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138 Cards in this Set
- Front
- Back
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prosody
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normal melodious intonation of speech that conveys the meaning of sentence structure
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alexia
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impairments in reading
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agraphia
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impairments in writing **in patients with aphasia it is always present
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agraphia without aphasia
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lesion in inferior parietal lobule of the language-dominant hemisphere
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alexia without agraphia
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lesion in the dominant occipital cortex extending to the posterior corpus callosum (often PCA infarct)
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gerstmann's syndrome
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agraphia
acalculia right-left disorientation finger agnosia |
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apraxia
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inability to carry out an action in response to verbal command in the absence of any comprehension deficit, motor weakness, or incoordination
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aphemia
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severe apraxia of the speech articulatory apparatus without a language disturbance
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cortical deafness
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bilateral lesions of the primary auditory cortex in Heschl's gyrus
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contralateral hemineglect
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lesion in the right parietal or frontal cortex
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allesthesia
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in a pt with hemineglect; erroneously report the location of a stimulus given to the left side of the body as being on the right
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allokinesia
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patient inappropriately moves the normal limb when asked to move the neglected limg
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spatial akinesia
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limb movements impaired when the limbs are located in the neglected hemispace
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anosognosia
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lack of awareness of the illness **not unique to right hemisphere lesions
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anosodiaphoria
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aware that they have severe deficits yet show no emotional concern or distress about it
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hemiasomatognosia
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deny that the left half of their body belongs to them
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Capgras syndrome
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patients insist that their friends or family members have all been replaced by identical looking imposters
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Fregoli syndrome
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patients believe that different people are actually the same person who is in disguise
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reduplicative paramnesia
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patients believe that a person, place or object exists as two identical copies
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where is the heteromodal association cortex
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frontal lobes and at the parieto-occipitotemporal junctions
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most common dominant hemisphere
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Left
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lesions of the left hemisphere cause?
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language dysfunction, even in left-handed individuals
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nondominant hemisphere specialized for what?
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certain nonverbal functions and is more important for complex visual spacial skills, emotional significance to events, and music perception
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lesion of the right hemisphere presentation?
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marked inattention to the contralateral side, even in individuals who are right hemisphere dominant for language
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dominant hemisphere lesions
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impairments of lanugage, detailed analytical abilities, and complex motor planning (praxis)
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non-dominant hemisphere lesions
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impairments of spatial attention and complex visual-spatial abilities, especially those involving spatial orientation and perception of overall gestalt
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posterior parietal and temporal association cortex more involved in?
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interpreting perceptual data and assigning meaning to sensory info
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anterior frontal association cortex more involved in?
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planning, control, and execution of actions
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where does auditory information reach the primary auditory cortex
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superior bank of the Sylvian fissure in the temporal lobe
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Wernicke's area?
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initial steps of language processing that enables certain sequences of sounds to be identified and comprehended
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where is wernicke's area
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corresponds to Brodmann's area 22; encompasses the posterior two-thirds of the superior temporal gyrus in the dominant hemisphere
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Broca's area?
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motor program that activates particular sequesnce of sounds to produce words and sentences
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where is broca's area
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corresponds to Brodmann's areas 44 and 45; opercular and triangular portions of the inferior frontal gyrus in the dominant hemisphere
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how do broca's and wernicke's communicate?
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via a subcortical white matter pathway called the arcuate fasciculus; also polysynaptic connections along the intervening peri-Sylvian cortex
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lexicon
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contained in posterior tempoparietal areas and used to map sounds to meaning for both comprehension and production
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information route in reading
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first reaches primary visual cortex in the occipital lobes, processed in visual association cortex, travels anteriorly via the angular gyrus to reach the language areas
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language problems with non-dominant lesion?
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may be difficult to judge the intended expression imparted by a tone of voice
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most common cause of abrupt onset aphasia
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cerebral infarct
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most common cause of Broca's aphasia
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infarct in the territory of the left MCA superior division
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most salient deficiency in Broca's aphasia
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decreased fluency of spontaneous speech; also lack prosody (normal melodic tone)
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why in Broca's aphasia is repetition impaired?
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disconnection of Broca's area from Wernicke's area
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commonly associated features in Broca's aphasia?
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dysarthria, right hemiparesis affected the face and arm more than the leg
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where are the lesions in little Broca's aphasia
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smaller lesions confined to the region of the frontal operculum
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what causes wernicke's aphasia
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lesion of wernicke's area and adjacent structures in the dominant temporoparietal lobes
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most common cause of wernicke's aphasia
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infarct in the left MCA inferior division territory
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visual deficit associated with wernickes
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contralateral visual field cut, especially of the right upper quadrant due to involvement of the optic radiation
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aphasia type: not fluent, doesn't comprehend, can't repeat?
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global aphasia
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aphasia type: not fluent, doesn't comprehend, can repeat?
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mixed transcortical aphasia
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aphasia type: not fluent, does comprehend, cannot repeat?
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Broca's aphasia
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aphasia type: not fluent, does comprehend, can repeat?
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transcortical motor aphasia
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aphasia type: fluent, does not comprehend, cannot repeat?
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Wernicke's aphasia
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aphasia type: fluent, does not comprehend, can repeat?
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transcortical sensory aphasia
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aphasia type: fluent, does comprehend, cannot repeat?
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conduction aphasia
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aphasia type: fluent, does comprehend, can repeat?
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anomic aphasia
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cause of conduction aphasia
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infarct in the peri-Sylvian area that interrupts the arcuate fasciculus or other pathways in the area of the supramarginal gyrus that connect the two
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cause of transcortical aphasias
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watershed infarct; spare broca's area, wernicke's area, and interconnections but damage other language areas in the frontal or temporoparietal cortices
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cause of transcortical motor aphasia
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ACA-MCA watershed infarct; destroys connections to other regions of the frontal lobe that are needed fro broca's to function but peri-sylvian connections left intact
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cause of transcortical sensory aphasia
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MCA-PCA watershed infarct; connections to structures in parietal lobe and temporal lobe that are needed for Wernicke's area to function are destroyed; peri-sylvian left intact
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patients who have aphasia always present with what
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agraphia
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agraphia without aphasia?
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legions in the inferior parietal lobule of the dominant hemisphere
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alexia without agraphia
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lesion in the dominant occipital cortex extending to the posterior corpus callosum, often a PCA infarct
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alexia with agraphia
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lesions of the dominant inferior parietal lobule in the region of the angular gyrus
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Gerstmann's syndrome cause
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dominant inferior parietal lobule in the region of the angular gyrus
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aphemia caused by?
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small lesion of the dominant frontal operculum restricted to Broca's area
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cortical deafness
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bilateral lesions of the primary auditory cortex in Heschl's gyrus (cannot identify a dog barking)
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lesion in pure word deafness
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infarct in the auditory area of the dominant hemisphere that extends to subcortical white matter to cut off the input from the other hemisphere
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consequence of callosotomy
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right hemisphere unable to access language function in the left hemisphere; agraphia of L hand, inability to name objects in L hand, inability to read in the L hemifield
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attention, alertness, and awareness depend on?
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medial and intralaminar thalamic nuclein; projections in the upper brainstem, hypothalamus, and basal forebrain; cingulate gyrus, medial and lateral fronto-parietal association cortex
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lesions of the right hemisphere affect memory how
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prominent and long-lasting deficits in attention to the contralateral side
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what regions are especially important for spatial analysis
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parietal association cortex at the junction of the parietal, temporal, and occipital lobes in non-dominant hemisphere
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higher-order info processing: "what" stream occurs where
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ventral occipital, temporal, and prefrontal
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higher-order info processing: "where" stream occurs where
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dorsal occipital, parietal, and prefrontal cortex
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parietal association cortex is where
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direectly in the dorsal stream, analyzing location and movement of visual objects in space
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most common cause of hemineglect syndrome
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infarcts of the R parietal or R frontal lobes
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alternate causes for hemineglect syndrome
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infarcts of the cingulate gyrus, thalamus, basal ganglia, or midbrain reticular formation
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marked ipsilateral gaze preference (toward the lesion) indicates
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acute frontal or parietal lesions
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patients with nondominant hemisphere lesions- personality affect?
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severe personality and emotional changes; bland or apathetic, decreased alertness and attention, irritability
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presentation of lesions of the R hippocampal formation (medial temporal sclerosis)
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deficits in visual-spatial memory
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what connects the frontal lobes to the amygdala
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uncinate fasciculus
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what connects the frontal lobes to the hippocampus
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cingulate gyrus and parahippocampal gyrus
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connection between thalamic nucleus and prefrontal cotex
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mediodorsal nucleus
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connection between prefrontal cortex and basal ganglia
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head of the caudate nucleus
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functions of the frontal lobe
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restraint, initiative, order (RIO)
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working memory
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ability to hold limited amt of info in an immediately available store while other cognitive functions are performed
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area of the brain assd with working memory
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dorsolateral prefrontal cortex
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dosolateral convexity lesion symptoms (frontal lobe)
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apathetic, lifeless, abulic state
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ventromedial orbitofrontal lesion
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impulsive, disinhibited, poor judgement
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saccades in frontal lobe lesions
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involvement of the frontal eye field can cause impaired saccades away from the lesion
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what would OKN look like in a patient with contralateral frontal lobe lesion
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subtle asymmetries with a decreased fast phase in one direction
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frontal release signs are?
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primitive reflexes normally seen in infants such as the grasp reflex, suck, snout, and root reflexes
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frontal gait abnormalities
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shuffling, unsteady, magnetic
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arrive at the primary visual cortex, then dorsal pathway goes where/does what
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projects to the parieto-occipital association area to answer the question "where"
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arrive at the primary visual cortex, then ventral pathway goes where/does what
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projects to the occipitotemporal association cortex to answer the question "what"
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how does blindsight work?
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primary visual cortex lesions; depends on info transmitted to association cortex by extrageniculatevisual pathways, bypassin the lateral geniculate nucleus and primary visual cortex
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inferior occipitotemporal cortex
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processes color and visual form involved in object ideintification
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prosopagnosia
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unable to recognize people by looking at their faces
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lesion for prosopagnosia
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occipitotemporal cortex (fusiform gyrus)
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achromatopsia
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central disorder of color perception
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color agnosia is caused by lesions where
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primary visual cortex of the dominant hemisphere extending into the right corpus callosum; is ass'd with alexia without agraphia and right hemianopia
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where is the lesion if the environment appears tilted or inverted (visual reorientation)
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vestibular or lateral medullary dysfunction
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palinopsia?
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lesions of the visual association cortex cause a previously seen object to reappear periodically
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palinopsia can be cause by what drug
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trazodone
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Balint's syndrome
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bilateral lesions of the dorosolateral parieto-occipital association cortex; **CLINICAL TRIAD:
1.) multianagnosia 2.) optic ataxia 3.) ocular ataxia |
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optic ataxia
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impaired ability to reach for or point to objects in space under visual guidance, but proprioceptive or auditory cues lead to ability to point
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ocular apraxia
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difficulty voluntarily directing one's gaze toward objects in peripheral vision through saccades
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lesion in Balint's syndrome
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dorsolateral parieto-occipital association cortex; ass'd symptoms may include inferior-quadrant visual field cuts, aphasia, hemineglect
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bilateral lesions of dorsolateral parieto-occipital cortex caused by?
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MCA-PCA watershed infarcts
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tinnitus is caused by
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peripheral auditory disorders affecting the typmanic membrane, middle ear ossibles, cochlea, or 8th cranial nerve
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self-audible bruits seen when
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AV malformations, carotid dissection, extracranial-to-intracranial pressure gradient that is produced by inc. ICP
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Bonnet syndrome
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visual hallucinations caused by visual loss
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two levels of consciousness
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content and level
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consciousness system that controls AAA includes
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upper brainstem, thalamic, hypothalamic, and basal forebrain activating systems, medial and lateral frontoparietal association cortex and cingulate gyrus
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attention includes at least two major functions
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1.) selective-focusing on a particular domain
2.) sustained- functions like vigilance, concentration, and nondistractability |
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cholinergic thalamus, hypothalamus, basal forebrain projections systems
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pedunculopontine and laterodorsal tegmental nuclie
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non-cholinergic thalamus, hypothalamus, basal forebrain projection system
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pontomesencephalic reticular formation
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nor-adrenergic cortex projection
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locus ceruleus and lateral tegmental area
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serotonergic cortex projection
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dorsal and medial raphe
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dopaminergic striatum, limbic, prefrontal cortex projection
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substantia nigra pars reticularis, ventral tegmental area
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ability to initiate spontaneous movement of contralateral limb
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prefrontal cortex
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anterior cingulate cortex important in what kind of attention?
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motivational factors of attention
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what do the superior colliculi, pretectal area, and pulvinar work together to accomplish
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directing visual attention toward relevant visual stimuli
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conscious awareness
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ability to combine varios forms of sensory, motor, emotional, and mnemonic information into an efficient summary of mental activity that can potentially be remembered at a later time
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delirium
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acute confusional state in which agitation and hallucinations are prominent
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most common causes of acute confusional states
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toxic or metabolic disorders, then infection, trauma, and seizures
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acute confusional states such as delirium
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develop over hours to weeks, have prominent attentional disturbances, tend to wax and wane over the course of hours, have marked slowing on the EEG, and are most often caused by metabolic or toxic disorders, alcohol withdrawl, head trauma, infection, and seizures
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chronic mental status changes
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develop over months to years, do not fluctuate as rapidly, and early on have less prominent disturbances in attention and a relatively normal EEG
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cortical dementia features
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disturbances in langugae, praxis, visual-spatial functions
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primary dementia ass'd with?
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neurodegenerative conditions for which treatments are not available
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secondary dementia assd with
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conditions that may be reversible
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B12 deficiency
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megaloblastic anemia along with subacute combined degeneration of the spinal cord (posterior columns more than corticospinal tracts)
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niacin deficiency
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pellagra- dementia, dermatitis, diarrhea (three Ds)
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pathophysiology of alzheimers disease
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cerebral atrophy, neuronal loss, amyloid plaques, neurofibrillary tangles
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changes are most severe in what areas in AD
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1.) medial temporal lobes (amygdala, hippocampal formation, enterohinal cortex)
2.) basal temporal cortex extending over lateral posterior temporal cortex, parieto-occipital cortex, and posterior cingulate gyrus 3.) frontal lobes |
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senile plaques composed of
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insoluble protein core containing B-amyloid, along with apoE, surrounded by abnormal axons/dendrites
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neurofibrillary tangles
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intracellular accumulations of hyperphosphorylated microtuble-associated proteins or paired helical filaments known as tau proteins
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what action is thought to promote the formation of toxic soluble B-amyloid oligomers
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cleavage at an intracellular location by y-secretase
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three locations that can cause early-onset disease in autosomal dominant families
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1.) APP gene (chrom 21)
2.) presenilin 1 gene (chrom 14) 3.) presenilin 2 gene (chrom 1) |
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cholinesterase inhibitors that show a modest improvement in cognitive function in patient's with AD
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donepezil, rivastigmine, galantamine
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