Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
48 Cards in this Set
- Front
- Back
|
Loss of language abilities following damage to dominant hemisphere
Cerebral infarct of left MCA most common cause Not due to motor or sensory deficits, although they may coexist Affects both written and spoken language |
Aphasia
|
|
|
Cannot speak or write normally
Struggle to get words out, but makes sense Very frustrated: aware of deficit Anomia: finding right name for something Comprehension generally intact Can understand spoken or written words Can carry out verbal instructions trouble with syntax Impaired repetition: involves arcuate fasciculus Reading aloud and writing impaired Often accompanied by right hemiparesis of arm & face |
Broca’s aphasia
|
|
|
Ability to generate speech is unimpaired
nonsensical speech, make up words Severe deficit in comprehension of language can’t understand spoken or written language can’t follow instructions Cannot repeat what they hear Lack of awareness of deficit: anosognosia Often accompanied by visual field deficit May involve damage to either/both of two areas Wernicke’s area (BA 22 in temporal lobe) Supramarginal and angular gyrus (areas 39 and 40) |
Wernicke’s aphasia
|
|
|
Larger lesion in area of angular gyrus of parietal lobe
Severe disorder of both reading and writing but auditory comprehension and speech are intact. Acalculia: problems with arithmetic Right-left disorientation Finger agnosia: can’t identify their fingers Visual field deficit Anomia |
Gerstmann’s syndrome (agraphic alexia or parietal alexia)
|
|
|
foreign accent syndrome
apraxia of speech articulation small lesion in operculum, sparing written language left MCA superior division infarct |
Aphemia
|
|
|
PCA lesion in dominant occipital cortex into corpus callosum
contralateral visual field deficit disconnection syndrome: connection between right visual areas and left hemisphere language centers lesioned cannot decode language-related visual information comprehends auditory information and can write and speak normally |
Alexia w/o Agraphia
Disconnection syndrome Splenium of Corpus Callosum affected |
|
|
Infarct in vicinity of supramarginal gyrus
Good comprehension and fluent speech But can’t repeat spoken words damage to arcuate fasiculus, sparing Broca and Wenicke areas. Normal fluency and comprehension Impaired naming, paraphasic errors |
Conduction Aphasia
disconnection syndrome (arcuate fasciculus |
|
|
Repetition intact
Motor - ACA-MCA watershed Sensory - MCA-PCA watershed Subcortical damage-thalamus Motor: Broca's but with repetition intact Damages connections from Broca's area to prefrontal cortex. Sensory: Wernicke's with reptition intact (MCA-PCA) Damages connections from Wernicke's to parietal and temporal lobes. Mixed: Global aphasia but repetition spared. Subcortical damage. |
Transcortical Aphasia
|
|
|
Early motor cortex activation, followed by a delayed inferior frontal signal in stutterers
Appear to initiate motor program before preparation of articulatory code |
Stutterering
|
|
|
Damage to both Wernicke and Broca areas.
Large MCA lesion or subcortical damage |
Global Aphasia
|
|
|
Developmental disorder primarily affecting reading
normal intelligence and spoken language Phonological hypothesis difficulty learning relationships between written alphabetic language and sounds (phonemes) of spoken language |
Dyslexia
|
|
|
Difficult with naming, may include paraphasias. May be category specific, associated with limited damage to areas of temporal lobe in 'what stream; of visual processing
|
Anomia Aphasia
|
|
|
reduced movement on contralateral side
Lack of spontaneous use of limbs |
Hemiakinesea.
|
|
|
Anosognosia
|
Unaware of deficits
|
|
|
Anosodiaphoria
|
Aware, but unconcerned of deficits
|
|
|
Hemiasomatognosia
|
Denial of neglected half body or a portion of it.
*Thinks it's someone elses |
|
|
Disconnection syndrome resulting from damage in supplementary motor area (or other areas in frontal or parietal lobe or corpus callosum)
Use of contralateral arm that is not under voluntary control |
Alien Hand Syndrome
|
|
|
Loss of color perception: loss of ability to identify or match colors, but can recall colors of familiar objects.
|
Achromatopsia
|
|
|
Cannot name (verbally) color because of disconnection between visual and language areas.
Damage to visual cortex of dominant hemisphere plus splenium of corpus callosum. |
Color anomia or color agnosia
|
|
|
Loss of ability to recognize people's faces visually
Right or bilateral lesions in inferior occipitotemporal cortex-right hemisphere is dominant in facial recognition |
Prosopagnosia
|
|
|
Belive those close to them (family members, friends) have been replaced by imposters.
Disconnection syndrome affecting link between limbic system and face area of occipitotemporal cortex. Patient's logical explanation of lack of emotional response. Can recognize by voice alone because limbic auditory connections are still intact |
Capgras Syndrome
|
|
|
Motion blindness, a selective loss of motion perception.
Damage in occipitoparietal Where Stream. Does not affect visual identification of shapes, objects, or faces. |
Akinetopsia
|
|
|
Associated with systemic hypotension within the framework of internal carotid disease.
Ocular apraxia Optic ataxia Simultanagnosia. Due to Bilateral lesions of dorsolateral pareito-occipital cortex, usually as a result of an MCA-PCA watershed infarct. May coexist with inferior quadrantanopia, aphasia, or hemineglect. |
Balint's syndrome
|
|
|
Difficulty voluntarily directing gaze (with a saccade) toward object of interest
|
Ocular apraxia
|
|
|
Cannot use visual information to accurately coordinate actions
|
Optic ataxia
|
|
|
Ability to describe and recognize details but inability to describe and recognize as a whole.
|
Simultanagnosia
|
|
|
diminished spontaneity
diminished verbal output (mutism) diminished motor behavior (including akinesia) personality changes lack of ability to plan or sequence Working memory deficits |
Abulia
Dorsolateral PFC Syndrome |
|
|
impuslivity
stimulus-driven behavior diminished social insight inappropriate behavior confabulation |
Disinhibited
Orbitomedial PFC Syndrome |
|
|
Affects 3-5% school-age children
Hereditary component, 5X more common in boys Hyperactivity Impaired attention Impulsivity |
Attention-deficit hyperactivity disorder (ADHD
|
|
|
imbalance in dopaminergic transmission in mesocortical pathways
Drugs that increase dopamine can cause psychosis Antipsychotic drugs decrease dopamine |
Schizophrenia
|
|
|
Degenerative disorder
Deficits in all basal ganglia pathways Prefrontal channel: deterioration of cognitive and executive functions Limbic channel: impaired impulse control and socially inappropriate behavior |
Huntington's Disease
|
|
|
Functions of Prefrontal Cortex
|
Goal-oriented behaviors : Setting goals, planning strategies, setting priorities, tracking progress
Social-emotional decision making : processing, evaluating and filtering social and emotional information Abstract reasoning Personality Working memory |
|
|
Gradual onset ages 35-60
Strong genetic component Accumulation of Tau tangles (no b-amyloid) Changes in personality/ social behavior, loss of initiative, & disinhibition Language deficits progressing to mutism Memory loss occurs later and is less severe |
Frontotemporal Dementias (e.g., Pick’s disease)
|
|
|
Onset may be rapid, stepwise
Typically develops between 60 and 75 Accounts for 10-20% 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
|
|
|
Onset after age 60, moderately rapid decline (death within 8 years)
Parkinsonism: bradykinesia, rigid muscles, shuffling walk, with or without tremor Visual hallucinations: an early symptom, distinguishes it from other dementias Cognitive problems: confusion, fluctuating attention, disorganized speech, executive dysfunction and visual-spatial impairment (e.g., apraxia). Memory deficits less prominent. REM behavioral sleep disorder: may precede onset of other symptoms by several years. Diagnosis primarily by process of elimination (Alzheimer’s, Parkinson’s and Progressive supranuclear palsy) |
Dementia with Lewy Bodies
|
|
|
Most cases are late-onset sporadic: interplay of genetics and environment
Gene for Apoliprotein E: APOEe4 is a "risk factor" while APOEe2 is considered protective. Those with higher educational levels and increased levels of physical activity are at reduced risk Early-onset familial: autosomal dominant, incidence of 1-5% Onset before 65 Mutations identified to date affect production or processing of b-Amyloid |
Alzheimer's Disease
|
|
|
Possible early stage Alzheimer’s: family and friends notice problems with memory
Early stage Alzheimer’s: decreased knowledge of current events and ability to perform complex tasks Mid-stage Alzheimer’s: major gaps in memory, confusion about date and season, require help with daily tasks Late Mid-stage Alzheimer’s: continued memory loss, significant changes in personality and behavior, extensive assistance required Late-stage Alzheimer’s: unable to speak or respond to environment, eventual loss of movement and muscle control (Frontal lobes) Average survival 8-10 year from diagnosis |
Stages of Alzheimer's
|
|
|
Reactions to medications.
Metabolic abnormalities Nutritional deficiencies Emotional problems Confusion, apathy and forgetfulness associated with depression are sometimes mistaken for dementia, particularly in older individuals. Bipolar disease, schizophrenia, and obsessive-compulsive disorder can be misdiagnosed as FTD Infections Normal-pressure hydrocephalus |
Differential diagnosis: treatable dementias
|
|
|
Degeneration of upper & lower motor neurons
weakness upper motor neuron signs - increased tone and reflexes lower motor neuron signs - atrophy and fasciculations affects brainstem nuclei excluding those controlling eye movements sensation and cognition normal Rapidly progressing disease onset ~ 50, survival 2-5 years Sporadic or hereditary Excitotoxic - blocking glutamate release prolongs survival |
ALS
Amyotrophic Lateral Sclerosis |
|
|
Autoimmune
Prevalence 0.1%, but 3-5% chance if relative affected Interaction of heredity and environmental factors 2X higher frequency in females Higher incidence in whites from northern climates Demyelination in CNS Slows/blocks conduction of action potential Usually relapsing-remitting Typical onset between 20 and 40, survival ~ 30 years |
Multiple Sclerosis
|
|
|
Synaptic Cell Adhesion Molecules (e.g., Neurexins and Neuroligins) connect pre- and post-synaptic specializations, regulate synaptic function, and may be disrupted in
|
autism, schizophrenia
|
|
|
poor vision caused by abnormal experience-dependent development
|
Amblyopia
|
|
|
Family linkage studies implicate genes important for neural development, e.g., neuroligins & neurexins
Evidence for abnormal structure/function Brain overgrowth early in development may interfere with development of connections between areas But possible growth arrest later because many autistic adults have reduced volume in specific cortical areas Pyramidal cells reduced in size and dendritic branching |
Autism Spectrum Disorders
|
|
|
Strong genetic component
Family studies have identified polymorphisms in genes important for migration ROBO1 which is important for development of commissural connections DCDC2 expressed at high levels in language areas Subtle abnormalites in dyslexics indicate expression levels or pattern of expression affected by mutation |
Dyslexia
|
|
|
Incidence of 1%
Believed to be polygenic, neural developmental disorder with late symptom onset 30% incidence in people with deletion in chromosome 22 DISC 1 (disrupted in schizophrenia): axon guidance and outgrowth Neuregulin: member of EGF family of proteins important at several stages in brain development |
Schizophrenia
|
|
|
X-linked dominant
Developmental regression in early childhood Mutation in MECP2 gene (codes for transciptional repressor that silences methylated genes) |
Rett Syndrome
|
|
|
Triplett repeats in FMR1 (RNA-binding protein)
Associated with immature dendritic morphology |
Fragile-X
|
|
|
Chromosome 21 trisomy
Results in overexpression of DSCAM, a cell-adhesion protein involved in neuronal differentiation and axon outgrowth |
Down’s syndrome
|
