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Lateralization & The Split Brain and Cortical Localization of Language
Lateralization & The Split Brain and Cortical Localization of Language
Ch. 16
Outline
The Dominant Left Hemisphere Tests of Cerebral Lateralization The Split-Brain Experiment Tests of Split-Brain Patients Differences Between the Left and Right Hemispheres Brocas Area Wernickes Area
Cross-cuing
Represents communication between hemispheres via a nonneural route For example: a red or green light is flashed in the left visual field; the split-brain patient was then asked to name the color: red or green
Cross-cuing
Most split-brain patients get 50% correct on this task (guessing, by chance); however one patient performed almost perfectly When the performance of this subject was carefully monitored, it was noticed that on the trials when the patient initially said (left hemisphere) the incorrect color, his head shook and the patient then changed their guess to the other color
Cross-cuing
Apparently, the right-hemisphere (who knew the correct answer) heard the incorrect guess of the left hemisphere, and signaled to the left hemisphere that it was wrong by shaking the persons head; when only first guesses were counted, performance fell to 50%
Helping-Hand Phenomenon
Occurs when the two hemispheres are presented with different information about the correct choice and then are asked to reach out and pick up the correct object from a collection in full view Usually the right hand will reach out to pick out what the left hemisphere saw, but the right hemisphere seeing what it thinks is an error being made causes the left hand to grab the right hand and pull it over to the other object
Analytic-Synthetic Theory
Suggests that there are two fundamentally different modes of thinking, an analytic mode (LH) and synthetic mode (RH), and that the neural circuitry for each is fundamentally different LH (pieces of the whole) operates in logical, sequential, analytic fashion RH (the whole) makes immediate, overall synthetic judgments
Motor Theory
Posits that LH is specialized for fine motor movement of which speech is but one example Two lines of evidence:
Lesions of the LH disrupt facial movements more than do RH lesions, even when they are not related to speech Degree of disruption of nonverbal facial movements is positively correlated with the degree of aphasia
Linguistic Theory
Based on the view that the primary function of the LH is language; this is based on studies of deaf people who communicate using ASL; this ability is lost if these people suffer damage to the LH, even when they are able to make the movements required (or is this just showing ASL is a language, and that language is highly analytical?)
Brocas Area
Inferior left prefrontal lobe in left hemisphere Damage leads to deficits primarily speech production (problems with expression) and also grammatical comprehension
Wernickes Area
Left temporal lobe, just posterior to the primary auditory cortex Damage leads to deficits to semantic language comprehension (problems with reception) and speech is imcomprehensible, despite having correct grammar, rhythm an intonation (word salad)
Conduction Aphasia
Damage to pathway connecting Brocas and Wernickes areas called the arcuate fasciculus Comprehension and spontaneous speech are intact but patient not able to repeat words they have just heard
Alexia
Damage to the left angular gyrus (area of left temporal and parietal cortex jost posterior to Wernickes) Inability to read despite intact language comprehension and production
Agraphia
Also due to damage to the left angular gyrus Inability to write despite intact language comprehension and production Involvement of LAG in alexia and agraphia show its responsible for language related visual input
Wernicke-Geshwind Model
Seven components in Left hemisphere: primary visual cortex, angular gyrus, primary auditory cortex, Wernickes area, arucate fasciculus, Brocas area, and primary motor cortex
Reading aloud
Primary visual cortex to left angular gyrus, which transmits visual code to auditory code Then to Wernickes area to arcuate fasciculus to Brocas to primary motor cortex to articulatory areas
Developmental Dyslexia
(1) Differences between brains of dyslexic and non-dyslexic readers have been reported, however none seems to play a critical role Example - dyslexics do not display the asymmetry of the planum temporale
Developmental Dyslexia
(2) Several types of dylexias and thus likely to have different causes and brain areas susceptible
Developmental Dyslexia
(3) Difficult to determine cause-and-effect of brain abnormalities Are these abnormalities the cause of dylexia or the result of lack of reading experience (brain develops differently as a result of different experience)?
Acquired Dyslexia
Two strategies for reading aloud:
Lexical procedure - based on specific stored information that has been acquired about written words - looks at it, recognizes it and says it Phonetic procedure - looks at words, recognizes letters, sounds them out and says word
Acquired Dyslexia
Surface Dyslexia - patients lose ability to to pronounce words based on the specific memories of the words (they lose their lexical procedure) Can pronounce non-words - wug Example: can pronoun words consistent with rules ( fish, river, or glass) but cant pronounce unusual words (have, lose, and steak are like cave, hose, and beak)
Acquired Dyslexia
Deep Dyslexia - patients lose ability to apply common rules of pronunciation ( they lose their phonetic procedure) Cant pronounce non-words Example: can say phonetically unusual words like aisle and yacht but not pronunciation rule-consistent words like fish, river, or glass
Acquired Dyslexia
Where are lexical and phonetic processes in the brain? Deep dyslexia (lose phonetic procedure) due to damage in LH Surface dyslexia (lose lexical) due to partial LH damage or RH damage