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183 Cards in this Set

  • Front
  • Back
Abulia
Dorsolateral prefrontal syndrome
Diminished spontaneity, verbal output (mutism), and motor behavior (including akinesia)
Personality changes
Lack of ability to plan or sequence; Working memory deficits
Perseveration (repetition of response without a stimulus) or impersistence
Incontinence
Impaired attentional capacity
Anosmia (loss of ability to smell)
Dorsolateral prefrontal syndrome
Diminished spontaneity, verbal output (mutism), and motor behavior (including akinesia)
Personality changes
Lack of ability to plan or sequence; Working memory deficits
Perseveration (repetition of response without a stimulus) or impersistence
Incontinence
Impaired attentional capacity
Anosmia (loss of ability to smell)
Abulia
Achromatopsia
Cortical color blindness; bilateral lesion of WHAT stream
Can’t ID or match colors, but can recall colors of familiar objects
Cortical color blindness; bilateral lesion of WHAT stream
Can’t ID or match colors, but can recall colors of familiar objects
Achromatopsia
ADHD
School-aged children; genetic component, 5X more common in males
Hyperactivity, impaired attention, impulsivity
Reduced activity in prefrontal cortex and basal ganglia
Genetic linkage suggests abnormal dopamine receptor/transporter/enzymes
Higher incidence in kids exposed to alcohol or tobacco in utero
Treated with stimulants to increase dopamine and NE levels in PFC (prefrontal cortex)
School-aged children; genetic component, 5X more common in males
Hyperactivity, impaired attention, impulsivity
Reduced activity in prefrontal cortex and basal ganglia
Genetic linkage suggests abnormal dopamine receptor/transporter/enzymes
Higher incidence in kids exposed to alcohol or tobacco in utero
Treated with stimulants to increase dopamine and NE levels in PFC (prefrontal cortex)
ADHD
Agnosia
No higher order sensory processing → inability to place significance on incoming sensation
No higher order sensory processing → inability to place significance on incoming sensation
Agnosia
Agraphia
Writing impairment; often occurs with aphasia
Can occur in isolation with lesion of inferior parietal lobe of dominant hemisphere
Writing impairment; often occurs with aphasia
Can occur in isolation with lesion of inferior parietal lobe of dominant hemisphere
Agraphia
AION
Anterior Ischemic Optic Neuropathy
Impaired blood supply to optic n.; common cause of sudden vision loss in pts over 50
Risk factors: diabetes, hypertension, elevated cholesterol
Impaired blood supply to optic n.; common cause of sudden vision loss in pts over 50
Risk factors: diabetes, hypertension, elevated cholesterol
AION
Anterior Ischemic Optic Neuropathy
Akinetopsia
“Motion blindness”; bilateral lesion of WHERE stream
Does not affect visual ID of shapes, objects, or faces; Can still detect tactile movement
“Motion blindness”; bilateral lesion of WHERE stream
Does not affect visual ID of shapes, objects, or faces; Can still detect tactile movement
Akinetopsia
Alexia
Reading impairment
Reading impairment
Alexia
Alexia with agraphia
Lesion in dominant parietal lobe – angular gyrus
Aphasia may be limited to dysnomia and paraphasias
Lesion in dominant parietal lobe – angular gyrus
Aphasia may be limited to dysnomia and paraphasias
Alexia with agraphia
Alexia without agraphia
PCA lesion in dominant occipital cortex into corpus callosum
Contralateral visual field deficit
Disconnection syndrome: between intact R visual areas and L hemisphere language centers
Can’t decode language-related visual information
Can still comprehend auditory speech and spoken and written language
PCA lesion in dominant occipital cortex into corpus callosum
Contralateral visual field deficit
Disconnection syndrome: between intact R visual areas and L hemisphere language centers
Can’t decode language-related visual information
Can still comprehend auditory speech and spoken and written language
Alexia without agraphia
Alien hand syndrome
Damage in supplementary motor area → disconnection syndrome
Movement of contralateral arm not under voluntary control
Damage in supplementary motor area → disconnection syndrome
Movement of contralateral arm not under voluntary control
Alien hand syndrome
Altitudinal scotoma
Lesion of the upper or lower branch of the retinal artery
Lesion of the upper or lower branch of the retinal artery
Altitudinal scotoma
Alzheimer’s disease
Neurodegeneration: B-amyloid plaques & tau tangles – temporal lobe (hippocampus)
Progressive
Memory affected first and most seriously
Disorientation, disinhibition, behavioral changes, aphasia
Final stages: loss of ability to walk, eat, etc… without assistance
Late onset sporadic: interplay of genetic and environment
APOE (transports cholesterol): APOEe4 = “risk factor”, APOEe2 = protective
Experience: Higher level of education and more physical activity = reduced risk
Early onset familial: autosomal dominant (1-5% of cases)
Onset before 65
Mutatations IDed that affect processing of amyloid precursor protein
Neurodegeneration: B-amyloid plaques & tau tangles – temporal lobe (hippocampus)
Progressive
Memory affected first and most seriously
Disorientation, disinhibition, behavioral changes, aphasia
Final stages: loss of ability to walk, eat, etc… without assistance
Late onset sporadic: interplay of genetic and environment
APOE (transports cholesterol): APOEe4 = “risk factor”, APOEe2 = protective
Experience: Higher level of education and more physical activity = reduced risk
Early onset familial: autosomal dominant (1-5% of cases)
Onset before 65
Mutatations IDed that affect processing of amyloid precursor protein
Alzheimer’s disease
Amaurosis fugax
“Fleeting darkness”; monocular vision loss for ~10 min; warning for retinal or cerebral infarct
Cause: stenosis of ipsilteral internal carotid → transient occlusion of the retinal artery
“Fleeting darkness”; monocular vision loss for ~10 min; warning for retinal or cerebral infarct
Cause: stenosis of ipsilteral internal carotid → transient occlusion of the retinal artery
Amaurosis fugax
Anomia
Difficulty with naming, may include paraphasias; may be category specific
Associated with limited damage to temporal lobe in WHAT stream
Difficulty with naming, may include paraphasias; may be category specific
Associated with limited damage to temporal lobe in WHAT stream
Anomia
Anosognosia
Unaware of functional deficits
Unaware of functional deficits
Anosognosia
Anton’s syndrome
Diseases of basilar artery → bilateral PCA ischemia or infarcts (bilateral lesion of primary visual cortex) → cortical blindness
Patient is not aware they are blind (anosognosia)
Diseases of basilar artery → bilateral PCA ischemia or infarcts (bilateral lesion of primary visual cortex) → cortical blindness
Patient is not aware they are blind (anosognosia)
Anton’s syndrome
Aphasia
Partial or complete loss of language abilities, often without loss of cognition, sensation, or ability to move the muscles used in speech
Common cause: cerebral infarct of left MCA
Partial or complete loss of language abilities, often without loss of cognition, sensation, or ability to move the muscles used in speech
Common cause: cerebral infarct of left MCA
Aphasia
Aphasias in bilinguals
Languages learned earlier and more fluently are less affected
Equal deficits if languages learned at the same time
Languages learned earlier and more fluently are less affected
Equal deficits if languages learned at the same time
Aphasias in bilinguals
Aphemia
Foreign accent syndrome
Apraxia of speech articulation, sparing written language
Results from small lesion in operculum of dominant hemisphere
Foreign accent syndrome
Apraxia of speech articulation, sparing written language
Results from small lesion in operculum of dominant hemisphere
Aphemia
Apraxia
Loss of ability to correctly perform a motor response in the absence of damage to language, primary motor, or cerebellar pathways
Exhibited in about 1/3 of aphasias
Loss of ability to correctly perform a motor response in the absence of damage to language, primary motor, or cerebellar pathways
Exhibited in about 1/3 of aphasias
Apraxia
Auditory disorders
Perception of spoken language affected; reading and writing spared
Perception of spoken language affected; reading and writing spared
Auditory disorders
Autism spectrum disorders
Strong genetic component – twins & siblings; Some variants X-linked – 4X higher in males
Family linkage studies implicate genes for neural development (neuroligins & neurexins)
Some cases documented de novo gene deletions and duplications relative to parents
Evidence for abnormal structure/function: Brain overgrowth in early development could interfere with development of connection between areas; Growth arrest later on is possible because many autistic adults have reduced volume in specific cortical areas; Pyramidal cells reduced in size and dendritic branching
Strong genetic component – twins & siblings; Some variants X-linked – 4X higher in males
Family linkage studies implicate genes for neural development (neuroligins & neurexins)
Some cases documented de novo gene deletions and duplications relative to parents
Evidence for abnormal structure/function: Brain overgrowth in early development could interfere with development of connection between areas; Growth arrest later on is possible because many effected adults have reduced volume in specific cortical areas; Pyramidal cells reduced in size and dendritic branching
Autism spectrum disorders
Balint’s syndrome
Usually from MCA-PCA watershed (systemic hypotension with internal carotid disease)
Bilteral lesion of WHERE stream; triad of symptoms
Simultagnosia: Can recognize and describe details, but can’t perceive visual scene as a whole
Optic ataxia: Can’t use visual info to accurately coordinate actions – NOT cerebellar ataxia; People can still point using auditory and other cues
Ocular apraxia: difficulty voluntarily directing gaze toward periphery through saccades
May coexist with inferior quadrantanopia, aphasia, or hemineglect
Usually from MCA-PCA watershed (systemic hypotension with internal carotid disease)
Bilteral lesion of WHERE stream; triad of symptoms
Simultagnosia: Can recognize and describe details, but can’t perceive visual scene as a whole
Optic ataxia: Can’t use visual info to accurately coordinate actions – NOT cerebellar ataxia; People can still point using auditory and other cues
Ocular apraxia: difficulty voluntarily directing gaze toward periphery through saccades
May coexist with inferior quadrantanopia, aphasia, or hemineglect
Balint’s syndrome
Bitemporal hemianopia
Bilateral lateral visual field
Bilateral lateral visual field defect
Bitemporal hemianopia
Broca’s aphasia
Expressive or motor aphasia
Lesion of left superior MCA; accompanied by R hemiparesis of arm and face
Telegraphic or stuttering style of speech (unless over-memorized), but still makes sense
Anomia; reading and writing also impaired
Impaired repetition; comprehension generally good – can carry out verbal instructions
Patient is frustrated and aware of deficits
Expressive or motor aphasia
Lesion of left superior MCA; accompanied by R hemiparesis of arm and face
Telegraphic or stuttering style of speech (unless over-memorized), but still makes sense
Anomia; reading and writing also impaired
Impaired repetition; comprehension generally good – can carry out verbal instructions
Patient is frustrated and aware of deficits
Broca’s aphasia
Capgras syndrome
Patient believes family and friends have been replaced by imposters
Disconnect between limbic system and “face” area of occipitotemporal cortex (WHAT)
“Imposters” “logically” explains lack of emotional response
Can recognize by voice alone because limbic-auditory connection is okay
Patient believes family and friends have been replaced by imposters
Disconnect between limbic system and “face” area of occipitotemporal cortex (WHAT)
“Imposters” “logically” explains lack of emotional response
Can recognize by voice alone because limbic-auditory connection is okay
Capgras syndrome
Color anomia/agnosia
Damage to visual cortex of dominant hemisphere + splenium of corpus callosum
May be seen with alexia w/o agraphia, usually with contralateral hemianopsia
Can’t verbally name color because of disconnection between visual and language areas
Damage to visual cortex of dominant hemisphere + splenium of corpus callosum
May be seen with alexia w/o agraphia, usually with contralateral hemianopsia
Can’t verbally name color because of disconnection between visual and language areas
Color anomia/agnosia
Conceptual Hemineglect
Anosognosia unaware of deficit
Anosodiaphoria unaware but unconcerned
Hemiasomatognosia denial of neglected half of body or a portion o fit
These are examples of ____ hemineglect.

Anosognosia unaware of deficit
Anosodiaphoria unaware but unconcerned
Hemiasomatognosia denial of neglected half of body or a portion o fit
Conceptual Hemineglect
Conduction aphasia
A disconnection sydrome
Damage to arcuate fasciculus, sparing Broca’s and Wernicke’s areas
Impaired repetition – responds with related words
Normal fluency and comprehension; impaired naming, paraphasic errors
A disconnection sydrome
Damage to arcuate fasciculus, sparing Broca’s and Wernicke’s areas
Impaired repetition – responds with related words
Normal fluency and comprehension; impaired naming, paraphasic errors
Conduction aphasia
Dementia with Lewy bodies
*aka corticobasal degeneration
Onset after 60; More frequent in males; Familial risk factor
Parkinsonism
Visual hallucination: could be an early symptom, distinguishes from other dementias
Cognitive problems: confusion, fluctuating attention, disorganized speech, executive dysfunction, visual-spatial impairment (apraxia)
Unlike Alzheimer’s: memory deficits less prominent
REM behavioral sleep disorder (may precede other symptoms by several years)
Diagnosis by process of elimination
Moderately rapid decline → death within 8 years
Neurodegeneration due to accumulation of alphasynuclein in substantia nigra and cortex
*aka corticobasal degeneration
Onset after 60; More frequent in males; Familial risk factor
Parkinsonism
Visual hallucination: could be an early symptom, distinguishes from other dementias
Cognitive problems: confusion, fluctuating attention, disorganized speech, executive dysfunction, visual-spatial impairment (apraxia)
Unlike Alzheimer’s: memory deficits less prominent
REM behavioral sleep disorder (may precede other symptoms by several years)
Diagnosis by process of elimination
Moderately rapid decline → death within 8 years
Neurodegeneration due to accumulation of alphasynuclein in substantia nigra and cortex
Dementia with Lewy bodies
Dichotic listening
Present separate stimuli to each ear to determine dominance
Present separate stimuli to each ear to determine dominance
Dichotic listening
Disconnection syndromes
Lesion in white matter affects communication between areas
Lesion in white matter affects communication between areas
Dissconnection syndrome
Disinhibited prefrontal syndrome
Orbitomedial prefrontal syndrome
Impulsive, stimulus-driven behavior
Diminished social insight; inappropriate humor
Confabulation
Emotional lability
Phineas Gage: No motor or speech deficits,
Perseveration (repetition of response without a stimulus) or impersistence
Incontinence with a lack of concern
Impaired attentional capacity
Anosmia (loss of ability to smell)
Orbitomedial prefrontal syndrome
Impulsive, stimulus-driven behavior
Diminished social insight; inappropriate humor
Confabulation
Emotional lability
Phineas Gage: No motor or speech deficits,
Perseveration (repetition of response without a stimulus) or impersistence
Incontinence with a lack of concern
Impaired attentional capacity
Anosmia (loss of ability to smell)
Disinhibited prefrontal syndrome
Dissection
Small tear in vessel allows blood to burrow into vessel wall – flap protrudes into vessel lumen – thrombus forms and possible embolus
Small tear in vessel allows blood to burrow into vessel wall – flap protrudes into vessel lumen – thrombus forms and possible embolus
Dissection
Down’s syndrome
Mental retardation
Extra copy of chromosome 21
Over-expression of DSCAM, cell-adhesion molecule promoting neuronal differentiation and axonal growth
Mental retardation
Extra copy of chromosome 21
Over-expression of DSCAM, cell-adhesion molecule promoting neuronal differentiation and axonal growth
Down’s syndrome
Dysarthria & Aphemia

motor or sensory problems?
Exclusively motor dysfunctions
Exclusively motor dysfunctions
Dysarthria & Aphemia
Dyslexia
Developmental with strong genetic component; mainly affects reading
Normal intelligence and spoken language
Phonological hypothesis: trouble learning phonetics, less common in less phonetically complex languages (ex: Japanese)
Early intervention can help “rewire” language areas
Family studies have IDed polymorphisms in genes important for neuronal migration, presumably affecting connections between visual and language centers
ROBO1 – important for development of commissural connections
DCDC2 – expressed at high levels in language areas
Subtle abnormalities indicate expression levels or pattern of expression affected by mutation, not complete loss
Developmental with strong genetic component; mainly affects reading
Normal intelligence and spoken language
Phonological hypothesis: trouble learning phonetics, less common in less phonetically complex languages (ex: Japanese)
Early intervention can help “rewire” language areas
Family studies have IDed polymorphisms in genes important for neuronal migration, presumably affecting connections between visual and language centers
ROBO1 – important for development of commissural connections
DCDC2 – expressed at high levels in language areas
Subtle abnormalities indicate expression levels or pattern of expression affected by mutation, not complete loss
Dyslexia
Embolism
Something lodges in and occlude a vessel (~1/3 of all strokes)
Something lodges in and occlude a vessel (~1/3 of all strokes)
Embolism
Encephalopathy
Diffuse brain dysfunction
Acute: metabolic or toxic
Hydrocephalus
Chronic: dementias, including Alzheimer’s
Diffuse brain dysfunction
Acute: metabolic or toxic
Hydrocephalus
Chronic: dementias, including Alzheimer’s
Encephalopathy
Fragile-X
Mental retardation involving a single gene
Triplet repeat in an RNA-binding protein (FMR1)
Associated with immature dendritic morphology
Mental retardation involving a single gene
Triplet repeat in an RNA-binding protein (FMR1)
Associated with immature dendritic morphology
Fragile-X
Frontal lobe degenerative
Huntington’s
Prefrontal channel: deterioration of cognitive and executive functions
Limbic channel: impaired impulse control and socially inappropriate behavior
Huntington’s is ____ lobe degeneration

Prefrontal channel: deterioration of cognitive and executive functions
Limbic channel: impaired impulse control and socially inappropriate behavior
Frontal lobe degenerative
Gerstmann’s syndrome
*aka agraphic alexia or parietal alexia
Larger lesion of angular gyrus
Severe agraphia and alexia; Acalculia (can’t do math); Right-left disorientation
Finger agnosia (can’t distinguish the fingers of the hand)
Auditory comprehension and speech are intact
Larger lesion of angular gyrus
Severe agraphia and alexia; Acalculia (can’t do math); Right-left disorientation
Finger agnosia (can’t distinguish the fingers of the hand)
Auditory comprehension and speech are intact
Gerstmann’s syndrome
*aka agraphic alexia or parietal alexia
Global aphasia
Wernicke’s + Broca’s
Lesion of MCA stem or subcortical damage
Wernicke’s + Broca’s
Lesion of MCA stem or subcortical damage
Global aphasia
Hemianopia, hemianopsia
Blindness in ½ of the visual field
Blindness in ½ of the visual field
Hemianopia, hemianopsia
Hemineglect
Sensation intact, lack of attention to and/or behavior consistent with perception
Usually results from acute lesion in right parietal and/or frontal cortex
Sensation intact, lack of attention to and/or behavior consistent with perception
Usually results from acute lesion in right parietal and/or frontal cortex
Hemineglect
Hemispatial neglect
Difficulty orienting body in space and performing tasks with spatial component
Line bisection bisect to right of midline
Cancellation tasks only cancel on right side
Drawing only draw right side of a scene)
Reading and writing only read right words and use ½ of the page to write
Failure to orient to objects in space contralateral to the lesion: wash or dress one side of the body, apply make-up to ½ of face, eat food on ½ of the plate
Difficulty orienting body in space and performing tasks with spatial component
Line bisection bisect to right of midline
Cancellation tasks only cancel on right side
Drawing only draw right side of a scene)
Reading and writing only read right words and use ½ of the page to write
Failure to orient to objects in space contralateral to the lesion: wash or dress one side of the body, apply make-up to ½ of face, eat food on ½ of the plate
Hemispatial neglect
Hemorrhage
Rupture of vessel, bleeding into tissue
Rupture of vessel, bleeding into tissue
Hemorrhage
Homonymous
Affecting the same part of the visual field of each eye
Affecting the same part of the visual field of each eye
Homonymous
Infarct
Necrosis by occlusion of blood flow (arterial or venous)
Necrosis by occlusion of blood flow (arterial or venous)
Infarct
Describe infarcts affecting primary visual cortex
Complete PCA → contralateral homonymous hemianopsia
Smaller infarcts → smaller corresponding areas of visual loss
Macular sparing is due to collateral MCA flow to occipital pole
Complete PCA → contralateral homonymous hemianopsia
Smaller infarcts → smaller corresponding areas of visual loss
Macular sparing is due to collateral MCA flow to occipital pole
Infarct affecting primary visual cortex
Ischemia
Deficiency of blood due to functional constriction or obstruction of a vessel
Deficiency of blood due to functional constriction or obstruction of a vessel
Ischemia
Hemorrhage
Rupture of vessel, bleeding into tissue
Rupture of vessel, bleeding into tissue
Hemorrhage
Homonymous
Affecting the same part of the visual field of each eye
Affecting the same part of the visual field of each eye
Homonymous
Infarct
Necrosis by occlusion of blood flow (arterial or venous)
Necrosis by occlusion of blood flow (arterial or venous)
Infarct
Infarct affecting primary visual cortex
Complete PCA → contralateral homonymous hemianopsia
Smaller infarcts → smaller corresponding areas of visual loss
Macular sparing is due to collateral MCA flow to occipital pole
Complete PCA → contralateral homonymous hemianopsia
Smaller infarcts → smaller corresponding areas of visual loss
Macular sparing is due to collateral MCA flow to occipital pole
Infarct affecting primary visual cortex
Ischemia
Deficiency of blood due to functional constriction or obstruction of a vessel
Deficiency of blood due to functional constriction or obstruction of a vessel
Ischemia
Ischemic core
Actual area of severely reduced blood flow; loss of oxygen and glucose, depletion of energy stores, direct damage to neurons and glia
Actual area of severely reduced blood flow; loss of oxygen and glucose, depletion of energy stores, direct damage to neurons and glia
Ischemic core
Ischemic penumbra
Moderately ischemic area with some collateral blood supply; area of secondary damage if reperfusion delayed
Moderately ischemic area with some collateral blood supply; area of secondary damage if reperfusion delayed
Ischemic penumbra
Lesion of optic chiasm
→ bitemporal hemianopsia; Common causes: pituitary tumor, aneurysm
lesion location resulting in bitemporal hemianopsia
Lesion of optic chiasm

common causes: pituitary tumor, aneurysm
LGN lesions
Caused by tumors, vascular accident
Lissencephaly
Mental retardation involving a single gene
One cause is loss of function in reelin, which guides neuronal migration
Mental retardation involving a single gene
One cause is loss of function in reelin, which guides neuronal migration
Lissencephaly
Mixed transcortical aphasia
Global aphasia, but with repetition intact
Caused by subcortical damage
Global aphasia, but with repetition intact
Caused by subcortical damage
Mixed transcortical aphasia
Monocular
Affecting one eye
Affecting one eye
Monocular
Motor intentional neglect
Hemiakinesia
No spontaneous use of limbs on contralateral side
But good muscle strength and coordination; Ask pt to raise limbs to test for extinction
Difficulty moving toward the side of space they are neglecting
No spontaneous use of limbs on contralateral side
But good muscle strength and coordination; Ask pt to raise limbs to test for extinction
Difficulty moving toward the side of space they are neglecting
Motor intentional neglect
Hemiakinesia
Multi-infarct dementia
Onset rapid or stepwise, usually ages 60-75, 10-20% of dementias
Biggest risk factor is high blood pressure
Confusion, problems with recent memory, inappropriate affect
Often with motor, sensory or other deficits
Onset rapid or stepwise, usually ages 60-75, 10-20% of dementias
Biggest risk factor is high blood pressure
Confusion, problems with recent memory, inappropriate affect
Often with motor, sensory or other deficits
Multi-infarct dementia
Optic nerve lesions
Glaucoma, optic neuritis (related to MS), elevated ICP, tumors → Monocular vision loss
caused by glaucoma, optic neuritis (related to MS), elevated ICP, tumors

result in monocular vision loss
Optic nerve lesions
Optic radiation lesion
Lower: Inferior MCA infarct; “pie in the sky”
Upper: Superior MCA infarct; “pie on the floor”
Both: PCA/MCA watershed infarct (with low BP) → contralateral homonymous hemianopia
These are lesions of which structure?

Lower: Inferior MCA infarct; “pie in the sky”
Upper: Superior MCA infarct; “pie on the floor”
Both: PCA/MCA watershed infarct (with low BP) → contralateral homonymous hemianopia
Optic radiation lesion
Optic tract lesions - visual field defect

Also, are they common?
Homonymous hemianopia.

Uncommon due to blood supply from small branches of several vessels
Uncommon due to blood supply from small branches of several vessels
Optic tract lesions
Paraphasia
Unintentional substitution of syllables, words, or phrases
Unintentional substitution of syllables, words, or phrases
Paraphasia
Pick’s disease
Frontotemporal dementia
Gradual anset ages 35-60, strong genetic component
Accumulation of Tau tangles
Changes in personality/social behavior, loss of initiative and inhibition
Laguage deficits → mutism
Memory loss less severe
Frontotemporal dementia
Gradual anset ages 35-60, strong genetic component
Accumulation of Tau tangles
Changes in personality/social behavior, loss of initiative and inhibition
Laguage deficits → mutism
Memory loss less severe
Pick’s disease
Prosopagnosia
Can’t recognize faces or learn new ones; bilateral lesion of WHAT stream
Can’t integrate, but can ID people with distinguishing features; Can ID by voice or other cues
Can’t recognize faces or learn new ones; bilateral lesion of WHAT stream
Can’t integrate, but can ID people with distinguishing features; Can ID by voice or other cues
Prosopagnosia
Psych disorders related to diffuse modulatory imbalance
Schizophrenia
Depression
Quadrantinopia with macular sparing
Retained vision in the center of the visual field due to collateral flow by MCA to the occipital pole
Retained vision in the center of the visual field due to collateral flow by MCA to the occipital pole
Quadrantinopia with macular sparing
Quadrantinopia/opsia
Blindness in ¼ of the visual field
Blindness in ¼ of the visual field
Quadrantinopia/opsia
Retrochiasmal lesions

visual field defects are ipsilateral or contralateral?
contralateral homonymous visual field deficits
→ contralateral homonymous visual field deficits
Retrochiasmal lesions
Rett syndrome
Mental retardation involving a single gene
X-linked dominant with developmental regression in early childhood
Mutation in MECP2 – codes for transcriptional repressor that silences methylated genes
Mental retardation involving a single gene
X-linked dominant with developmental regression in early childhood
Mutation in MECP2 – codes for transcriptional repressor that silences methylated genes
Rett syndrome
Schizophrenia
Language problems due to disorganization of thought processes
Dopamine transmission imbalance in mesocoritcal pathways
Believed to be polygenic, neural developmental disorder with late onset
30% incidence in people with deletion in chromosome 22
Mutations in DISC 1, which controls axon guidance and outgrowth
Mutations in Neuregulon, an EGF protein – important at several stages in brain development
Language problems due to disorganization of thought processes
Dopamine transmission imbalance in mesocoritcal pathways
Believed to be polygenic, neural developmental disorder with late onset
30% incidence in people with deletion in chromosome 22
Mutations in DISC 1, which controls axon guidance and outgrowth
Mutations in Neuregulon, an EGF protein – important at several stages in brain development
Schizophrenia
Scotoma
Black, dark brown, purplish or white region of visual loss
Black, dark brown, purplish or white region of visual loss
Scotoma
Sensory neglect
Ignore stimuli in contralateral hemisphere
Sensory extinction: when stimuli presented simultaneously to both sides, only perceived on intact side
Visual neglect most common
Intact vision demonstrated by presenting stimulus only to the left visual field
Ignore stimuli in contralateral hemisphere
Sensory extinction: when stimuli presented simultaneously to both sides, only perceived on intact side
Visual neglect most common
Intact vision demonstrated by presenting stimulus only to the left visual field
Sensory neglect
Sign language and aphasias in deaf
Sign language uses same areas as spoken language, but usually more bilateral
Left hemisphere damage → syndromes comparable to Broca’s and Wernicke’s
Right hemisphere damage → visual-perceptual problems
Split-brain patients
Corpus callosum cut to treat epilepsy; reveals language comprehension in non-dominant hemisphere, even though they can’t speak; confabulation by dominant hemisphere to explain actions of isolated right hemisphere
Corpus callosum cut to treat epilepsy; reveals language comprehension in non-dominant hemisphere, even though they can’t speak; confabulation by dominant hemisphere to explain actions of isolated right hemisphere
Split-brain patients
Sudden and severe attack
Stroke
Stroke
Sudden and severe attack
Stuttering
Developmental with strong genetic component (twins); boys less likely to improve
Apparently, abnormal cortical activation patterns during speech initiate motor program before preparation of articulatory code
Often situation specific
Developmental with strong genetic component (twins); boys less likely to improve
Apparently, abnormal cortical activation patterns during speech initiate motor program before preparation of articulatory code
Often situation specific
Stuttering
Supranuclear palsy
Widespread neurodegeneration in midbrain-diencephalon junction
Dementia
Parkinsonism
Loss of vertical eye movements and wide-eyed stare
Rigidity of neck rather than limbs
Bradykinesia and frequent falls
Widespread neurodegeneration in midbrain-diencephalon junction
Dementia
Parkinsonism
Loss of vertical eye movements and wide-eyed stare
Rigidity of neck rather than limbs
Bradykinesia and frequent falls
Supranuclear palsy
Thrombus
Blood clot formed on vessel wall underlying atherosclerotic plaque; causes occlusion
Blood clot formed on vessel wall underlying atherosclerotic plaque; causes occlusion
Thrombus
TIA
EMERGENCY: indicator of potential stroke; ~10 min; more than 10 min → permanent cell damage; more than 1 hr → distinguishable infarct
EMERGENCY: indicator of potential stroke; ~10 min; more than 10 min → permanent cell damage; more than 1 hr → distinguishable infarct
TIA
Transcortical aphasias
Often caused by watershed infarcts, also subcortical damage
Repetition intact
Often caused by watershed infarcts, also subcortical damage
Repetition intact
Transcortical aphasias
Transcortical motor aphasia
Broca’s, but with repetition intact
ACA-MCA watershed
Lesion in connection from Broca’s to prefrontal cortex
Broca’s, but with repetition intact
ACA-MCA watershed
Lesion in connection from Broca’s to prefrontal cortex
Transcortical motor aphasia
Transcortical sensory aphasia
Wernicke’s, but with repetition intact
MCA-PCA watershed
Lesion in connection from Wernicke’s to parietal and temporal lobes
Wernicke’s, but with repetition intact
MCA-PCA watershed
Lesion in connection from Wernicke’s to parietal and temporal lobes
Transcortical sensory aphasia
Wada’s procedure
Anesthetize hemispheres separately to determine dominance
Anesthetize hemispheres separately to determine dominance
Wada’s procedure
Wernicke’s aphasia
Receptive or sensory aphasia
Lesion of left inferior MCA; often with contralateral superior quadrantanopia
Damage to Wernicke’s area (BA 22) and/or Supramarginal and angular gyrus (BA 39 & 40)
Word salad: fluent, effortless speech, but nonsensical
Anomia; reading and writing also impaired; Paraphasia
Impaired repititon
Anosognosia
Receptive or sensory aphasia
Lesion of left inferior MCA; often with contralateral superior quadrantanopia
Damage to Wernicke’s area (BA 22) and/or Supramarginal and angular gyrus (BA 39 & 40)
Word salad: fluent, effortless speech, but nonsensical
Anomia; reading and writing also impaired; Paraphasia
Impaired repititon
Anosognosia
Wernicke’s aphasia
inability to handle stress → weakened prefrontal cortex functions → overactivation of limbic circuits; Treatment balances serotonergic and noradrenergic systems
depression
depression
inability to handle stress → weakened prefrontal cortex functions → overactivation of limbic circuits; Treatment balances serotonergic and noradrenergic systems