, and responds to information

disorders that cause slow processing speed

parkinson’s, MS

types of executive functions

planning, problem solving, reasoning, shifting between tasks, working and strategic memory, behavior

symptoms of executive dysfunction

poor judgement and planning, impulsive, abulia (loss of willpower), akinesia or motor impersistence

tests for frontal lobe

crossed response inhibition, contrasting motor programs, go-no-go, primitive reflexes, verbal fluency, stroop task

parts of the pre-frontal cortex

dorsolateral, ventrolateral, orbitofrontal, ventromedial, dorsomedial

case of phineas gage

had damage to his orbitofrontal cortex and was not able to control his behavior after

parts of the brain involved in ADHD

PFC (executive function), basal ganglia (hyperactivity), limbic system (emotion)

cognitive impairments that occur after a TBI

attention, executive function, processing speed, memory

how is level of severity classified in TBI

depends of level of alertness, duration of post-traumatic amnesia, and duration of LOC

glasgow coma scale

assesses level of consciousness based on eye opening, verbal response, and motor response (larger score is better)

retrograde amnesia

loss of memory of events that occurred before injury (more recent = more susceptible)

anterograde amnesia

loss of memory of events that occurred after the injury, difficulty forming new memories

cause of anterograde amnesia

damage to hippocampus

predictor of the outcome of recovering from a TBI

duration of post-traumatic amnesia

function of galveston orientation and amnesia test (GOAT)

evaluate progression of amnesia following a TBI

when is post-traumatic amnesia considered to have ended

a score of greater than 75 is achieved on 3 consecutive administrations of the GOAT

updated TBI classification framework

clinical, biomarker, imaging, and modifier pillars

what was wrong with the old TBI classification system

it did not say anything about where, volume, or effects of the injury

dorsal visual processing stream

the where pathway, spatial locations and movement of objects

ventral visual processing stream

the what pathway, recognizing objects and patterns

impairments caused by dorsal stream lesions

hemineglect, simultanagnosia, optic ataxia, ocular apraxia, balint’s syndrome

tests for hemi-inattention and neglect

line bisecting, clock drawing, describe a scene

why is a lesion to the right side more detrimental to visual attention

the right hemisphere attends to the left and a little to the right

why is visual neglect of the right side rare

redundant processing from both hemispheres

prognosis of inattention/neglect

most recover within 6 months

anosognosia

denial of illness or unawareness of deficits

anosodiaphoria

aware of severe deficits but not concerned about it

asomatognosia

disturbance in the sense of ownership for one’s body or body part (denial their body belongs to them)

simultanagnosia

impaired ability to perceive scene as a whole and can only perceive parts at a time, difficulty scanning a complex scene

optic ataxia

impaired ability to reach for or point to something under visual guidance (proprioception intact)

ocular apraxia

difficulty voluntarily directing gaze toward objects in peripheral vision

balint’s syndrome

triad of simulatanagnosia, optic ataxia, ocular apraxia

impairments of ventral stream lesions

agnosias, achromatopsia

agnosia

failure to recognize previously familiar stimuli

apperceptive agnosia

unable to identify and copy something

associative agnosia

unable to name the item but can copy it

prosopagnosia

unable to recognize people by their faces (or anything other specific recognition)

what can someone with prosopagnosia do

describe parts of a face, discern age and gender, recognize emotions

what is involved in praxis

generating an idea, motor planning, and execution

apraxia

problem with the integration of cognition and motor info that leads to the inability to plan and execute skilled movements

types of praxis

buccofacial, ideomotor, ideational, constructional, limb kinetic, oral

ideomotor praxis

perform simple previously learned commands

ideational praxis

ability to sequence multi-step tasks

pragmatics

social use of language that includes intonation, gestures, and facial expressions

prosody

variation in pitch, rhythm, and loudness to convey meaning beyond the words themself

assessments of expressive language

naming tests and fluency tests

assessments of receptive language

evaluated by following instructions

areas involved in verbal repetition

wernicke’s, broca’s, arcuate fasciculus

function of wernicke’s area

comprehension

function of broca’s area

speech production

other names for expressive aphasia

motor, broca’s

problem in broca’s aphasia

cannot produce language

phonemic paraphasia

mixing up the sounds in a word

semantic paraphasia

saying horse instead of zebra

other names for receptive aphasia

sensory, wernicke’s

problem in wernicke’s aphasia

cannot understand what is being said

common errors in receptive aphasia

word substitutions, neologisms, logorrhea

types of declarative/explicit memory

semantic (facts) and episodic (experiences)

types of nondeclarative/implicit memory

skills, priming, classical conditioning, nonassociative learning

steps of multi-store memory

sensory memory → if paid attention to transferred to short term memory → kept alive with working memory

how is memory moved to long term

retention (temporary storing) then consolidation

cause of discrepancy between recall and recognition tasks

problem with retrieval

stages of memory

encoding (learning), storage, retrieval

where does encoding of memory happen

prefrontal cortex

parts of the brain involved in storage and retrieval

medial temporal lobe of the hippocampus stores until consolidation then the thalamus and basal forebrain store

types of memory assessments

orientation of who/where/date, free recall, cued recall, recognition (multiple choice), long term memories

how does a distractor effect memory

interferes with the storage and recency effect so you dont remember the last few words

prospective memory

remembering to do something in the future

additional requirement of prospective memory

anterior FPC is needed for monitoring of the completion of the task

causes of memory deficits

poor encoding or retrieval, poor consolidation, decay, interference

frontal lobe dysfunction effect on memory

less strategic encoding leads to less accurate retrieval

hippocampal dysfunction effect on memory

no consolidation so new memories are not stored

part of memory most effected by neurological illnesses

encoding and storage

functions of the left (dominant) hemisphere

complex motor processes, language