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183 Cards in this Set
- Front
- Back
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agnosias
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decreased or impaired ability for recognition, identification, naming
individual is away of stimulus and acknowledge it but cannot recognize and name |
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lesion of what lobe will cause agnosias?
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temporal lobe
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what areas of brain contain face recognition?
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areas of occipital cortex and superior temporal sulcus
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prosopagnosia
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bilateral inferior occipitotemporal temporal (fusiform) gyrus
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function of right parietal lobe is involved with
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spatial visual relationships
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what lobe has the widest repertoire of functions of all association cortices?
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frontal lobe
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fxn of frontal lobe
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define personality, appreciation of self
integration of inputs from medial dorsal nucleus of thalamus all association cxs and limbic system to produce analysis and appropriate behavior |
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frontal lobe functions are divided into 3 executive functions:
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1. restraint
2. initiative 3. order |
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disinhibition -damage to
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orbitofrontal lesions
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disinhibition causes
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impaired restraint, inappropriate affect (jocularity or rage/vulgarity), impulsiveness, unconcern for the future, labile emotions
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abulia -lesion where?
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dorsolateral lesions
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abulia -describe
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blunted initiative and ambition
problem solving deficits diminished planning abilities apathy perseveration behavior distractibility |
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limited insight and poor judgement -lesion where?
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orbitofrontal lesions
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limited insight and poor judgement -describe
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disordered thoughts and memories
wrong choices of response selection of plan for immediate circumstance or future |
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what are the six major structures of limbic system?
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limbic lobe
hippocampal formation amygdala nucleus basalis of Meynert septal area and nuclei anterior perforated substance (primary olfactory tubercle) |
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what are the major pathways of the limbic system?
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1. fornix (alveus --> fimbria --> fornix)
2. stria terminalis 3. mamillothalamic tract (part of limbic system) |
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ancillary structures of the limbic system
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nucleus accumbens
VTA reticular formation ventral pallidum diencephalon: hypothalamus, thalamus (anterior and mediodorsal nucleus), habenula |
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4 limbic system functions
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1. olfaction
2. memory 3. emotions and drives 4. homeostasis, autonomic and neuroendocrine control |
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key structure for memory
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hippocampus
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key structure for emotions and drives
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amygdala
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papez circuit is suited to consolidation of what function?
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memory from short term to long term
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emotions can influence memories.
emotions are found more ______ memory are found more ______ in the brain |
emotions are more rostral
memory is more caudal |
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declarative memory includes what functions?
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EVERYDAY MEMORY - availability of facts and events in the conscious mind:
daily episodes words and their meanings history |
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nondeclarative memory includes what functions?
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PROCEDURAL, MOTOR, and PERCEPTURAL MEMORY-operating largely on subconscious level:
motor skills associations priming cues puzzle solving skills |
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what brain structures are involved in declarative memory?
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hippocampal formation
entorhinal cortex mammillary bodies medial diencephalon (anterior and mediodorsal thalamus, septal n) |
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what brain structures are involved in nondeclarative memory?
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cortical association areas
assoc with nonpyramidal areas such as cerebellum, basal ganglia, parietal and frontal cortex |
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site of short-term memory storage (declarative)
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hippocampus and related structures
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site of long-term memory storage (declarative)
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cortical sites
-Wernicke's -temporal |
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site of short-term memory storage (nondeclarative)
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unknown
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long-term potentiation
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form of synaptic plasticity where increase in EPSP amplitude for an equivalent amount of transmitter
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long-term depression
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long-lasting decrease in synaptic efficacy in hippocampus, cortex, amygdala, cerebellum, basal ganglia
decrease in EPSP amplitude for an equivalent amount of transmitter released into synapse |
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mechanisms of LTP
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more functional receptors inserted new AMPA receptors into postsynaptic membrane leading to LTP
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mechanism of LTD
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fewer functional receptors
deletion or internalization of AMPA from the postsynaptic membrane leads to LTD |
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how does LTP and LTD induce long term mechanisms?
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PKA activates transcription that leads to enhanced gene expression, protein synthesis, protein synthesis, long-lasting increases in PKA/synapse structure
Changes in dendritic spine MORPHOLOGY and NUMBER Neurotrophins contribute to protein synthesis |
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lesion of the medial temporal lobe (hippocampus and parahippocampal gyrus) and/or medial diencephalic system produces:
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ANTEROGRADE AMNESIA - new experiences are not saved, cannot form/consolidate new memories
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lesion of cortical association areas (frontal/parietal/temporal lobes) produce what memory deficit?
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RETROGRADE AMNESIA in which past experiences are not recalled long term memories are not stored
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HM underwent bilateral temporal lobectomy for intractable seizures
--causes what memory deficit? |
unable to form NEW MEMORIES
no short term memory |
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HM contributions
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declarative and nondeclarative are independent
established that memory begins in temporal lobe: parahippocampal gyrus and hippocampus |
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nucleus basalis and septal nuclei are sources of what transmitter?
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ACh
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what disease has decreased functional cholinergic activity in terminal limbic and cortical areas
-linked to impaired memory capabilities |
Alzheimer's disease
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caused by thiamine deficiency
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Wernicke-Korsakoff
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what disease results in bilateral lesion of mammilary bodies, medial dorsal thalamus and other diencephalic structures of the cerebellum?
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Wernicke-Korsakoff
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wernicke-korsakoff causes what symptoms?
common in what type of pts? |
causes BOTH anterograde and retrograde amnesia and motor disturbances characteristically: confusion, ataxis, opthalmoplegia
associated with chronic alcoholism and malnutrition |
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people with amnesia struggle to remember past events and may also struggle to___________
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envision the future
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what structure is involved in imagination? constructing an abstract scene of the future
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hippocampus
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lost memories are
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impaired ability to imagine the future
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________ is based on stitching together fragments of multiple similar situations from memory to careate a new mental vision
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imagination
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right nondominant parietal cortex lesions produces what?
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hemineglect syndrome
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left dominant parietal and/or frontal cortex lesions produces
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apraxias
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apraxias
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the inability to perform learned motor tasks despite preservation of necessary basic motor, sensory and cognitive capacities
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each describable emotion physiologically has 3 parts in common:
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1-subjective internal feeling itself
2-visceral motor responses 3- somatic behavior responses |
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what is the NODAL POINT linking cortical and subcortical areas involved in emotional processing and subjective learning?
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amygdala
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what types of sensory info inputs into AMYGDALA?
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vision
audition smell taste somatosensory |
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amygdala output areas control:
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somatomotor and autonomic responses
guides normal, reasoned behavior |
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what structure:
mediates neural processes that invest sensory experience with emotional significance? |
amygdala!
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amygdala strongly influences
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autonomic
neuroendocrine regulation emotional aspects of memory, olfaction, behavioral drives |
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what structure attaches emotional significance to perceptions made in association cortex: anxiety, fear, anger aggression, affection, love etc
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amygdala
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contralateral sensory neglect syndrome
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lesion of non-dominant hemisphere in region of inferior parietal lobe involving supramarginal and angular gyri
-individual ignores left side sensory stimuli of all modalities and motor functions shoe extreme right side preference |
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anosognosia
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conceptual neglect, lack of awareness of or denial of a deficit or illness
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anosodiaphoria
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awareness of deficit but unconcerned
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hemiasomatoagnosia
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denial that left side of body belongs to them
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what lobe contains the Where stream?
what fasciculus? |
parietal lobe
superior longitudinal fasciculus |
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what lobe contains the What stream?
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temporal lobe
inferior longitudinal fasciculus |
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lesions of supramarginal gyrus (area 40) on dominant side (left) leads to
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apraxias
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lesion of the angular gyrus on dominant side (left) leads to
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alexia and agraphia
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lesion of left parieto-occipital cortex esp supramarginal gyrus (area 40)
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apraxia (cannot strategize)
inability to perform a complex motor act (pantomime or imitate) even though there is no direct damage to motor or sensory (proprioception) systems and no deficits in comprehension |
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what area contains engrams for programming skilled motor acts that are transferred to left motor association cortex and left premotor cortex
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left supramarginal gyrus
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angular gyrus (area 39) is crucial for what skill?
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reading
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damage on left dominant parietal lobe particularly angular gyrus
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alexia
agraphia with or without aphasia depending on extend of lesion |
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Gerstmann's syndrome
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lesion of dominant inferior region of parietal lobe including angular gyrus and some surrounding areas
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symptoms of Gerstmann's syndrome
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agraphia
acalculia finger agnosia left-right disorientation |
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alexia without agraphia can occur with what type of lesion?
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CAN WRITE BUT CANNOT READ WHAT THEY WROTE
disconnection syndome lesion of left occipital cortex and/or splenium of corpus callosum due to PCA -left hemifield is destroyed info from right hemifield is not able to be transferred from right cortex to left language areas |
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disconnection syndrome
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failure of underlying connections to transfer information btwn primary sensory areas and association areas and between association areas
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what artery infarct will affect Wernicker's area?
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left MCA inferior division or PCA infarct
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what artery infarct will affect genu of corpus callosum?
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ACA and pericallosal artery
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what area has the greatest influence over both left and right motor cortices?
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left premotor area
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lesion of the areas that disconnect supramarginal gyrus from left premotor areas will also disconnect
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right premotor gyru
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Anton's syndrome
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cortical blindness area 17
individual can still detect light versus dark and movement due to spared pathway to tectum |
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visual agnosia
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areas 18 and 19
unable to recognize objects visually they see objects but they have no meaning with no acuity problems and no naming deficits due to aphasias |
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achromatopsia
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areas 18 and 19
loss of color perception would is black and white |
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Balint's syndrome
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dorsal parietal cortex
simultanagnosia - cant get the big picture optic ataxia - visually guided reaching (hand-eye coordination is disrupted) ocular apraxia - voluntary scanning of a scene |
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left lateral temporal cortex lesion will lead to
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difficulties in language and word processing
aphasia and other symptoms disrupt the What? stream |
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temporal lobe lesions produce impaired what?
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ability to recognize, identify and name
agnosias |
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prosopagnosia - lesion where?
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bilateral inferior occipitotermporal temporal (fusiform) gyrus
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what are the symptoms of prosopagnosia?
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inability to recognize familiar faces
right hemisphere lesion results in inability to recognize unfamiliar faces as faces |
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what other areas in the brain besides inferior occipitotemporal is involved in face recognition?
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occipital cortex
superior temporal sulcus |
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what area is the CEO? defines are personality, has widest repertoire of functions of all association cortices
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frontal lobe
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frontal lobe functions in 3 executive functions including:
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restraint
initiative order |
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all connection in the brain lead to:
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the prefrontal cortex
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function of prefrontal cortex
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balances internal drives with external contingencies to judge (put value on) perceptions and plan appropriate behavior
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orbitofrontal region function
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monitor or modulate limbic driven functions and behavior
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what acts as an integrator and comparator of the current situation with past experiences to plan, plot, initiate the correct behavior?
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frontal cortex
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what links emotions to moral judgements?
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frontal lobe
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what evaluates immediate and future consequences of choices at hand
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frontal lobe
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frontal lobe deficits leads to
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mismatch of behavior and circumstances that drive behavior
altered cognitive motor and personality traits |
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frontal lobe deficits leads to what traits?
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disinhibition
abulia limited insight poor judgement |
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disinhibition -lesion of what?
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orbitofrontal
impaired restraint inappropriate affect impulsiveness unconcern for the future labile emotions |
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abulia - lesion of what?
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dorsolateral
blunted initiative and ambition problem solving deficits diminished planning abilities apathy preservation behavior distractibility |
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limited insight and poor judgement due to lesion of what?
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orbitofrontal
disordered thoughts and memories wrong choices of response selection of plan for immediate circumstance or future |
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depression
NT prob? where? |
decreased NE and serotonin in frontal lobes, prefrontal cortex, possibly orbitofrontal cortex
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anxiety disorders
NT prob? tx |
increased nonadrenergic, serotonergic functional tone form LC and raphe
tx: benzodiazepines/GABA |
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OCD caused by
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deficits in serotonin in terminal regions:
head of caudate cingulate gyrus orbital frontal cortex from raphe nuclei SSRIs are frequently effective |
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schizophrenia
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hyperactivity of dopaminergic pathways from VTA --> nucleus accumbens, ventral pallidum, prefrontal cortex, limbic cortex
classic antipsychotic meds are dopamine-receptor antagonists glutamate/GABA/NE/5-HT may also play roles |
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seizures, epilepsy, limbic structures localized to dysfunction to
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temporal lobes
orbital frontal cingulate gyrus |
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why are temporal lobes, orbital frontal, cingulate gyrus more prone to seizure generation?
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lowest thresholds for seizure generation
lots of glutamate, low GABA more subtle than generalized seizures |
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anti-seizure meds do what?
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enhance GABA-ergic NTs
quell hyperexcitable neuronal membrane |
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what percentage of cerebral cortex is association cortex?
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80%
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unimodal
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primary association cortex for specific input modalities
ie Somatosensory, auditory, visual ultimately involved in primary sensation higher order processing: quantitation, directional qualities, initial recognition |
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heteromodal
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secondary assoc cortex has MULTIPLE INPUT modalities from thalamus and multiple connections with other association areas and limbic system
complex integration and flavoring with contextual, emotional motivational influences |
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motor association (premotor) cortex -fxn
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formulation of motor program for primary motor cortex
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arcuate fasciculus connects
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broca's to wernicke's
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parietal association cortex -basic function
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attention to external and internal stimuli
more reflexive than focused |
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temporal association cortex -basic function
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recognition and identification of nature of stimulus particularly complex mutlimodal stimuli
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frontal association cortex
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planning and selection of approp behavior focused attention on problem rather than reflexive
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which hemisphere?
concerned with details analytical functions? |
LEFT/dominant
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which hemisphere?
parallel-like processing of mult inputs simultaneously to give whole picture? |
RIGHT/nondominant
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which hemisphere?
specialized for nonverbal functions related more to visual-spatial attention and skills |
RIGHT/nondominant
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which hemisphere?
processes info in a serial like and sequential manner? |
LEFT/dominant
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which hemisphere?
functions: language skilled motor formulation arithmetic: sequential and analytical calculation skills musical ability: sequential and analytical skills of musicians sense of direction: set of written directions |
LEFT/dominant
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impairment of what side will cause:
aphasia analytical abilities complex motor planning and strategies |
LEFT
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impairment of what side?
lose spatial attention (neglect syndrome) complex usual-spatial behaviors involving orientation and perception of big picture |
RIGHT/Nondominant
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what hemisphere?
prosody: emotion conveyed in tone or voice visual spatial analysis and spatial attention arithmetic-line up columns on page musical ability - untrained musicians or complex pieces sense of direction: finding one's way by sense of spatial orientation |
RIGHT/nondominant
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Broca's aphasia deficits - also called agrammatic aphasia
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spontaneous speech
auditory comprehension repetition of sentences naming reading writing associated deficits - right sided motor weakness (hemiparesis or hemiplegia) and apraxia |
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where is lesion site for broca's aphasia?
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left frontal region
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Wernicke's aphasia deficits
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spontaneous speech
auditory comprehension -severely impaired repetition - poor, corresponds to severity to comprehension deficits reading-can read but dont understand writing: content is meaningless associated deficits-unaware of their own deficit |
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where is the lesion site of Wernicke's?
do they have paralysis? |
posterior superior temporal regions of the left hemisphere with extension into the inferior parietal lobule
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conduction aphasia deficits
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Spontaneous speech: Fluent and paraphasic. Patient is aware of the errors and makes efforts at self correction.
Auditory comprehension: Normal, adequate for normal conversation. Repetition: Poor repetition is the distinctive feature of conduction aphasia (can repeat common words). Naming: The symptoms are variable, literal paraphasias are often observed. Reading: Severe impairment in reading aloud but reading comprehension is normal. Writing: It is impaired to significant degree. Writing errors are related to omissions, substitutions, and reversals of letters. Associated deficits: Some may show sensory loss and visual field defects. |
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conduction aphasia lesion site
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arcuate fasciculus in the left hemisphere-traditional explanation
often brain damage in the left parietal lobe involving supramarginal and low post centraly gyri |
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global aphasia
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sum of the deficits of Broca's and Wernicke's
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global aphasia lesion site
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Large lesions of the left middle cerebral artery territory that includes frontal, temporal, and parietal lobes.
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transcortical motor aphasia
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Spontaneous speech: Speech is usually comprised of one or two word responses and echolalic (repeat what you say).
Auditory comprehension: Relatively intact Repetition: Normal Naming: Impaired, perseveration and fragmentation observed on confrontation naming |
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what is the differentiating factor between transcortical motor aphasia and broca's?
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repetition is good in transcortical not broca's
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transcortical sensory aphasia
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Spontaneous speech: Speech is usually fluent, but paraphasic and echolalic.
Auditory comprehension: Severely impaired Repetition: Excellent Naming: Impaired. These patients are unable to either identify the object or name it. Reading: Reading aloud is preserved but reading comprehension is severely impaired. Writing: Impaired, parallels that of Wernicke’s aphasia. Associated deficits: Sensory functions impaired. Some have visual field defects. |
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transcortical sensory aphasia
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left posterior temporal occipital lobe
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mixed transcortical aphasia (isolation of the speech area, rare)
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Spontaneous speech: No spontaneous speech, echolalic.
Auditory comprehension: Severely impaired Repetition: Relatively good Naming: Impaired Reading: Reading aloud as well as reading comprehension is severely impaired. Writing: Impaired Associated deficits: Paresis |
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mixed transcortical speech lesion site
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extensive cortical damage to both cerebral hemisphere with relative preservation of neurons in perysylvian cortex
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anomia
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have word finding problems
will find this in almost all aphasics TIA can give you just anomia |
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aphasia
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It is a language impairment resulting from damage to certain areas of the brain (i.e., left hemisphere in right handed individuals) that are responsible for the interpretation and formulation of language.
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crossed aphasia
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right hemisphere lesion in right handers
rare 1-2% prevalence c |
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causes of aphasia
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1. cerebro-vascular accident
2. trauma 3. intracranial tumors 4. infections |
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localization
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determine site of insulting lesion
The neurologic deficit produced by a lesion in any given area of the nervous system are characteristic of the area involved and relatively independent of the type of lesion |
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mode of onset
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acute: vascular, trauma, seizure
subacute: inflammation, infection chronic: mass or tumor, chronic inflammation, chronic infection |
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neurologic examination -looks at what?
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mental status
cranial nerve motor sensory cerebellum: coordination gait |
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mode of onset
what would take YEARS for symptoms to occur? |
degenerative diseases
tumor |
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what would take MONTHS/WEEKS for symptoms to occur?
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chronic inflammation
chronic infection tumor |
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what will take weeks and days for onset of sx?
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demyelination
subacute infection subacute inflammation |
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what will take days and hours for onset of sx?
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acute infection
acute inflammation |
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what will be abrupt in onset of sx?
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vascular
trauma seizures |
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define NonREM sleep
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idling brain in a moveable body
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define REM sleep
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highly active brain in a paralyzed body
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schizophrenia
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HYPERACTIVITY of dopaminergic pathway from VTA to nucleus accumbens, ventral pallidum, prefrontal cortex, limbic cortex
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antipsychotic drugs are
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dopamine receptor antagonists
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OCD
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deficits in serotonin in terminal regions:
head of caudate cingulate gyrus orbital frontal cortex from raphe nuclei |
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how do you treat OCD?
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SSRIs to increase serotonin levels
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anxiety disorders
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increase nonadrenergic serotonergic functional tone from LC and raphe
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schizophrenia
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HYPERACTIVITY of dopaminergic pathway from VTA to nucleus accumbens, ventral pallidum, prefrontal cortex, limbic cortex
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antipsychotic drugs are
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dopamine receptor antagonists
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OCD
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deficits in serotonin in terminal regions:
head of caudate cingulate gyrus orbital frontal cortex from raphe nuclei |
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how do you treat OCD?
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SSRIs to increase serotonin levels
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anxiety disorders
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increase nonadrenergic serotonergic functional tone from LC and raphe
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how do you treat anxiety disorders?
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benzodiazepines
GABA |
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depression (opposite of anxiety disorder)
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decreased NE and 5-HT in frontal lobes, prefrontal cortex, possibly orbitofrontal cortex
gluatamate orbitofrontal cortex glutamate and dopamine may be important |
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4As of cortical lesions
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aphasia
apraxia agnosia anopia |
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4Ds of bulbar lesion
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dysphagia
dysarthria diplopia drooping eyelid |
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alzheimer's -deterioration where?
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nucleus basalis and septal nucleus projecting to limbic and cortical areas - decrease in functional cholinergic activity interminal limbic areas and cortical areas--linked to imparied memory capabilities
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what helps SLOW DOWN memory deficits in alzheimers?
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centrally acting cholinergic meds
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Wernicke-Korsakoff
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thiamine deficiency (chronic alcoholism and malnutrition) causes anterograde and retrograde amnesia
motor disturbances confusion and ataxia, opthalmoplegia |
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lesions are where in Wernicke-Korsakoff?
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bilateral lesions of mammillary bodies, medial dorsal thalamus and other diencephalic structures and cerebellum
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artery infarct for Wernicke's area
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posterior infarct
left MCA inferior |
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artery infarct for Broca's area
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left MCA superior division infarct
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artery infarct for genu of corpus callosum
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Anterior cerebral artery/pericallosal artery infarct
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lesion of left occipital cortex and/or splenium of corpus callosum frequently due to what vascular infarct?
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posterior cerebral artery
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esion of left occipital cortex and/or splenium of corpus callosum leads to what deficits?
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alexia without agraphia
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lesion of SM gyrus/Wernicke's (where Engrams are contained) leads to what deficits?
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L and R apraxia
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lesion at genu of corpus callosum causes what deficit?
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L apraxia
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lesion of left MCA superior divison/left premotor/broca's area-deficits?
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L and R apraxia
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Cortical blindness: individual can still detect light vs dark and movement due to spared pathway to tectum
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Anton's syndrome
area 17 |
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unable to recognize objects visually
objects are seen but have no meaning with no acuity problems and no naming deficits due to aphasias |
visual agnosia area 18 and 19
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loss of color perception, world now black and white
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achromatopsia area 18 and 19
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simultanagnosia - cant get the big picture
optic ataxia ocular apraxia |
Balint's syndrome
dorsal parietal cortex |
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impaired restraint
inappropriate affect impulsiveness unconcern for future labile emotions |
disinhibition (orbitofrontal lesions)
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blunted initiative and ambition
problem solving deficits diminished planning abilities apathy perseveration behavior (stuck in a rut) distractability |
abulia (dorsolateral lesions)
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disordered thought and memories
wrong choices of response selectio nof plan for immediate circumstance or future |
limited insight and poor judgement (orbitofrontal lesions)
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