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65 Cards in this Set

  • Front
  • Back
What are the common elements of all languages?
1. Phonemes
2. Grammar
3. Symbols (for written languages)
4. Sensitive periods
5. Genetic base: FOXP2 gene in people with certain language problems
What language characteristics do we share with songbirds?
Sensitive periods
Genetic Base (calls even in isolated birds have components of the actual call)
What is aphasia?
Language impairment due to brain injury.
What is paraphasias?
Substitution of a word by sound, an incorrect word, or an unintended word.
What is a neologism?
The creation of an entirely new word by the substitution of a phoneme.
What is agraphia?
impairment of writing
What is alexia?
impairment of reading.
What is apraxia?
The impairment of complex, sequential motor movements.
What are the characteristics of aphasia?
a. Paraphasias and neologisms
b. Nonfluent speech
c. Agraphia
d. Alexia
e. Apraxia sometimes
What are the characteristics of Broca's Aphasia?
1) Labored, hesitant speech
2) Comprehension intact
3) Anomia and usually alexia and apraxia
What are the characteristics of Wernicke's aphasia?
1) Verbally fluent, but many paraphasias and often neologisms
2) Cannot repeat words
3) Comprehension poor or nonexistent; alexia may or may not be present
4) Syntax intact
What are the characteristics of global aphasia? Why?
1) Loss of all or almost all language-related ability

Both Broca's and Wernicke's areas affected.
What are the characteristics of conduction aphasia?
1) Fluent speech
2) Intact comprehension
3) Inability to repeat words—phonemic paraphasias
What is the Wernicke-Geschwind connectionist model?
Deficits can be understood as breaks in an interconnected network of components, each which is involved with a particular feature of language or production.
How is language processing the same in hearing impaired people?
a. Left hemisphere processes many language functions the same as hearing people, and in the same areas of the brain
b. Right hemisphere also activated, but implication of this unclear
A common trait of dyslexia patients is the anomalies of what?
arrangement of cortical cells, especially in areas of the frontal and temporal cortical regions.
What is micropolygyria?
Excessive cortical folding.
What are ectopias?
Nests of extra cells.
When do the anomalies associated with dyslexia most likely occur?
During the middle of gestation during active cell migration.
What are common brain abnormalities associated with dyslexia?
--disorganization of the planum temporale: ectopias, micropolygyria --activation of more anterior and less visual areas, disruption of angular gyrus transmission
What is deep dyslexia?
Can read concrete but not abstract words, cannot read nonsense words, verbal paraphasias
What is surface dyslexia?
Can read nonsense words fine, cannot do irregular words
What is the gene associated with dyslexia?
DYXC1 - This is a gene that only accounts for some dyslexia (9% of the general population)
What is the "Final motor pathway" for speech?
Broca's area and adjacent frontal areas
What is the brain region associated with "Phoneme identification"?
inferior frontal, temporal, parietal lobes
What is the brain region associated with "seeing words"?
posterior left hemisphere
What is the brain region associated with "hearing words"?
temporal lobes
What is the brain region associated with "repeating words"?
motor, supplementary motor, and cerebellar and insular areas
What is the brain region associated with "generating verbs"?
large portions of the left hemisphere
What is the brain region associated with "semantic categories"?
Many, including the frontal area.
Which side of the visual field has an advantage for verbal material?
Which side of the visual field has an advantage for non-verbal material?
What ear has an advantage for right-handed people?
The right ear.
Which side of the brain typically exhibits a larger planum temporale?
Which side of the brain does music more excite?
What parts of the brain does perfect pitch involve?
Left hemisphere and possibly planum temporale.
What area of the brain did Phineas Gage likely damage?
primarily orbitofrontal
What are the behavioral characteristics of individuals with orbitofrontal-type (Disinhibited) of prefrontal damage?
Stimulus-driven behavior (utilization behavior)
--Diminished social insight (they don't know the rules any more) --Distractible and impulsive
--Emotional lability: apathy alternating with bouts of euphoria, silliness, perseveration
What are the behavioral characteristics of individuals with dorsolateral(dysexecutive)-type of prefrontal damage?
Diminished judgment, planning, insight and temporal organization (can't read the cues any more)
--Cognitive impersistence (i.e., short attention span)
--Motor programming deficits (possibly aphasia and apraxia) --Diminished self-care (again, failure to read cues)
What are the behavioral characteristics of individuals with mediofrontal(apathetic)-type of prefrontal damage?
--Diminished spontaneity, verbal and motor behavior; diminished prosody, slow responses
--Urinary incontinence
--Lower-extremity weakness and sensory loss
What does damage to postcentral gyrus cause?
What is astereognosis?
The inability to identify items by touch.
What can happen if both the postcentral gyrus and the parietal areas get injured?
Instead of simple astereognosis, multi-modal tasks can also be impaired.
What do bilateral lesions at temporo-occipital-parietal junctions cause?
What is prosopagnosia?
The inability to recognize either their own or others' faces.
--faces may or may not be recognized as faces, but are not recognized as who they are
--may also get losses of ability in other specific categories, e.g., birds, cars
What can right inferior parietal damage produce?
hemispatial neglect
What is hemispatial neglect?
The total ignoring of parts of the visual field even though no visual-field defect is present.
--May be an attention problem
What other symptoms usually accompany hemispatial neglect?
--simultaneous extinction, and often denial of illness
--may involve polymodal cells in parietal
What are some ways to reverse damage done to the brain?
a. treatment involving dissolving clots (thrombolytics)
b. inhibiting Na+ or Ca++ channels
c. blocking glutamate receptors to stop excitotoxicity
What causes apoptosis?
excessive intercellular calcium and zinc
What does diaschisis mean?
The distant inhibitory effects of brain lesions that seem to be reversible.
What does lesion momentum refer to?
The slower the momentum of the lesion (occuring over a long period of time, or a smaller "mass" [size] of the lesion) the more likely the brain can recover (or dynamically reroute) from the damage.
How much recovery is normally seen in patients with aphasia? When does that recovery usually happen?
Some. Usually occurs in the first three months.
What are some ways the brain regrows and reorganizes after an injury?
Axons can re-grow and can get collateral sprouting
What is collateral sprouting?
Neurons near the damage site recognize the damage and respond by developing new sprouts or branches which over time take over the function of the damaged parts.
What is the best way to improve the function of a limb that has stopped functioning?
Force the limb to do work (constraint-induced-movement therapy)
Can new neurons be grown in the brain?
Yes, especially in motor areas.
What is the likely area of the brain associated with the onset of Alzheimer's Disease?
Ml postsynaptic Ach receptors in nucleus basalis of Meynart
What are the two theories of the mechanism of Alzheimer's Disease?
a. Build-up of neuritic plaques with amyloid core
b. Genetic abnormality in APO-E preventing removal of beta-amyloid
What are the current treatments of Alzheimer's Disease?
Cholinesterase inhibitors
What do Cholinesterase inhibitors affect?
AchE, BuChE, or both
How does donezipil treat Alzheimer's Disease?
It is a cholinesterase inhibitor affecting AchE
How does tacrin treat Alzheimer's Disease?
It is a cholinesterase inhibitor affecting AchE and BuChE.
How do cholinesterase inhibitors work to slow down Alzheimer's Disease?
They stop breakdown of AchE and also might slow degeneration by affecting growth factor or inhibiting amyloid deposition.
How successful are current Alzheimer's Disease treatments?
They vary, some showing a significant arresting of the disease, others only showing a small delay of degeneration.