Psy3242 - User contributions [en]

Wernicke's aphasia

Admin — Mon, 28 Apr 2008 10:12:31 GMT

Admin:

[[Category:Neuropsychological syndromes]]

[http://www.http://www.youtube.com/watch?v=aVhYN7NTIKU] Wernicke's Aphasia

Pascual-Leone et al. (1995)

Admin — Fri, 18 Apr 2008 16:13:26 GMT

Admin:

[[Category:Plasticity Symposium]]

==Introduction==

----

Pascula-Leone, Wassermann, Sadato, and Hallett (1995) conducted a study to examine the representation of the motor cortical outputs in relation to a preceding activity. This study emphasized the importance of the correlation between precise timing and skill acquisition. More specifically, the current study focused exclusively on six blind participants, who were proficient in reading Braille, which requires the use of the tip of the index finger in order to discriminate between differential patterns of raised dots. The finger is subject to side-to-side movements “at a constant amplitude and speed to enhance this sensory discrimination by the pressure receptors in the skin” (Pascula-Leone et. al., 1995). In previous studies, it has been found that the sensorimotor representation of the reading finger is enlarged in these blind, proficient Braille readers when compared to the same finger of the opposite hand, or with either finger in normal, sighted individuals. The extent to which this modulation is enlarged would very well question the size and stability of these cortical representations, for it seems unlikely that such an enlargement would inhibit a proficient Braille reader from the use of his/her other fingers. This dilemma has led to the hypothesis that if this transformation in the motor cortical output is taking place during skill acquisition that requires the use of a specific body part, it should also be expected to reduce to a baseline after learning of the relevant task has occurred. Thus, the cortical representation gives rise to a dynamic, flexible system, whose activation is dependent upon the previous activity (Pascula-Leone et. al., 1995). The flexibility of this system led the researchers in the current study to further investigate the stability as well as the size of this motor cortical output representation in proficient Braille readers.

==Method==

----

Six proficient Braille readers (four men and two women), with ages ranging from 44 to 57 years, participated in this study. These participants were all completely blind before the age of ten, learned to read Braille before the age of 13, and all used the right index finger for character recognition and the left index for line spacing. The experiment tested participants on two different Mondays, which were separated by one week. All Braille readers were tested two times per days (once in the morning and once in the evening). It should be noted that one of the days, in which the participant was tested, was considered to be a “work day,” where he/she read Braille for four to six hours. In contrast, the participants were required to request one of the two testing days off from work without notifying the experimenter, in which they read no Braille. This date was referred to as the “control day” and used as a means of comparison in statistical procedures following the experiment. Using the focal Transcranial Magnetic Stimulation (TMS), this instrument mapped the motor cortical outputs to the left first dorsal interosseous (FDI) as well as the right abductor digiti minimi (ADM) muscles (Pascula-Leone et. al., 1995). Additionally, electrodes were connected to the participant’s finger muscles to evaluate the extent to which the brain areas connected to this cortical modulation were enlarged.

==Results==

----

The findings of the current study support the aforementioned hypothesis that the motor cortical representation is comprised of a dynamic and flexible system, whose organization is largely dependent upon the previous, relevant task. In other words, the current experiment was able to show significant changes in the motor cortical outputs that rapidly adjust to meet the demands and successful completion of the required task.

==Discussion==

----

This study highlights the developmental characteristic of plasticity in the brain. It shows that this phenomenon is ongoing and not limited to brain damaged individuals. For instance, skill acquisition requires the growth of new neurons that adapt to the relevant task. A case study reported in the article discussed a 54-year-old female, who was blind from birth, due to a rare eye condition called Retrolental Fibroplasia. This disease is most salient in infants and usually results from high concentrations of oxygen, which causes abnormal growth of the fibrous tissue behind the lens to take place (Pascula-Leone et. al., 1995). Like the participants in the experimental design, she, too, was a proficient Braille reader, who showed an enlarged motor cortical representation of the right, reading hand (FDI) in contrast to that of her left FDI. After a period of nine months, this subject was tested again, and results from this experiment showed a significant reduction in the cortical output map of the right FDI. Stunned by this finding, researchers were notified of the participant’s recent vacation, in which she did not engage in any Braille reading. Consequently, she was asked to return to the laboratory at the end of work week and surprisingly, they found a “return” to the enlargement of the motor cortical output map that was documented in the first experiment. Based on this reported case study, along with the findings of the current experiment, it can be concluded that skill acquisition relies on plastic changes in the neural network that must adapt to the demands of the new task. Proficiency in learning may very well rely on a rapid modulation of the cortical representation, which gives rises to a correlation between precision of time and skill acquisition. However, the development of this capacity has also been shown to consist of intracortical connections that become latent due to lack of exposure and practice of the relevant skill. Additionally, a point should be made about this latency, for on the days that did not involve Braille reading, these participants were still most likely engaging in tasks that required the use of similar body parts, and thus the motor cortical outputs were adjusted for these activities. This finding gives rise to the plastic component of the brain, in that the “rewiring” of this neural network results in a failure to rapidly respond after prolonged exposure to a task that requires the use of the same body parts (Pascula-Leone et. al., 1995). While this study certainly highlights the underlying neural mechanisms of the plasticity phenomenon, studies involving non-proficient Braille readers should be investigated to assess the types of neural changes that take place following similarly delayed exposure to training.

==References==

----

Pascual-Leone, A., Wassermann, E. M., Sadato, N., Hallett, M. (1995). The role of reading activity on the modulation of motor cortical outputs to the reading hand in braille readers. Annals of Neurology, 38, 910- 915.

Pascual-Leone et al. (1995)

Admin — Fri, 18 Apr 2008 16:12:41 GMT

Admin:

[[Category:Plasticity Symposium]]

''Introduction''

----

Pascula-Leone, Wassermann, Sadato, and Hallett (1995) conducted a study to examine the representation of the motor cortical outputs in relation to a preceding activity. This study emphasized the importance of the correlation between precise timing and skill acquisition. More specifically, the current study focused exclusively on six blind participants, who were proficient in reading Braille, which requires the use of the tip of the index finger in order to discriminate between differential patterns of raised dots. The finger is subject to side-to-side movements “at a constant amplitude and speed to enhance this sensory discrimination by the pressure receptors in the skin” (Pascula-Leone et. al., 1995). In previous studies, it has been found that the sensorimotor representation of the reading finger is enlarged in these blind, proficient Braille readers when compared to the same finger of the opposite hand, or with either finger in normal, sighted individuals. The extent to which this modulation is enlarged would very well question the size and stability of these cortical representations, for it seems unlikely that such an enlargement would inhibit a proficient Braille reader from the use of his/her other fingers. This dilemma has led to the hypothesis that if this transformation in the motor cortical output is taking place during skill acquisition that requires the use of a specific body part, it should also be expected to reduce to a baseline after learning of the relevant task has occurred. Thus, the cortical representation gives rise to a dynamic, flexible system, whose activation is dependent upon the previous activity (Pascula-Leone et. al., 1995). The flexibility of this system led the researchers in the current study to further investigate the stability as well as the size of this motor cortical output representation in proficient Braille readers.

''Method''

----

Six proficient Braille readers (four men and two women), with ages ranging from 44 to 57 years, participated in this study. These participants were all completely blind before the age of ten, learned to read Braille before the age of 13, and all used the right index finger for character recognition and the left index for line spacing. The experiment tested participants on two different Mondays, which were separated by one week. All Braille readers were tested two times per days (once in the morning and once in the evening). It should be noted that one of the days, in which the participant was tested, was considered to be a “work day,” where he/she read Braille for four to six hours. In contrast, the participants were required to request one of the two testing days off from work without notifying the experimenter, in which they read no Braille. This date was referred to as the “control day” and used as a means of comparison in statistical procedures following the experiment. Using the focal Transcranial Magnetic Stimulation (TMS), this instrument mapped the motor cortical outputs to the left first dorsal interosseous (FDI) as well as the right abductor digiti minimi (ADM) muscles (Pascula-Leone et. al., 1995). Additionally, electrodes were connected to the participant’s finger muscles to evaluate the extent to which the brain areas connected to this cortical modulation were enlarged.

''Results''

----

The findings of the current study support the aforementioned hypothesis that the motor cortical representation is comprised of a dynamic and flexible system, whose organization is largely dependent upon the previous, relevant task. In other words, the current experiment was able to show significant changes in the motor cortical outputs that rapidly adjust to meet the demands and successful completion of the required task.

''Discussion''

----

This study highlights the developmental characteristic of plasticity in the brain. It shows that this phenomenon is ongoing and not limited to brain damaged individuals. For instance, skill acquisition requires the growth of new neurons that adapt to the relevant task. A case study reported in the article discussed a 54-year-old female, who was blind from birth, due to a rare eye condition called Retrolental Fibroplasia. This disease is most salient in infants and usually results from high concentrations of oxygen, which causes abnormal growth of the fibrous tissue behind the lens to take place (Pascula-Leone et. al., 1995). Like the participants in the experimental design, she, too, was a proficient Braille reader, who showed an enlarged motor cortical representation of the right, reading hand (FDI) in contrast to that of her left FDI. After a period of nine months, this subject was tested again, and results from this experiment showed a significant reduction in the cortical output map of the right FDI. Stunned by this finding, researchers were notified of the participant’s recent vacation, in which she did not engage in any Braille reading. Consequently, she was asked to return to the laboratory at the end of work week and surprisingly, they found a “return” to the enlargement of the motor cortical output map that was documented in the first experiment. Based on this reported case study, along with the findings of the current experiment, it can be concluded that skill acquisition relies on plastic changes in the neural network that must adapt to the demands of the new task. Proficiency in learning may very well rely on a rapid modulation of the cortical representation, which gives rises to a correlation between precision of time and skill acquisition. However, the development of this capacity has also been shown to consist of intracortical connections that become latent due to lack of exposure and practice of the relevant skill. Additionally, a point should be made about this latency, for on the days that did not involve Braille reading, these participants were still most likely engaging in tasks that required the use of similar body parts, and thus the motor cortical outputs were adjusted for these activities. This finding gives rise to the plastic component of the brain, in that the “rewiring” of this neural network results in a failure to rapidly respond after prolonged exposure to a task that requires the use of the same body parts (Pascula-Leone et. al., 1995). While this study certainly highlights the underlying neural mechanisms of the plasticity phenomenon, studies involving non-proficient Braille readers should be investigated to assess the types of neural changes that take place following similarly delayed exposure to training.

''References''

----

Pascual-Leone, A., Wassermann, E. M., Sadato, N., Hallett, M. (1995). The role of reading activity on the modulation of motor cortical outputs to the reading hand in braille readers. Annals of Neurology, 38, 910- 915.

Oliver Sacks

Admin — Fri, 18 Apr 2008 16:06:33 GMT

Admin: formatting

[[Category:Neuropsychological profiles]]

''Biography''

Oliver Sacks is a practicing neurologist, who is most famous for his books featuring patients' case studies he has encountered throughout his career. He was born July 9, 1933 in London, England. He was brought up among a family of doctors and scientists, his mother was a surgeon and his father was a general practitioner. Oliver followed in his family’s foot steps. He earned his medical degree from Queen’s College at Oxford University. He completed his residencies at Mt. Zion Hospital in San Francisco and at UCLA. Later he moved to New York to begin his practice. He began working as a consulting neurologist at Beth Abraham Hospital in New York City. This hospital was the place where he met with many of the people that inspired his books, all beginning with the patients with sleeping sickness, whom he treated with L-Dopa to bring out of their vegetative state. A recount of this was used to make his book Awakenings.

Sacks has been published many times throughout his career. He has received many acknowledgements for his literary achievements including the Lewis Thomas Prize by Rockefeller University, which recognized him as a poet. He is an honorary member of the American Academy of Arts and Letters and the American Academy of Arts and Sciences. The New York Times referred to him as “the poet laureate of medicine.” He has written many best selling books; besides his own works, he has greatly participated to neurological literature through his collaborations with and contributions to the works of many other professionals in the field.

''Books''
*Migraine (1970)
*Awakenings (1973)
*A Leg to Stand On (1984)
*The Man Who Mistook His Wife for a Hat (1985)
*Seeing Voices: A Journey into the World of the Deaf (1990)
*An Anthropologist on Mars (1995)
*The Island of the Colorblind (1996
*Uncle Tungten: Memories of a Chemical Boyhood (2001)
*Oaxaca Journal (2002
*Musicophilia: Tales of Music and the Brain (2007)

''Recognition''

Oliver Sacks has received recognition throughout his career for his exemplary work. These include honorary degrees, awards, memberships, among others.
He has honorary fellowships to a variety of different organizations:
*American Academy of Arts and Letters
*American Academy of Arts and Sciences
*American Neurological Association
*Association of British Neurologists
*Jonathan Edwards College, Yale University
*New York Academy of Sciences
*New York Institute for the Humanities at NYU
*Queen’s College, Oxford
*Royal College of Physicians
*University of California, Santa Cruz, Cowell College

Sacks has inducted as a member to the following groups:
*Alpha Omega Alpha
*American Academy of Neurology
*American Fern Society
*Authors’ Guild
*British Pteridological Society
*Bronx County and NY State Medical Societies
*New York Mineralogical Club
*New York Stereoscopic Society
*PEN
*Society for Neuroscience

He has received 11 honorary degrees from Universities around the world, including:
*1990 Georgetown University, Doctor of Humane Letters
*1991 Tufts University, Doctor of Science
*1991 College of Staten Island, CUNY, Doctor of Humane Letters
*1991 New York Medical College, Doctor of Science
*1992 Medical College of Pennsylvania, Doctor of Medical Science
*1992 Bard College, Doctor of Science
*2001 Queen's University, Kingston, Ontario, Doctor of Laws
*2003 Karolinska Institutet, Stockholm, Doctor of Medical Science
*2005 Gallaudet University, Doctor of Laws
*2005 University of Oxford, Doctor of Civil Law
*2006 Pontificia Universidad Católica de Perú

In addition he has received many awards for his work:
*1970 Alpha Omega Alpha, Albert Einstein College of Medicine
*1973 Book of the Year, The Observer, AWAKENINGS
*1974 Hawthornden Prize for Imaginative Literature, AWAKENINGS
*1988 American Psychiatric Association, Oskar Pfister Award
*1989 American Academy & Institute of Arts and Letters, Harold D. Vursell Memorial Award
*1989 Guggenheim Fellowship (for work on the neuro-anthropology of Tourette’s Syndrome)
*1991 The Scriptor Award, University of Southern California, AWAKENINGS
*1991 Odd Fellows Social Concern Book Award, SEEING VOICES
*1991 Prix Psyche'
*1991 National Headache Foundation, Professional Support Award
*1991 American Academy of Neurology, Presidential Citation
*1991 American Neurological Association, Special Presidential Award
*1991 The Royal National Institute for the Deaf, Communicator of the Year Award
*1991 Assn of Neuroscience Depts & Programs, Award for Education in Neuroscience
*1994 George S. Polk Award for Magazine Reporting, "An Anthropologist on Mars"
*1994 National Association of Science Writers Award, "An Anthropologist on Mars"
*1995 Esquire/Apple/Waterstone's Book of the Year, AN ANTHROPOLOGIST ON MARS
*1996 Mainichi Publishing Culture Award, Tokyo, Best Natural Science Book, SEEING VOICES
*2000 Cornell University, A.D. White Professor-at-Large
*2001 New York Times Editors’ Choice, UNCLE TUNGSTEN
*2002 Lewis Thomas Prize for the Scientist as Poet, Rockefeller University
*2002 Alfred P. Sloan Foundation fellowship (Music and the Brain)
*2002 Jewish Quarterly Wingate Prize, UNCLE TUNGSTEN
*2004 National Science Foundation Public Communication Award
*2004 Tanner Lecturer in Human Values, Yale University
*2004 Coalition of Voluntary Mental Health Associations, Mental Health Award
*2004 E.A. Wood Scientific Writing Award, American Crystallographic Association
*2004 New York City Mayor’s Award for Excellence in Science and Technology
*2004 Literature Award of the German Chemical Industry Fund, UNCLE TUNGSTEN

''Currently''
Oliver Sacks work has brought him around the world. He has encountered many people of a variety of cultures. However, he continues to reside in New York. He currently holds the position of Professor of Clinical Neurology and Clinical Psychiatry at the Columbia University Medical Center.
[[Image:Example.jpg]][[Image:Example.jpg]]

'''Links'''
[[]]

Pascual-Leone et al. (1995)

Admin — Thu, 17 Apr 2008 12:00:27 GMT

Admin:

[[Category:Plasticity Symposium]]

'''Introduction'''

----

Pascula-Leone, Wassermann, Sadato, and Hallett (1995) conducted a study to examine the representation of the motor cortical outputs in relation to a preceding activity. This study emphasized the importance of the correlation between precise timing and skill acquisition. More specifically, the current study focused exclusively on six blind participants, who were proficient in reading Braille, which requires the use of the tip of the index finger in order to discriminate between differential patterns of raised dots. The finger is subject to side-to-side movements “at a constant amplitude and speed to enhance this sensory discrimination by the pressure receptors in the skin” (Pascula-Leone et. al., 1995). In previous studies, it has been found that the sensorimotor representation of the reading finger is enlarged in these blind, proficient Braille readers when compared to the same finger of the opposite hand, or with either finger in normal, sighted individuals. The extent to which this modulation is enlarged would very well question the size and stability of these cortical representations, for it seems unlikely that such an enlargement would inhibit a proficient Braille reader from the use of his/her other fingers. This dilemma has led to the hypothesis that if this transformation in the motor cortical output is taking place during skill acquisition that requires the use of a specific body part, it should also be expected to reduce to a baseline after learning of the relevant task has occurred. Thus, the cortical representation gives rise to a dynamic, flexible system, whose activation is dependent upon the previous activity (Pascula-Leone et. al., 1995). The flexibility of this system led the researchers in the current study to further investigate the stability as well as the size of this motor cortical output representation in proficient Braille readers.

'''Method'''

----

Six proficient Braille readers (four men and two women), with ages ranging from 44 to 57 years, participated in this study. These participants were all completely blind before the age of ten, learned to read Braille before the age of 13, and all used the right index finger for character recognition and the left index for line spacing. The experiment tested participants on two different Mondays, which were separated by one week. All Braille readers were tested two times per days (once in the morning and once in the evening). It should be noted that one of the days, in which the participant was tested, was considered to be a “work day,” where he/she read Braille for four to six hours. In contrast, the participants were required to request one of the two testing days off from work without notifying the experimenter, in which they read no Braille. This date was referred to as the “control day” and used as a means of comparison in statistical procedures following the experiment. Using the focal Transcranial Magnetic Stimulation (TMS), this instrument mapped the motor cortical outputs to the left first dorsal interosseous (FDI) as well as the right abductor digiti minimi (ADM) muscles (Pascula-Leone et. al., 1995). Additionally, electrodes were connected to the participant’s finger muscles to evaluate the extent to which the brain areas connected to this cortical modulation were enlarged.

'''Results'''

----

The findings of the current study support the aforementioned hypothesis that the motor cortical representation is comprised of a dynamic and flexible system, whose organization is largely dependent upon the previous, relevant task. In other words, the current experiment was able to show significant changes in the motor cortical outputs that rapidly adjust to meet the demands and successful completion of the required task.

'''Discussion'''

----

This study highlights the developmental characteristic of plasticity in the brain. It shows that this phenomenon is ongoing and not limited to brain damaged individuals. For instance, skill acquisition requires the growth of new neurons that adapt to the relevant task. A case study reported in the article discussed a 54-year-old female, who was blind from birth, due to a rare eye condition called Retrolental Fibroplasia. This disease is most salient in infants and usually results from high concentrations of oxygen, which causes abnormal growth of the fibrous tissue behind the lens to take place (Pascula-Leone et. al., 1995). Like the participants in the experimental design, she, too, was a proficient Braille reader, who showed an enlarged motor cortical representation of the right, reading hand (FDI) in contrast to that of her left FDI. After a period of nine months, this subject was tested again, and results from this experiment showed a significant reduction in the cortical output map of the right FDI. Stunned by this finding, researchers were notified of the participant’s recent vacation, in which she did not engage in any Braille reading. Consequently, she was asked to return to the laboratory at the end of work week and surprisingly, they found a “return” to the enlargement of the motor cortical output map that was documented in the first experiment. Based on this reported case study, along with the findings of the current experiment, it can be concluded that skill acquisition relies on plastic changes in the neural network that must adapt to the demands of the new task. Proficiency in learning may very well rely on a rapid modulation of the cortical representation, which gives rises to a correlation between precision of time and skill acquisition. However, the development of this capacity has also been shown to consist of intracortical connections that become latent due to lack of exposure and practice of the relevant skill. Additionally, a point should be made about this latency, for on the days that did not involve Braille reading, these participants were still most likely engaging in tasks that required the use of similar body parts, and thus the motor cortical outputs were adjusted for these activities. This finding gives rise to the plastic component of the brain, in that the “rewiring” of this neural network results in a failure to rapidly respond after prolonged exposure to a task that requires the use of the same body parts (Pascula-Leone et. al., 1995). While this study certainly highlights the underlying neural mechanisms of the plasticity phenomenon, studies involving non-proficient Braille readers should be investigated to assess the types of neural changes that take place following similarly delayed exposure to training.

'''References'''

----

Pascual-Leone, A., Wassermann, E. M., Sadato, N., Hallett, M. (1995). The role of reading activity on the modulation of motor cortical outputs to the reading hand in braille readers. Annals of Neurology, 38, 910- 915.

User talk:Mnguyen

Admin — Wed, 09 Apr 2008 14:44:49 GMT

Admin:

Mai-han,

Thanks for getting started! [[User:Admin|Dr. St. John]] 15:35, 28 February 2008 (EST)

==Corsi task==

The Corsi page image looks nice. Make sure your text flows a little better. For example, some of the "instructions" are written in third person, past tense, and some in second person, present tense. [[User:Admin|Dr. St. John]] 10:44, 9 April 2008 (EDT)

User talk:Hmetzger

Admin — Wed, 09 Apr 2008 14:42:25 GMT

Admin:

== Recent edits ==

Glad you've gotten started. I replaced the links you had to external images and embedded them on the page. Take a look at how I did it (by going your your pages and hitting Edit). You should add some subheadings to the pages (like "Recent edits" above); you do this as follows:

<nowiki>==Recent edits==</nowiki>

Be sure to also edit your pages for clarity of writing. [[User:Admin|Dr. St. John]] 10:42, 9 April 2008 (EDT)

Iowa gambling task

Admin — Wed, 09 Apr 2008 14:40:26 GMT

Admin:

[[Category:Neuropsychological methods]]

[[Image:Decks.jpg|thumb|300pxl|Iowa Gambling Task methodology.]]

The Iowa Gambling Task was created by A. Bechara, H. Damasio, D. Tranel,
and A. R. Damasio (1997) of the University of Iowa. It was designed to examine emotion and cognition interaction in decision making. The area of the brain reqired to perfom the Iowa Gambling Task accurately is the dorsolateral and lateral orbital prefrontal cortex. This area of the brain is involved in making right and wrong decisions, predicting future events, and mediating conflict, which are requirements to complete the IGT correctly.

The Iowa Gambling Task requires the participant to choose cards from four different decks. Each card has a different amount of money on it and can either result in a gain of profit or a loss. Two of the decks, the green and red, have low monetary rewards but lower losses. These are called the advantageous decks. The other two decks, yellow and blue, have high rewards but even higher losses. The IGT is fixed so that if a person picks cards from the advantageous decks, profit will be made, and if the person picks from the disadvantageous decks, the results are monetary deficits. Most participants begin the task by picking cards from the disadvantageous deck, with the high rewards and even higher losses. After a few trials, the participant should see the pattern of loss and begin choosing from the green and read advantageous decks.

[[Image:Aggressionbrain.jpg|thumb|300pxl|Prefrontal cortex and other brain regions.]]
Studies done on the Iowa Gambling Task show differences between age and sex. A study done by Wood, Busemeyer, Coling, Cox, and Davis (2005) indicated that both older and younger adults perform well on the IGT, but have different means of doing so. Older adults (65-88 yrs.) depend on accurate representations of wins and losses depicted through the IGT. Young adults (18-34 yrs.) rely on the learning from the task and memory.

Another study based on sex was performed by Overman, Graham, Redmond, Eubank, Boettcher, Samplawski, and Walsh (2006). The data indicated that women need a personal moral dilemma presented during the Iowa Gambling Task to achieve results close to those of the men. Men's better performance is not because men are mathematically more gifted; instead, women need the personal moral dilemma to activate the dorsolateral prefrontal cortex and lateral orbital prefrontal cortex already activated in men during the IGT.

Iowa gambling task

Admin — Wed, 09 Apr 2008 14:39:55 GMT

Admin: added embedded images

[[Category:Neuropsychological methods]]

[[Image:Decks.jpg|thumb|200pxl|Iowa Gambling Task methodology.]]

The Iowa Gambling Task was created by A. Bechara, H. Damasio, D. Tranel,
and A. R. Damasio (1997) of the University of Iowa. It was designed to examine emotion and cognition interaction in decision making. The area of the brain reqired to perfom the Iowa Gambling Task accurately is the dorsolateral and lateral orbital prefrontal cortex. This area of the brain is involved in making right and wrong decisions, predicting future events, and mediating conflict, which are requirements to complete the IGT correctly.

The Iowa Gambling Task requires the participant to choose cards from four different decks. Each card has a different amount of money on it and can either result in a gain of profit or a loss. Two of the decks, the green and red, have low monetary rewards but lower losses. These are called the advantageous decks. The other two decks, yellow and blue, have high rewards but even higher losses. The IGT is fixed so that if a person picks cards from the advantageous decks, profit will be made, and if the person picks from the disadvantageous decks, the results are monetary deficits. Most participants begin the task by picking cards from the disadvantageous deck, with the high rewards and even higher losses. After a few trials, the participant should see the pattern of loss and begin choosing from the green and read advantageous decks.

[[Image:Aggressionbrain.jpg|thumb|200pxl]]
Studies done on the Iowa Gambling Task show differences between age and sex. A study done by Wood, Busemeyer, Coling, Cox, and Davis (2005) indicated that both older and younger adults perform well on the IGT, but have different means of doing so. Older adults (65-88 yrs.) depend on accurate representations of wins and losses depicted through the IGT. Young adults (18-34 yrs.) rely on the learning from the task and memory.

Another study based on sex was performed by Overman, Graham, Redmond, Eubank, Boettcher, Samplawski, and Walsh (2006). The data indicated that women need a personal moral dilemma presented during the Iowa Gambling Task to achieve results close to those of the men. Men's better performance is not because men are mathematically more gifted; instead, women need the personal moral dilemma to activate the dorsolateral prefrontal cortex and lateral orbital prefrontal cortex already activated in men during the IGT.

File:Decks.jpg

Admin — Wed, 09 Apr 2008 14:38:52 GMT

Admin:

File:Aggressionbrain.jpg

Admin — Wed, 09 Apr 2008 14:38:37 GMT

Admin:

Auguste D. (patient)

Admin — Wed, 09 Apr 2008 14:36:48 GMT

Admin: added formatting

[[Category:Neuropsychological profiles]]

[[Image:Augusted.jpg|thumb|200pxl|Auguste D.]]

Auguste D. was a 51-year-old woman from Frankfurt, Germany. She was admitted to a Frankfurt hospital on November 25, 1901. Auguste's symptoms were disorientation, unpredictable behavior, hallucinations, a reduced ability to comprehend and recall information, as well as psychosocial impairment. She was initially examined by Alois Alzheimer and that followed for a period of five years, until Auguste D.'s death in April of 1906.

Over this period of time, Alzheimer constructed 32 sheets of observation, compiled a case study of Auguste D., and created an attestation about his findings. He also obtained writing samples, which are Auguste's attempts to write her name, and four pictures of her.

Here are a few examples of her assessments and questionings as recorded by Dr. Alzheimer:

'''November 26, 1901'''
*Dr. A: What is your first name?
*Patient: Auguste
*Dr. A: What is your last name?
*Patient: Auguste
*Dr. A: What is your husband's name?
*Patient: Auguste

When eating cauliflower and pork, Auguste is asked what she is consuming. She answers spinach.

When items are showed to her, a short moment later, she cannot remember them. When not being examined, Auguste constantly talks about twins. In attempts to write out her name, Auguste can write Mrs. but forgets the rest.

'''November 29, 1901'''
*Dr. A: What year is it?
*Patient: 1800
*Dr. A: What is the name of the 11th month?
*Patient: The last one, if not the last one.

Auguste has no problem recalling the color of snow, soot, sky, and meadows. She knows how many hands, fingers, and legs she has. She can correctly read letters but cannot understand what she reads. When it comes to simple math such as multiplication of small numbers, Auguste cannot answer correctly and replies with random phrases and words. Physically, Auguste is fairly normal, just a little weak.

She died in 1906, after pneumonia after being hospitalized for five years. A year after her death, Dr. Alzheimer published his composition under the title "A characteristic serious disease of the cerebral cortex." He characterized his patient with initial symptoms of jealousy toward her husband, followed by rapidly increasing memory impairments and disorientation. Dr. Alzheimer was uncertain of what was causing the disease and called it "peculiar." He noted, however, that several cases were beginning to pop up. When looking at Auguste D.'s brain after her death, the only peculiarity he noticed were in the brain's neurofibrils, and the fibrils around them, but he could not explain why this was. Alzheimer knew it was some form of dementia, but scholars and medical people still debate if it was what we call now Alzheimer's Disease.

Auguste D. (patient)

Admin — Wed, 09 Apr 2008 14:34:26 GMT

Admin: added embedded image

[[Category:Neuropsychological profiles]]

[[Image:Augusted.jpg|thumb|200pxl|Auguste D.]]

Auguste D. was a 51-year-old woman from Frankfurt, Germany. She was admitted to a Frankfurt hospital on November 25, 1901. Auguste's symptoms were disorientation, unpredictable behavior, hallucinations, a reduced ability to comprehend and recall information, as well as psychosocial impairment. She was initially examined by Alois Alzheimer and that followed for a period of five years, until Auguste D.'s death in April of 1906.

Over this period of time, Alzheimer constructed 32 sheets of observation, compiled a case study of Auguste D., and created an attestation about his findings. He also obtained writing samples, which are Auguste's attempts to write her name, and four pictures of her.

Here are a few examples of her assessments and questionings as recorded by Dr. Alzheimer:

November 26, 1901:
Dr. A: What is your first name?
Patient: Auguste
Dr. A: What is your last name?
Patient: Auguste
Dr. A: What is your husband's name?
Patient: Auguste

When eating cauliflower and pork, Auguste is asked what she is consuming. She answers spinach.

When items are showed to her, a short moment later, she cannot remember them. When not being examined, Auguste constantly talks about twins. In attempts to write out her name, Auguste can write Mrs. but forgets the rest.

November 29, 1901
Dr. A: What year is it?
Patient: 1800
Dr. A: What is the name of the 11th month?
Patient: The last one, if not the last one.

Auguste has no problem recalling the color of snow, soot, sky, and meadows. She knows how many hands, fingers, and legs she has. She can correctly read letters but cannot understand what she reads. When it comes to simple math such as multiplication of small numbers, Auguste cannot answer correctly and replies with random phrases and words. Physically, Auguste is fairly normal, just a little weak.

She died in 1906, after pneumonia after being hospitalized for five years. A year after her death, Dr. Alzheimer published his composition under the title "A characteristic serious disease of the cerebral cortex." He characterized his patient with initial symptoms of jealousy toward her husband, followed by rapidly increasing memory impairments and disorientation. Dr. Alzheimer was uncertain of what was causing the disease and called it "peculiar." He noted, however, that several cases were beginning to pop up. When looking at Auguste D.'s brain after her death, the only peculiarity he noticed were in the brain's neurofibrils, and the fibrils around them, but he could not explain why this was. Alzheimer knew it was some form of dementia, but scholars and medical people still debate if it was what we call now Alzheimer's Disease.

File:Augusted.jpg

Admin — Wed, 09 Apr 2008 14:33:39 GMT

Admin:

Corpus callosum

Admin — Wed, 09 Apr 2008 14:32:52 GMT

Admin: replaced gif with jpg

[[Category:Brain areas]]

[[Image:Callosum.jpg|thumb|200pxl|The corpus callosum in a human brain.]]

The Corpus Callosum, which contains more than 200 million nerve fibers, connects the left and the right hemispheres of the brain. It is the largest pathway in the human brain and runs right down the middle. When it comes to communication between both hemispheres, the corpus callosum is the main pathway used. Communication is needed when the body needs to coordinate movement or create complex thoughts and ideas. There are other smaller pathways the brain also uses to communicate between hemispheres, but the Corpus Callosum is the most important. The next main pathway is the Anterior Commisure, but it contains a mere 50,000 nerve fibers as compared to the 200 million of the Corpus Callosum.

As the human body develops, so does the Corpus Callosum. The actual structure of the Corpus Callosum finishes developing between 12 and 16 weeks in utero; however, although the structure has finised growing, the fibers in it continue to become more effective and efficient as one grows into an adolescent. By the age of 12, the Corpus Callosum will funtction just as well as it will in adulthood.

The Corpus Callosum does not complete growth in all people. In some developmental cases, the fibers will not completely connect the two hemispheres. This occurs in utero, and if the pathway is not created during prenatal development, it never will develop correctly. Some people are also born completely without a Corpus Callosum.These disorders can be a result of prenatal infections or viruses, genetic abnormalities, toxic metabolic conditions, like Fetal Alcohol Syndrome, and blockage of the growth of the Corpus Callosum by something like a cyst in the fetus. A few names of disorders are Agenisis of the Corpus Callosum, Hypoplasia, and Dysgenesis. Many people with an abnormal Corpus Callosum live completely healthy lives, while others may need medication through their lifetime. A person with a CC disorder may have Epilepsy, a slow down in reaching the milestones of development (crawling, walking, talking, etc.), and frequent migrane headaches. With medication or other therapy, person suffering from a CC disorder can lead completely normal lives.

File:Callosum.jpg

Admin — Wed, 09 Apr 2008 14:32:35 GMT

Admin:

Corpus callosum

Admin — Wed, 09 Apr 2008 14:31:26 GMT

Admin: added embedded image

[[Category:Brain areas]]

[[Image:Callosum.gif|thumb|200pxl|The corpus callosum in a human brain.]]

The Corpus Callosum, which contains more than 200 million nerve fibers, connects the left and the right hemispheres of the brain. It is the largest pathway in the human brain and runs right down the middle. When it comes to communication between both hemispheres, the corpus callosum is the main pathway used. Communication is needed when the body needs to coordinate movement or create complex thoughts and ideas. There are other smaller pathways the brain also uses to communicate between hemispheres, but the Corpus Callosum is the most important. The next main pathway is the Anterior Commisure, but it contains a mere 50,000 nerve fibers as compared to the 200 million of the Corpus Callosum.

As the human body develops, so does the Corpus Callosum. The actual structure of the Corpus Callosum finishes developing between 12 and 16 weeks in utero; however, although the structure has finised growing, the fibers in it continue to become more effective and efficient as one grows into an adolescent. By the age of 12, the Corpus Callosum will funtction just as well as it will in adulthood.

The Corpus Callosum does not complete growth in all people. In some developmental cases, the fibers will not completely connect the two hemispheres. This occurs in utero, and if the pathway is not created during prenatal development, it never will develop correctly. Some people are also born completely without a Corpus Callosum.These disorders can be a result of prenatal infections or viruses, genetic abnormalities, toxic metabolic conditions, like Fetal Alcohol Syndrome, and blockage of the growth of the Corpus Callosum by something like a cyst in the fetus. A few names of disorders are Agenisis of the Corpus Callosum, Hypoplasia, and Dysgenesis. Many people with an abnormal Corpus Callosum live completely healthy lives, while others may need medication through their lifetime. A person with a CC disorder may have Epilepsy, a slow down in reaching the milestones of development (crawling, walking, talking, etc.), and frequent migrane headaches. With medication or other therapy, person suffering from a CC disorder can lead completely normal lives.

File:Callosum.gif

Admin — Wed, 09 Apr 2008 14:30:31 GMT

Admin:

User talk:Kmcastino

Admin — Wed, 09 Apr 2008 14:28:52 GMT

Admin:

== Good start! ==

Looks like you were able to start your pages off - good! Let me know if you need any help. [[User:Admin|Dr. St. John]] 13:01, 8 February 2008 (EST)

== Suggestions ==

Kelly, glad to see you've got even more online now. The Alzheimer's Disease article can certainly be expanded, although you may want to wait until we get to that topic in a couple of weeks. Try using subheadings to organize your articles (see me if you don't know how). For the Palmeri article, it may help to import some of the figures from that paper. [[User:Admin|Dr. St. John]] 06:34, 27 March 2008 (EST)

== Paul Broca Picture ==

Kelly, I added your picture to the [[Paul Broca]] article. Go to that page and use the edit tab to see how I did it. [[User:Admin|Dr. St. John]] 10:25, 9 April 2008 (EDT)

== Subheadings ==

You had trouble with subheadings on the Palmeri article page. Subheadings are made like this:

<nowiki>== Subheadings ==</nowiki>

I fixed it on that page, you can now add them to your other pages if you choose.

[[User:Admin|Dr. St. John]] 10:28, 9 April 2008 (EDT)

Palmeri et al. (2002)

Admin — Wed, 09 Apr 2008 14:27:34 GMT

Admin: fixed subheadings for Kelly

[[Category:Synesthesia Symposium]]

==Participant==

Participant was WO, an adult male who has experienced lexical synesthesia since early childhood. WO's mother, maternal grandfather and maternal great uncle all experienced synethesia.Lexical synesthesia is when achromatic words (black, white, grey) and numbers reliably appear colored. During synesthesia there is a binding of color to visual forms.

==Procedure==
First,Palmeri et al (2002) tested WO's color associations with a list of 100 common monosyllabic words. He was tested twice; the sessions were separated by moren than a month. WO was 97 percent consistent across the two trials. Then the researchers tested WO's synesthesia elicited by local and global forms. For instance, out of small 2s the researchers made a 5. The synethesia person could either see the small 2s (local) or the large 5(global). In synesthesia from motion-defined stimuli, WO was able to identify the digit and saw the associated color for each of the digits. In synesthesia from binocularly defined stimuli, Palmeri et al. (2002) created individual digits by using random-dot stereograms, the digit was visible because of the disparity between the dots using 3D red/green glasses. Results from the stroop interference was significantly slowed for WO when the ink colors were incongruent with the synesthetic colors. In tests were WO had to pick out a 2 in a number of 5s, WO was able to pick out the 2 because it "popped out" to him. But when WO had to pick out the 8 among 6s, WO had a harder time because the synesthetic color for 6s and 8s was a similar blusih color. One conclusion from this paper is that "binding in lexical synethesia occurs during central visual processing and not during later more conceptual processing" (Palmeri et al, 4130). The results were consistent with previous research by Similek et al. and Ramachandran and Hubbard.

Alzheimer's Disease

Admin — Wed, 09 Apr 2008 14:26:40 GMT

Admin: fixed formatting

[[Category:Neuropsychological syndromes]]

Someone develops Alzheimer's Disease every 71 seconds. Alzheimer's Disease is a progessive neuro de-generative disorder that accelerates cell loss. In recent years researchers have found that exercise improves memory,concentration, and abstract reasoning among older adults, and may even delay the onset of Alzheimer's disease. Aerobic exercise increases blood flow to the brain which nourishes brain cells and allows them to function more effectively. A recent study showed that exercise actually promotes the growth of new neurons(brain cells) in the hippocampus--the part of the brain that controls memory and learning. Scientists previously believed that once brain cells died, they were not replaced. According to previous research, chemicals, obesity, and smoking have all been linked to Alzheimer's. People who described themselves as goal-oriented and able to control impulses were less likely to develop Alzheimer's Disease according to a study of 997 people. Baby monkeys exposed to lead showed Alzheimer's like symptoms including amyloid plague, years later, according to a recent study. At the University of Alabama at Birmingham, mice who drank the equivalent of five sodas a day for six months did worse on memory tasks than those who drank water. The mice that had sodas had more than twice the amyloid plaque in their brains (which is a sign of Alzheimer's) than the others.The treatment costs of Alzheimer's Disease(AD) in the United States is estimated to be 100 billion. AD is the fourth common cause of death after heart disease, cancer and stroke. The neurobehavioral hallmark of probable AD is a gradual onset and continuous cognitive decline. The neuropathology of AD can only be confirmed by biopsy or autospy which includes the presence of neurofibillary tangles and amyloid or senile plaques. They occur in normal elderly persons but they occur in much larger numbers throughout the brains of AD patients and affect the functioning of the hippocampi. The brains of AD victims also have large numbers of granulovascuolar organelles which are small clusters of dead brain cell material that collect in the neurons in the hippocampi. Atrophy or shriveled cortex or shrunken cortex is a sign of dead nuerons that are present in Alzheimer's Disease.

Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques and tangles were among the abnormalities that Dr. Alois Alzheimer saw in the brain of Auguste D., although he called them different names.

* Plaques build up between nerve cells. They contain deposits of a protein fragment called beta-amyloid (BAY-tuh AM-uh-loyd). Tangles are twisted fibers of another protein called tau (rhymes with “wow”).

* Tangles form inside dying cells. Though most people develop some plaques and tangles as they age, those with Alzheimer’s tend to develop far more. The plaques and tangles tend to form in a predictable pattern, beginning in areas important in learning and memory and then spreading to other regions.

Scientists are not absolutely sure what role plaques and tangles play in Alzheimer’s disease. Most experts believe they somehow block communication among nerve cells and disrupt activities that cells need to survive.

At a scientific meeting in November 1906, German physician Alois Alzheimer presented the case of “Frau Auguste D.,” a 51-year-old woman brought to see him in 1901 by her family. Auguste had developed problems with memory, unfounded suspicions that her husband was unfaithful, and difficulty speaking and understanding what was said to her. Her symptoms rapidly grew worse, and within a few years she was bedridden. She died in Spring 1906, of overwhelming infections from bedsores and pneumonia.

Dr. Alzheimer had never before seen anyone like Auguste D., and he gained the family’s permission to perform an autopsy. In Auguste’s brain, he saw dramatic shrinkage, especially of the cortex, the outer layer involved in memory, thinking, judgment and speech. Under the microscope, he also saw widespread fatty deposits in small blood vessels, dead and dying brain cells, and abnormal deposits in and around cells.

The condition entered the medical literature in 1907, when Alzheimer published his observations about Auguste D. In 1910, Emil Kraepelin, a psychiatrist noted for his work in naming and classifying brain disorders, proposed that the disease be named after Alzheimer.

User talk:Kmcastino

Admin — Wed, 09 Apr 2008 14:25:17 GMT

Admin:

Paul Broca

Admin — Wed, 09 Apr 2008 14:24:18 GMT

Admin:

[[Category:Neuropsychological profiles]]

[[Image:PaulBroca.jpg|thumb|200px|Paul Broca]]
Pierre Paul Broca (June 28, 1824 – July 9, 1880) was a French physician, anatomist, and anthropologist. He was born in Sainte-Foy-la-Grande, France.

Broca advanced the science of cranial anthropometry by developing many new types of measuring instruments (craniometers) and numerical indices. The uses that reputable scientists, including racist ones, made of Broca's measurements and conclusions have been analyzed by Stephen Jay Gould in The Mismeasure of Man (1981) and by his biographer, Francis Schiller. Broca's work is also featured in Carl Sagan's book Broca's Brain.

Early on in life in his native France, at the tender age of 17 he started his monumental life as a prosector and he eventually became Secretary of the Societé-Anatomique. As a neurological clinician but also as a researcher, he wrote effusively- well over 500 presentations (none ever considered mediocre). A classic 900 page monograph on aneurysms came forth from his gifted pen and he even experimented with hypnotism on a series of surgical cases. Even with considerably opposition, he helped introduce the microscope in the diagnosis of cancer. But he is best known amongst so many other accomplishments for his contribution to neurology the concept of functional localization by cerebral convolution. And with his aged father looking on with silent admiration in a memorable meeting in 1862 he demonstrated the brain lesion of his first patient who had suffered from aphémie (renamed aphasia later by Armand Trousseau (1801-1867)). From this presentation and from other ongoing observations he concluded that the integrity of the left frontal convolution was responsible and necessary for articular speech (David Ferrier 1843-1928) is responsible for naming this region "Broca’s convolution- the motor speech area."

Paul Broca's patient was Monsieur LeBorgne. Tan. Tan was only able to say the word "Tan." He is also responsible for the study of Aphasia known as Broca's aphasia. In a patient with Broca's aphasia, words like "in" "and" "but" "above" "about" and "so on" are often omitted. There is also telegraphic speech. There is difficulties in language production (especially of novel utterances). May be able to use well practiced expressions without obvious difficulty and may be able to sing well known songs. Broca's area is located in the left frontal lobe just forward from the primary motor cortex on the posterior surface of the 3rd frontal gyrus, encompassing Brodman's 44 and part of area 6. Non-fluent speech but articulation is good. Speech is often slow, deliberte and effortful and may have only a very simple grammatical structure. When PET is used to examine resting brain function, patients with Broca's aphasia show underactivation in left frontal regions.

Paul Broca discovered that speech was impaired following damage to the posterior portion of the third convolution of the left frontal lobe(often called Broca's area). Broca's aphasia is known as expressive, nonfluent, or motor aphasia. The degree of speech loss highly correlates to the degree of oral apraxia. Apraxia refers to a difficulty miming or performing learned motor skills on command. Patients severely affected with oral apraxia may be unable to poke their tongue out or whistle on verbal command or in imitation of the examinar. Tan was found at postmortem to have a lesion of the third frontal gyrus. The right hand is often paralyzed because the lesion that causes Broca's aphasia may also encroach on the motor strip for the hand. The major feature of Broca's aphasia is severe nonfluency of speech, which may be extreme to render the patient mute. Speech is often limited to a few stereotyped expressions and expletives. Often the comprehension of numbers and symbols is also impaired. Their non-verbal memory is good; they have no difficulty recognizing doctors and other caregivers and they can follow a simple schedule. They are also emotionally fragile and easily angered or brought to tears.

Paul Broca

Admin — Wed, 09 Apr 2008 14:24:01 GMT

Admin:

[[Category:Neuropsychological profiles]]

[[Image:PaulBroca.jpg|thumb|300px|Paul Broca]]
Pierre Paul Broca (June 28, 1824 – July 9, 1880) was a French physician, anatomist, and anthropologist. He was born in Sainte-Foy-la-Grande, France.

Broca advanced the science of cranial anthropometry by developing many new types of measuring instruments (craniometers) and numerical indices. The uses that reputable scientists, including racist ones, made of Broca's measurements and conclusions have been analyzed by Stephen Jay Gould in The Mismeasure of Man (1981) and by his biographer, Francis Schiller. Broca's work is also featured in Carl Sagan's book Broca's Brain.

Early on in life in his native France, at the tender age of 17 he started his monumental life as a prosector and he eventually became Secretary of the Societé-Anatomique. As a neurological clinician but also as a researcher, he wrote effusively- well over 500 presentations (none ever considered mediocre). A classic 900 page monograph on aneurysms came forth from his gifted pen and he even experimented with hypnotism on a series of surgical cases. Even with considerably opposition, he helped introduce the microscope in the diagnosis of cancer. But he is best known amongst so many other accomplishments for his contribution to neurology the concept of functional localization by cerebral convolution. And with his aged father looking on with silent admiration in a memorable meeting in 1862 he demonstrated the brain lesion of his first patient who had suffered from aphémie (renamed aphasia later by Armand Trousseau (1801-1867)). From this presentation and from other ongoing observations he concluded that the integrity of the left frontal convolution was responsible and necessary for articular speech (David Ferrier 1843-1928) is responsible for naming this region "Broca’s convolution- the motor speech area."

Paul Broca's patient was Monsieur LeBorgne. Tan. Tan was only able to say the word "Tan." He is also responsible for the study of Aphasia known as Broca's aphasia. In a patient with Broca's aphasia, words like "in" "and" "but" "above" "about" and "so on" are often omitted. There is also telegraphic speech. There is difficulties in language production (especially of novel utterances). May be able to use well practiced expressions without obvious difficulty and may be able to sing well known songs. Broca's area is located in the left frontal lobe just forward from the primary motor cortex on the posterior surface of the 3rd frontal gyrus, encompassing Brodman's 44 and part of area 6. Non-fluent speech but articulation is good. Speech is often slow, deliberte and effortful and may have only a very simple grammatical structure. When PET is used to examine resting brain function, patients with Broca's aphasia show underactivation in left frontal regions.

Paul Broca discovered that speech was impaired following damage to the posterior portion of the third convolution of the left frontal lobe(often called Broca's area). Broca's aphasia is known as expressive, nonfluent, or motor aphasia. The degree of speech loss highly correlates to the degree of oral apraxia. Apraxia refers to a difficulty miming or performing learned motor skills on command. Patients severely affected with oral apraxia may be unable to poke their tongue out or whistle on verbal command or in imitation of the examinar. Tan was found at postmortem to have a lesion of the third frontal gyrus. The right hand is often paralyzed because the lesion that causes Broca's aphasia may also encroach on the motor strip for the hand. The major feature of Broca's aphasia is severe nonfluency of speech, which may be extreme to render the patient mute. Speech is often limited to a few stereotyped expressions and expletives. Often the comprehension of numbers and symbols is also impaired. Their non-verbal memory is good; they have no difficulty recognizing doctors and other caregivers and they can follow a simple schedule. They are also emotionally fragile and easily angered or brought to tears.

Paul Broca

Admin — Wed, 09 Apr 2008 14:23:02 GMT

Admin:

[[Category:Neuropsychological profiles]]

[[Image:PaulBroca.jpg|thumb|300pxl]]
Pierre Paul Broca (June 28, 1824 – July 9, 1880) was a French physician, anatomist, and anthropologist. He was born in Sainte-Foy-la-Grande, France.

Broca advanced the science of cranial anthropometry by developing many new types of measuring instruments (craniometers) and numerical indices. The uses that reputable scientists, including racist ones, made of Broca's measurements and conclusions have been analyzed by Stephen Jay Gould in The Mismeasure of Man (1981) and by his biographer, Francis Schiller. Broca's work is also featured in Carl Sagan's book Broca's Brain.

Early on in life in his native France, at the tender age of 17 he started his monumental life as a prosector and he eventually became Secretary of the Societé-Anatomique. As a neurological clinician but also as a researcher, he wrote effusively- well over 500 presentations (none ever considered mediocre). A classic 900 page monograph on aneurysms came forth from his gifted pen and he even experimented with hypnotism on a series of surgical cases. Even with considerably opposition, he helped introduce the microscope in the diagnosis of cancer. But he is best known amongst so many other accomplishments for his contribution to neurology the concept of functional localization by cerebral convolution. And with his aged father looking on with silent admiration in a memorable meeting in 1862 he demonstrated the brain lesion of his first patient who had suffered from aphémie (renamed aphasia later by Armand Trousseau (1801-1867)). From this presentation and from other ongoing observations he concluded that the integrity of the left frontal convolution was responsible and necessary for articular speech (David Ferrier 1843-1928) is responsible for naming this region "Broca’s convolution- the motor speech area."

Paul Broca's patient was Monsieur LeBorgne. Tan. Tan was only able to say the word "Tan." He is also responsible for the study of Aphasia known as Broca's aphasia. In a patient with Broca's aphasia, words like "in" "and" "but" "above" "about" and "so on" are often omitted. There is also telegraphic speech. There is difficulties in language production (especially of novel utterances). May be able to use well practiced expressions without obvious difficulty and may be able to sing well known songs. Broca's area is located in the left frontal lobe just forward from the primary motor cortex on the posterior surface of the 3rd frontal gyrus, encompassing Brodman's 44 and part of area 6. Non-fluent speech but articulation is good. Speech is often slow, deliberte and effortful and may have only a very simple grammatical structure. When PET is used to examine resting brain function, patients with Broca's aphasia show underactivation in left frontal regions.

Paul Broca discovered that speech was impaired following damage to the posterior portion of the third convolution of the left frontal lobe(often called Broca's area). Broca's aphasia is known as expressive, nonfluent, or motor aphasia. The degree of speech loss highly correlates to the degree of oral apraxia. Apraxia refers to a difficulty miming or performing learned motor skills on command. Patients severely affected with oral apraxia may be unable to poke their tongue out or whistle on verbal command or in imitation of the examinar. Tan was found at postmortem to have a lesion of the third frontal gyrus. The right hand is often paralyzed because the lesion that causes Broca's aphasia may also encroach on the motor strip for the hand. The major feature of Broca's aphasia is severe nonfluency of speech, which may be extreme to render the patient mute. Speech is often limited to a few stereotyped expressions and expletives. Often the comprehension of numbers and symbols is also impaired. Their non-verbal memory is good; they have no difficulty recognizing doctors and other caregivers and they can follow a simple schedule. They are also emotionally fragile and easily angered or brought to tears.

Paul Broca

Admin — Wed, 09 Apr 2008 14:21:18 GMT

Admin: added image

[[Category:Neuropsychological profiles]]

[[Image:PaulBroca.jpg]]
Pierre Paul Broca (June 28, 1824 – July 9, 1880) was a French physician, anatomist, and anthropologist. He was born in Sainte-Foy-la-Grande, France.

Broca advanced the science of cranial anthropometry by developing many new types of measuring instruments (craniometers) and numerical indices. The uses that reputable scientists, including racist ones, made of Broca's measurements and conclusions have been analyzed by Stephen Jay Gould in The Mismeasure of Man (1981) and by his biographer, Francis Schiller. Broca's work is also featured in Carl Sagan's book Broca's Brain.

Early on in life in his native France, at the tender age of 17 he started his monumental life as a prosector and he eventually became Secretary of the Societé-Anatomique. As a neurological clinician but also as a researcher, he wrote effusively- well over 500 presentations (none ever considered mediocre). A classic 900 page monograph on aneurysms came forth from his gifted pen and he even experimented with hypnotism on a series of surgical cases. Even with considerably opposition, he helped introduce the microscope in the diagnosis of cancer. But he is best known amongst so many other accomplishments for his contribution to neurology the concept of functional localization by cerebral convolution. And with his aged father looking on with silent admiration in a memorable meeting in 1862 he demonstrated the brain lesion of his first patient who had suffered from aphémie (renamed aphasia later by Armand Trousseau (1801-1867)). From this presentation and from other ongoing observations he concluded that the integrity of the left frontal convolution was responsible and necessary for articular speech (David Ferrier 1843-1928) is responsible for naming this region "Broca’s convolution- the motor speech area."

Paul Broca's patient was Monsieur LeBorgne. Tan. Tan was only able to say the word "Tan." He is also responsible for the study of Aphasia known as Broca's aphasia. In a patient with Broca's aphasia, words like "in" "and" "but" "above" "about" and "so on" are often omitted. There is also telegraphic speech. There is difficulties in language production (especially of novel utterances). May be able to use well practiced expressions without obvious difficulty and may be able to sing well known songs. Broca's area is located in the left frontal lobe just forward from the primary motor cortex on the posterior surface of the 3rd frontal gyrus, encompassing Brodman's 44 and part of area 6. Non-fluent speech but articulation is good. Speech is often slow, deliberte and effortful and may have only a very simple grammatical structure. When PET is used to examine resting brain function, patients with Broca's aphasia show underactivation in left frontal regions.

Paul Broca discovered that speech was impaired following damage to the posterior portion of the third convolution of the left frontal lobe(often called Broca's area). Broca's aphasia is known as expressive, nonfluent, or motor aphasia. The degree of speech loss highly correlates to the degree of oral apraxia. Apraxia refers to a difficulty miming or performing learned motor skills on command. Patients severely affected with oral apraxia may be unable to poke their tongue out or whistle on verbal command or in imitation of the examinar. Tan was found at postmortem to have a lesion of the third frontal gyrus. The right hand is often paralyzed because the lesion that causes Broca's aphasia may also encroach on the motor strip for the hand. The major feature of Broca's aphasia is severe nonfluency of speech, which may be extreme to render the patient mute. Speech is often limited to a few stereotyped expressions and expletives. Often the comprehension of numbers and symbols is also impaired. Their non-verbal memory is good; they have no difficulty recognizing doctors and other caregivers and they can follow a simple schedule. They are also emotionally fragile and easily angered or brought to tears.

User talk:Prea

Admin — Thu, 27 Mar 2008 11:39:08 GMT

Admin: /* Nice Edit */

==Nice Edit==

Prea, your edit to [[Wada test]] looks nice! I made a few formatting changes to pretty it up a bit; take a look. [[User:Admin|Dr. St. John]] 11:30, 19 March 2008 (EST)

== Hemiplegia ==

I like the figure you found for [[Hemiplegia]]. Looks good. I organized the Resources part so it looks a little better. [[User:Admin|Dr. St. John]] 06:39, 27 March 2008 (EST)

Hemiplegia

Admin — Thu, 27 Mar 2008 11:38:00 GMT

Admin: fixed resources

[[Category:Neuropsychological syndromes]]

Hemiplegia describes the condition of a brain damaged individual who is unable to intentionally move parts of his or her body on the side opposite that of the brain damage. Hemplegia usually occurs as a result of a loss of blood supply in the mid-cerebral artery due to aneurysm, hemorrhage, or clot. It may also be caused by a head injury, epilespy, and/or tumor. In addtion, damage to subcortical structures, such as the basal ganglia, may result in hemplegia, since such structures are often served by the mid-cerebral artery.

[[Image:Example.jpg]] http://www.humanillnesses.com/original/images/hdc_0001_0003_0_img0192.jpg

== Resources ==

*[http://www.ninds.nih.gov/disorders/alternatinghemiplegia/alternatinghemiplegia.htm NIH site]
*[http://www.wisegeek.com/what-are-some-causes-of-hemiplegia.htm Online encyclopedia site]
*Stirling, John. Introducing Neuropsychology
*Ogden, Jenni A. Fractured Minds: A Case Study Approach to Clincial Neuropsychology

User talk:Carson3816

Admin — Thu, 27 Mar 2008 11:35:59 GMT

Admin:

== Good Work ==

Good work on your edits. I really like that you found a picture of Luria. He looks like a friendly guy! [[User:Admin|Dr. St. John]] 06:35, 27 March 2008 (EST)

User talk:Kmcastino

Admin — Thu, 27 Mar 2008 11:34:20 GMT

Admin: /* Good start! */

User talk:Prea

Admin — Wed, 19 Mar 2008 16:30:10 GMT

Admin:

==Nice Edit==

Prea, your edit to [[Wada test]] looks nice! I made a few formatting changes to pretty it up a bit; take a look. [[User:Admin|Dr. St. John]] 11:30, 19 March 2008 (EST)

Wada test

Admin — Wed, 19 Mar 2008 16:29:14 GMT

Admin: cleaned up apostrophes

[[Category:Neuropsychological methods]]

== Overview ==

[[Image:wada.jpg|right]]
The Wada Test, officially referred to as the intracarotid sodium amobarbital procedure or ISAP, is named after Dr. Juhn E. Wada, the first physician who performed it. It is used to determine localization, that is which functions are located in which part of the brain. The test consists of administering a drug, sodium amytal, to the internal carotid artery one hemisphere at a time, thereby inducing a temporary lesion lasting only a few minutes. Before injecting the drug, the patient is given tests measuring his or her abilities in speech, object naming, and memory. While one hemisphere is anesthetized, the neuropsychologist then tests the other hemisphere to evaluate how well it manages speech, naming, and memory.

== Tests ==

The tests used for the Wada procedure vary depending on the center. The Montreal Neurological Instituted technique, however, can be used as a guide on the types of tests given and how the results are used. Memory tests usually consist in showing the patient five items that test both his or her verbal and visual memory. For example, the patient may be asked to memorize two pictures of an object, an actual object, a word, and then a sentence. After the anesthetic wears off, the patient will be asked to recall or choose among a number of items, the original five items shown when only one hemisphere was awake. If the majority of items cannot be remembered, the temporal lobe and hippocampus that stayed awake cannot mediate memory. This information is important because if temporal lobe needs to be removed, for a person with epilepsy for example, the removal would not cause a problem since this lobe is already known to be dysfunctional. Likewise if the other hemisphere was the one with the epileptic focus, removing that temporal lobe and the hippocampus may cause amnesia in the individual.

== Modern Uses of the Wada Test ==

Functional MRI (fMRI) has increasingly been taking the place of the Wada test, which can be more invasive and less accurate. The fMRI, on the other hand, has been used to directly visualize the origin of seizures and to detect blood flow changes. The Wada procedure, however, does not usually cause long term problems and for a person who suffers from constant seizures, completing the Wada procedure successfully can be life-changing.

== Difference in Brain Organization between Right and Left-Handers? ==

The Wada Test put to rest the belief that the left hander's brain was the mirror image of the right hander's brain. Results from the test showed the pattern of lateralization found in most right-handers was the same in about 70% of left-handers. Of the 30% remaining, half showed the opposite pattern (known as reversed asymmetry) and the other half showed language and spatial skills distributed in both hemispheres (referred to as bi-lateral distribution).

== Resources ==

*http://www.epilepsy.com/epilepsy/surgery_wada
*http://www-personal.umich.edu/~gusb/wadadesc.html
*Stirling, John. Introducing Neuropsychology
*Ogden, Jenni A. Fractured Minds: A Case Study Approach to Clincial Neuropsychology.

Wada test

Admin — Wed, 19 Mar 2008 16:28:43 GMT

Admin: put picture to right and fixed Resources list

[[Category:Neuropsychological methods]]

== Overview ==

[[Image:wada.jpg|right]]
The Wada Test, officially referred to as the intracarotid sodium amobarbital procedure or ISAP, is named after Dr. Juhn E. Wada, the first physician who performed it. It is used to determine localization, that is which functions are located in which part of the brain. The test consists of administering a drug, sodium amytal, to the internal carotid artery one hemisphere at a time, thereby inducing a temporary lesion lasting only a few minutes. Before injecting the drug, the patient is given tests measuring his or her abilities in speech, object naming, and memory. While one hemisphere is anesthetized, the neuropsychologist then tests the other hemisphere to evaluate how well it manages speech, naming, and memory.

== Tests ==

The tests used for the Wada procedure vary depending on the center. The Montreal Neurological Instituted technique, however, can be used as a guide on the types of tests given and how the results are used. Memory tests usually consist in showing the patient five items that test both his or her verbal and visual memory. For example, the patient may be asked to memorize two pictures of an object, an actual object, a word, and then a sentence. After the anesthetic wears off, the patient will be asked to recall or choose among a number of items, the original five items shown when only one hemisphere was awake. If the majority of items cannot be remembered, the temporal lobe and hippocampus that stayed awake cannot mediate memory. This information is important because if temporal lobe needs to be removed, for a person with epilepsy for example, the removal would not cause a problem since this lobe is already known to be dysfunctional. Likewise if the other hemisphere was the one with the epileptic focus, removing that temporal lobe and the hippocampus may cause amnesia in the individual.

== Modern Uses of the Wada Test ==

Functional MRI (fMRI) has increasingly been taking the place of the Wada test, which can be more invasive and less accurate. The fMRI, on the other hand, has been used to directly visualize the origin of seizures and to detect blood flow changes. The Wada procedure, however, does not usually cause long term problems and for a person who suffers from constant seizures, completing the Wada procedure successfully can be life-changing.

== Difference in Brain Organization between Right and Left-Handers? ==

The Wada Test put to rest the belief that the left handerâ��s brain was the mirror image of the right handerâ��s brain. Results from the test showed the pattern of lateralization found in most right-handers was the same in about 70% of left-handers. Of the 30% remaining, half showed the opposite pattern (known as reversed asymmetry) and the other half showed language and spatial skills distributed in both hemispheres (referred to as bi-lateral distribution).

== Resources ==

*http://www.epilepsy.com/epilepsy/surgery_wada
*http://www-personal.umich.edu/~gusb/wadadesc.html
*Stirling, John. Introducing Neuropsychology
*Ogden, Jenni A. Fractured Minds: A Case Study Approach to Clincial Neuropsychology.

Wada test

Admin — Wed, 19 Mar 2008 16:25:07 GMT

Admin: moved picture to our site

[[Category:Neuropsychological methods]]

== Overview ==

The Wada Test, officially referred to as the intracarotid sodium amobarbital procedure or ISAP, is named after Dr. Juhn E. Wada, the first physician who performed it. It is used to determine localization, that is which functions are located in which part of the brain. The test consists of administering a drug, sodium amytal, to the internal carotid artery one hemisphere at a time, thereby inducing a temporary lesion lasting only a few minutes. Before injecting the drug, the patient is given tests measuring his or her abilities in speech, object naming, and memory. While one hemisphere is anesthetized, the neuropsychologist then tests the other hemisphere to evaluate how well it manages speech, naming, and memory.

== Tests ==

The tests used for the Wada procedure vary depending on the center. The Montreal Neurological Instituted technique, however, can be used as a guide on the types of tests given and how the results are used. Memory tests usually consist in showing the patient five items that test both his or her verbal and visual memory. For example, the patient may be asked to memorize two pictures of an object, an actual object, a word, and then a sentence. After the anesthetic wears off, the patient will be asked to recall or choose among a number of items, the original five items shown when only one hemisphere was awake. If the majority of items cannot be remembered, the temporal lobe and hippocampus that stayed awake cannot mediate memory. This information is important because if temporal lobe needs to be removed, for a person with epilepsy for example, the removal would not cause a problem since this lobe is already known to be dysfunctional. Likewise if the other hemisphere was the one with the epileptic focus, removing that temporal lobe and the hippocampus may cause amnesia in the individual.

[[Image:wada.jpg]]

== Modern Uses of the Wada Test ==

Functional MRI (fMRI) has increasingly been taking the place of the Wada test, which can be more invasive and less accurate. The fMRI, on the other hand, has been used to directly visualize the origin of seizures and to detect blood flow changes. The Wada procedure, however, does not usually cause long term problems and for a person who suffers from constant seizures, completing the Wada procedure successfully can be life-changing.

== Difference in Brain Organization between Right and Left-Handers? ==

The Wada Test put to rest the belief that the left hander’s brain was the mirror image of the right hander’s brain. Results from the test showed the pattern of lateralization found in most right-handers was the same in about 70% of left-handers. Of the 30% remaining, half showed the opposite pattern (known as reversed asymmetry) and the other half showed language and spatial skills distributed in both hemispheres (referred to as bi-lateral distribution).

== Resources ==

http://www.epilepsy.com/epilepsy/surgery_wada
http://www-personal.umich.edu/~gusb/wadadesc.html
Stirling, John. Introducing Neuropsychology
Ogden, Jenni A. Fractured Minds: A Case Study Approach to Clincial Neuropsychology.

File:Wada.jpg

Admin — Wed, 19 Mar 2008 16:24:29 GMT

Admin:

User talk:Ktreynolds

Admin — Thu, 06 Mar 2008 21:29:04 GMT

Admin:

Kaitlin,

Thanks for getting started! Let me know if you need any help. [[User:Admin|Dr. St. John]] 16:29, 6 March 2008 (EST)

User talk:Mnguyen

Admin — Thu, 28 Feb 2008 20:35:54 GMT

Admin:

Mai-han,

Thanks for getting started! [[User:Admin|Dr. St. John]] 15:35, 28 February 2008 (EST)

Main Page

Admin — Wed, 20 Feb 2008 17:49:02 GMT

Admin: /* Your Assignment */

==PSY 324-2 Neuropsychology==

These pages are for the Spring, 2008 Neuropsychology class at Rollins College. You must be a member of the class to create an account, and you must have an account in order to edit the pages.

==First Steps==

Your first assignment is to create a user account and to edit your user page.

*[[Special:Userlogin|Create Your Account]] - you may select anything for your user name
*Edit your user page - up in the upper right corner (for Firefox users; upper left for IE users - but use Firefox if you have it), you will see your new user name with a little icon of a person next to it. It will be red. Click it. This takes you to your user page. Edit the page (click the Edit tab at the top) and type in your real name and anything else you wish. (Check out [[User:Admin |my user page]] for reference.)

==Your Assignment==

You will be assigned:

*One [[:Category:Neuropsychological syndromes|syndrome]]
*One [[:Category:Neuropsychological methods|method or test]]
*One [[:Category:Neuropsychological profiles|profile of a neuropsychologist or famous case]]
*One [[:Category:Brain areas|brain region of interest]]

and will contribute an article on each of these. In addition, you will be responsible (as a team) to do one write-up of a symposium article and presentation (either the [[:Category:Plasticity Symposium|Plasticity Symposium]] or the [[:Category:Synesthesia Symposium|Synesthesia Symposium]]).

===To start an article===

Select from the links above to see a list of all syndromes, methods, scientists, and brain areas. Select from the list the one you were assigned and begin editing. For the most part, what you type in the edit window is what you will get. If you'd like help with any of the more advanced features (creating titles, bold text, uploading images, etc.), see me.

The good thing about a wiki is you can easily continue to edit your articles throughout the semester.

===Other responsibilities===

It is also permissible (and encouraged) to make small contributions to other people's articles, whether it be fixing minor typos, providing links to your article or other articles as appropriate, or even adding unique content. All contributions on a wiki are logged, so I will be able to credit all of your contributions.

Main Page

Admin — Wed, 20 Feb 2008 17:43:49 GMT

Admin: added symposium links

==PSY 324-2 Neuropsychology==

These pages are for the Spring, 2008 Neuropsychology class at Rollins College. You must be a member of the class to create an account, and you must have an account in order to edit the pages.

==First Steps==

Your first assignment is to create a user account and to edit your user page.

*[[Special:Userlogin|Create Your Account]] - you may select anything for your user name
*Edit your user page - up in the upper right corner (for Firefox users; upper left for IE users - but use Firefox if you have it), you will see your new user name with a little icon of a person next to it. It will be red. Click it. This takes you to your user page. Edit the page (click the Edit tab at the top) and type in your real name and anything else you wish. (Check out [[User:Admin |my user page]] for reference.)

==Your Assignment==

You will be assigned:

*One [[:Category:Neuropsychological syndromes|syndrome]]
*One [[:Category:Neuropsychological methods|method or test]]
*One [[:Category:Neuropsychological profiles|profile of a neuropsychologist or famous case]]
*One [[:Category:Brain areas|brain region of interest]]

and will contribute an article on each of these. In addition, you will be responsible (as a team) to do one write-up of a symposium article and presentation (either the [[:Category:Plasticity Symposium|Plasticity Symposium]] or the [[:Category:Synesthesia Symposium|Synesthesia symposium]]).

===To start an article===

Select from the links above to see a list of all syndromes, methods, scientists, and brain areas. Select from the list the one you were assigned and begin editing. For the most part, what you type in the edit window is what you will get. If you'd like help with any of the more advanced features (creating titles, bold text, uploading images, etc.), see me.

The good thing about a wiki is you can easily continue to edit your articles throughout the semester.

===Other responsibilities===

It is also permissible (and encouraged) to make small contributions to other people's articles, whether it be fixing minor typos, providing links to your article or other articles as appropriate, or even adding unique content. All contributions on a wiki are logged, so I will be able to credit all of your contributions.

Speling et al. (2006)

Admin — Wed, 20 Feb 2008 17:42:10 GMT

Admin:

[[Category:Synesthesia Symposium]]

Aleman et al. (2001)

Admin — Wed, 20 Feb 2008 17:41:45 GMT

Admin:

[[Category:Synesthesia Symposium]]

Nikolic et al. (2007)

Admin — Wed, 20 Feb 2008 17:41:25 GMT

Admin:

[[Category:Synesthesia Symposium]]

Kim et al. (2006)

Admin — Wed, 20 Feb 2008 17:41:05 GMT

Admin:

[[Category:Synesthesia Symposium]]

Palmeri et al. (2002)

Admin — Wed, 20 Feb 2008 17:40:34 GMT

Admin:

[[Category:Synesthesia Symposium]]

Witthoft and Winawer (2006)

Admin — Wed, 20 Feb 2008 17:40:13 GMT

Admin:

[[Category:Synesthesia Symposium]]

Category:Synesthesia Symposium

Admin — Wed, 20 Feb 2008 17:39:46 GMT

Admin:

Articles presented during the Synesthesia Symposium (March 24-26).

Hancock et al. (2006)

Admin — Wed, 20 Feb 2008 17:38:14 GMT

Admin:

[[Category:Synesthesia Symposium]]

Ptito et al. (2005)

Admin — Wed, 20 Feb 2008 17:37:25 GMT

Admin:

[[Category:Plasticity Symposium]]

Cohen et al. (1997)

Admin — Wed, 20 Feb 2008 17:37:02 GMT

Admin:

[[Category:Plasticity Symposium]]

Hamilton et al. (2000)

Admin — Wed, 20 Feb 2008 17:36:42 GMT

Admin:

[[Category:Plasticity Symposium]]

Sadato et al. (1996)

Admin — Wed, 20 Feb 2008 17:36:24 GMT

Admin:

[[Category:Plasticity Symposium]]